Acute Kidney Injury BMJ

Acute kidney injury
Straight to the point of care
Last updated: Mar 05, 2020

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Risk factors 4
Aetiology 7
Pathophysiology 7
Classification 8
Case history 8
Diagnosis 10
Recommendations 10
History and exam 28
Investigations 34
Differentials 47
Criteria 48
Management 50
Recommendations 50
Treatment algorithm overview 74
Treatment algorithm 76
Emerging 119
Primary prevention 119
Secondary prevention 120
Patient discussions 120
Follow up 122
Monitoring 122
Complications 123
Prognosis 124
Guidelines 125
Diagnostic guidelines 125
Treatment guidelines 125
Evidence tables 127
References 131
Disclaimer 142
Acute kidney injury Overview
Summary
Commonly associated with sepsis, hypovolaemia, and/or hypotension (pre-kidney AKI and intrinsic AKI);
nephrotoxins such as aminoglycoside antibiotics (e.g., gentamicin), intravenous iodinated contrast, ethylene
OVERVIEW
glycol, or rarer forms of AKI such as vasculitis or interstitial nephritis (intrinsic AKI); or urinary outflow
obstruction (post-kidney AKI).
Usually occurs in patients with intercurrent illness, without symptoms or signs specific to the kidneys, and is
only diagnosed when kidney function tests are performed. Patients may present in many different ways (e.g.,
with sepsis, hypotension, decreased urine output, lower urinary tract symptoms, or oedema).
Suspect AKI when there is an acute rise in serum creatinine and/or a fall in urine output. More severe AKI
can be complicated by hyperkalaemia and acidaemia along with uraemic encephalopathy or pericarditis.
Pulmonary oedema can also occur in patients with AKI secondary to obstructive uropathy or renal artery
stenosis (flash pulmonary oedema) but is usually iatrogenic due to over-enthusiastic fluid resuscitation.
The mainstay of management is supportive care, with treatment of the underlying cause. Give particular
attention to the prompt treatment of sepsis, optimisation of volume status, correction of acidaemia or
electrolyte complications, avoidance of nephrotoxins, and relief of any obstruction.
Renal replacement therapy may be needed for severe AKI with complications that do not respond to medical
management.
Prompt recognition and treatment is important; AKI occurs in 10% to 20% of emergency admissions and has
an inpatient mortality >20% (>35% for stage 3 AKI).
Definition
Acute kidney injury (AKI), previously known as acute renal failure (ARF), is an acute decline in kidney
function, leading to a rise in serum creatinine and/or a fall in urine output.[1] The change in terminology
emphasises that kidney injury presents as a disease spectrum from mild kidney injury to severe kidney
failure.[1] [2] [3] A standardised definition is important to facilitate clinical care and research.[4] AKI may
be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction,
or intrinsic kidney disease. The resulting effects include impaired clearance and regulation of metabolic
homeostasis, altered acid/base and electrolyte regulation, and impaired volume regulation.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 05, 2020.
BMJ Best Practice topics are regularly updated and the most recent version
3
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subject to our disclaimer. © BMJ Publishing Group Ltd 2022. All rights reserved.
Acute kidney injury Theory
Epidemiology
The reported incidences of AKI vary, and are confounded by differences in diagnosis, definition criteria,
or hospital discharge coding.[6] [7] UK Renal Registry data, covering a population of 9.1 million people
THEORY
in England over a 3 month period in 2017, produced an annual estimated AKI rate of 10,400 per million
population (95% CI 10,000 to 10,400).[8] AKI is seen in 10% to 20% of people admitted to hospital as
emergencies, with an inpatient mortality >20%.[3] [9] [10] The overall incidence of AKI in the ICU is higher
at 20% to 50% and it is associated with mortality over 50%.[11] [12] There is some evidence to suggest that
AKI is becoming more common, perhaps because of more aggressive medical and surgical interventions in
older patients who are at higher risk of developing AKI as a complication.[13] One study found the incidence
of AKI not requiring dialysis among a large population of hospitalised patients to have increased from 323
to 522 per 100,000 person-years between 1996 and 2003.[14] Prediction scores have been developed for
outcomes of AKI, but have had variable success.[15] [16]
Acute tubular necrosis (ATN) accounts for 45% of cases of AKI. ATN is caused by sepsis in 19% of ICU
patients. Pre-kidney AKI, obstruction, glomerulonephritis, vasculitis, acute interstitial nephritis, acute on
chronic kidney disease and atheroembolic injury account for most of the remainder.[17] [18]
The incidence of contrast nephropathy varies, and is reported to be the third most common cause of AKI in
hospitalised patients. In a study of 7500 patients undergoing percutaneous intervention for coronary artery
disease, 3.3% of all patients experienced AKI, defined as a rise in serum creatinine of 38 micromols/L (0.5
mg/dL) or more, and 25% of patients with a baseline creatinine of at least 153 micromols/L (2.0 mg/dL)
experienced AKI.[19]
Up to 7% of patients hospitalised with AKI require renal replacement therapy.[20] In the ICU, the mortality
rate exceeds 50% in patients with multi-organ failure who require dialysis.[17] [18] [20] Minor rises in
creatinine (≥26.5 micromols/L [0.3 mg/dL]) are associated with an increased risk of hospital mortality,
increased risk of chronic kidney disease, and higher odds of progressing to end-stage kidney failure.
Risk factors
Strong
advanced age
Advanced age is associated with chronic kidney disease, underlying vascular disease of the kidneys,
and other comorbid medical conditions that predispose to AKI.
underlying kidney disease

Associated with increased susceptibility to AKI, particularly contrast-related AKI. Risks increase with
increasing severity of chronic kidney disease.[5]
diabetes mellitus
AKI incidence rates of 9% to 38% have been reported in patients with diabetes and chronic kidney
disease undergoing contrast exposure.[49]
sepsis
May result in acute tubular necrosis, infectious glomerulonephritis, pre-kidney AKI from hypotension, or
drug-induced injury from medicines used in treatment. Highest risk with bacteraemia.
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Mar 05, 2020.
iodinated contrast
Intravenous iodinated contrast has previously been reported to cause contrast-induced AKI.[5]
However, the association has been questioned more recently by large population studies that have
failed to demonstrate this risk.[40] [41] [42] Risk of contrast-induced AKI increases with intra-arterial
THEORY
administration and with increasing volume of contrast medium.[3]
exposure to nephrotoxins (e.g., aminoglycosides, vancomycin + piperacillin-

ta zobactam, cancer therapies, non-steroidal anti-inflammatory drugs, or
ACE inhibitors)
May precede and lead to AKI.[5] [50] [51]
excessive fluid loss

From haemorrhage, vomiting, diarrhoea, or sweating; hospitalised patients may have insufficient
replacement fluids.
surgery
May precede AKI from pre-kidney, intrinsic, or post-kidney causes. Cardiothoracic surgery is
particularly high risk, although off-pump approaches may limit this risk.[52]
haemorrhage
The resulting impaired kidney perfusion supports pre-kidney AKI as cause of AKI or ischaemia
resulting in acute tubular necrosis.
recent vascular intervention

May be associated with atheroembolic injury or contrast-induced AKI.
cardiac arrest
May precede pre-kidney AKI or acute tubular necrosis, especially if there is severe and prolonged
kidney ischaemia.
pancreatitis
There may be severe third spacing of fluid leading to intravascular volume depletion resulting in pre-
kidney failure.
trauma
There may be impaired kidney perfusion causing pre-kidney AKI, rhabdomyolysis predisposing to
pigment-induced injury, or ischaemia causing acute tubular necrosis.
malignant hypertension
Malignant hypertension may cause AKI.[5]
myeloproliferative disorders, such as multiple myeloma

Intratubular precipitation of light chains in times of volume contraction is associated with kidney injury,
especially in cases of contrast exposure with volume contraction in myeloma patients. Hypercalcaemia
predisposes to pre-kidney AKI.[5] [53]
5
connective tissue disease
May present with AKI (e.g., systemic lupus erythematosus, scleroderma, anti-neutrophil cytoplasmic
antibody-associated glomerulonephritis, anti-glomerular basement membrane disease).[5]
THEORY
sodium-retaining states (e.g., congestive heart failure, cirrhosis, nephrotic

syndrome)
Associated with chronic kidney disease, but may present with AKI.[5]
drug overdose
May precede AKI due to direct toxicity, rhabdomyolysis, and volume depletion.
nephrolithiasis
May lead to AKI if significant obstruction is present.
Weak
drug abuse
AKI from nephrotoxicity, ischaemia.
alcohol abuse
Suspect pigment-induced AKI if rhabdomyolysis is present (e.g., after prolonged loss of
consciousness).
excessive exercise
Suspect pigment-induced AKI due to rhabdomyolysis.
recent blood transfusion

AKI may be present from intravascular haemolytic transfusion reaction, deposition of immune
complexes.
malignancy
May lead to post-kidney AKI if mass effect is causing outflow obstruction, or AKI may result in
association with myeloproliferative disorders or chemotherapy-related toxicities (i.e., tumour lysis).
Immune complex glomerulonephritis may result from the malignancy.
genetic susceptibility
There is preliminary evidence that a genetic predisposition for AKI may exist, especially with
apolipoprotein E (APO-E) genes.[47] Genome-wide searches have found other protective candidates,
but much more work is needed to validate these findings.[48]
use of renin-angiotensin system inhibitors

Found to be a predictor of risk of postoperative AKI, but may be a marker rather than a mediator
of risk. It is unclear whether there is any benefit to stopping agents prior to surgery in high-risk
patients.[54]
proton pump inhibitors
Proton pump inhibitors may increase risk of AKI; however, more studies are needed to clarify this
association.[55]
THEORY
herbal therapy
Case reports suggest that herbs and dietary supplements could potentially contribute to kidney
injuries.[56]
Aetiology
Aetiology of AKI may be multifactorial, generally classified into pre-kidney, intrinsic, and post-kidney
causes.[21]
• Pre-kidney AKI can be due to various causes of reduced kidney perfusion, such as hypovolaemia,
haemorrhage, sepsis, third spacing of fluid (such as in severe pancreatitis), overdiuresis, or other
causes of reduced kidney perfusion such as heart failure. Hepatorenal syndrome, a form of pre-kidney
AKI not responsive to fluid administration, is seen in cases of severe liver disease. Renovascular
disease, especially with the recent addition of an ACE inhibitor to a patient with bilateral renal artery
stenosis, is also a consideration, as this sometimes leads to acute tubular necrosis (ATN).
• Intrinsic kidney failure may be multifactorial. ATN, rapidly progressive glomerulonephritis, and
interstitial nephritis are the most common aetiologies. Vascular diseases, including haemolytic
uraemic syndrome, thrombotic thrombocytopenic purpura, scleroderma renal crisis, atheromatous
embolisation, and thrombosis, are also potential causes. Severe ischaemic injury may result in cortical
necrosis.
• Post-kidney AKI results from mechanical obstruction of the urinary outflow tract. Retroperitoneal
fibrosis, lymphoma, tumour, prostate hyperplasia, strictures, renal calculi, ascending urinary infection
(including pyelonephritis), and urinary retention are common causes.
Pathophysiology
Pre-kidney AKI results from impaired kidney perfusion and the changes seen are appropriate physiological
responses. The kidney's response to a lower perfusion pressure is to enhance sodium and water re-
absorption. Baroreceptors in the carotid artery and aortic arch respond to lower blood pressure with
sympathetic stimulation. This, along with vasoconstriction of the glomerular efferent arteriole and dilation
of the afferent arteriole, is intended to maintain glomerular filtration within a relatively narrow range.
Decreasing perfusion promotes activation of the renin/angiotensin/aldosterone system. Angiotensin II,
a potent vasoconstrictor, stimulates aldosterone release, promoting sodium and water resorption at the
collecting duct. Low blood volume is also a stimulus to the hypothalamus promoting antidiuretic hormone
release and increased tubular water re-absorption, concentrating the urine.
Acute tubular necrosis (ATN) due to prolonged or severe ischaemia, the most common form of AKI, is
preceded by impaired kidney perfusion and tissue hypoxaemia, yielding direct microvascular endothelial
injury and tubular ischaemia typically most severe in the early proximal tubule and the outer medullary
segments.[22] [23] Hypoxaemia results in increased reactive oxygen species, reduction in available
adenosine triphosphate, and cellular dysfunction and death.[24] Additionally, complement system activation,
direct neutrophil activation, membrane attack complex activation, cytokines, chemokines, and vasoactive
hormones have been studied and may be contributory.[25] [26] [27] [28] [29] [30] [31] [32] [33] ATN may also
7
result from exposure to drugs, endotoxins, or radiocontrast media. Animal models suggest direct cytotoxic
effects of the contrast as well as vasoconstriction in the kidney resulting in impaired medullary blood flow,
increased viscosity, and hypoxaemia.[34] [35] [36] [37] [38] [39] However, the association with radiocontrast
exposure is controversial, as population studies do not replicate risk.[40] [41] [42]
THEORY
Kidney injury associated with obstruction results from increased intratubular pressure yielding tubular
ischaemia and atrophy. Evidence also suggests injury results from an influx of monocytes and macrophages.
Cytokines, free radicals, proteases, and tumour necrosis factor-beta are released, causing irreversible tubular
injury and fibrosis when obstruction becomes chronic.[43] [44] [45] [46]
There is preliminary evidence that a genetic predisposition for AKI may exist, especially with apolipoprotein E
(APO-E) genes.[47] Genome-wide searches have found other protective candidates, but much more work is
needed to validate these findings.[48]
Classification
Kidney Disease: Improving Global Outcomes (KDIGO) definition of
AKI[1]
Any of the following:
• Increase in serum creatinine by ≥26 micromol/L (≥0.3 mg/dL) within 48 hours; or

• Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred
within the prior 7 days; or
• Urine volume <0.5 mL/kg/hour for 6 hours.
Classification based on pathophysiology[5]

• Pre-kidney (pre-renal) AKI: injury due to impaired kidney perfusion.
• Intrinsic AKI: direct injury to the kidney parenchyma.
• Post-kidney (post-renal) AKI: injury due to urinary outflow obstruction.
Case history
Case history #1
A 65-year-old male smoker with diabetes mellitus, hypertension, dyslipidaemia, and chronic kidney
disease presents with chest pain. ECG changes suggest an acute myocardial infarction. He is taken for
an urgent coronary angiogram. Three days later, he is noticed to have developed an elevated serum
creatinine, oliguria, and hyperkalaemia.
Case history #2
A 35-year-old man with a history of congenital valvular heart disease undergoes a dental procedure
without appropriate antibiotic prophylaxis. Several weeks later, he presents with fever and respiratory
distress. He is intubated, and Streptococcus viridans is isolated in all blood cultures drawn at the time
of admission. Echocardiography demonstrates a mitral valve vegetation. Laboratory tests reveal a rising
serum creatinine and a reduction in urine output. Urinalysis reveals more than 20 white blood cells, more
than 20 red blood cells, and red cell casts. Urine culture is negative. Kidney ultrasound is unremarkable.
THEORY
Serum erythrocyte sedimentation rate is elevated.
Other presentations
Rarer presentations include AKI secondary to:
• Vasculitis
• AKI may be associated with systemic symptoms such as arthralgia, myalgia, and/or rash.
Urinalysis will demonstrate blood and protein.
• Interstitial nephritis
• Patients may present with fever, rash, and/or arthralgia with leucocytes on urinalysis. There
may be a history of a new medication being commenced.
• Atheroembolic injury
• AKI may occur following vascular catheterisation or systemic anticoagulation resulting from
atheroembolic injury.
• Obstruction
• AKI secondary to abdominal masses or an enlarged bladder may be found on examination or

by imaging. Patients may be otherwise asymptomatic.
9
Acute kidney injury Diagnosis
Recommendations
Urgent
Consider the possibility of AKI whenever a patient presents with an acute illness or shows a
deterioration in their early warning scores.[1] [3] [62]
• AKI is easily missed; most patients present asymptomatically, with non-specific symptoms or with
symptoms solely related to the precipitating illness (e.g., sepsis).
• AKI occurs in 10% to 20% of emergency admissionsand has an inpatient mortality >20%
(>35% in stage 3 AKI).[3] [9] [10]
Look for signs of sepsis and manage promptly. [9] [63]
• Perform a septic screen and implement your local care bundle (e.g., Sepsis Six) if infection is
suspected.
Recognise and treat hypovolaemia promptly with an immediate bolus of crystalloid

intravenous fluid. [1] [62] [13] [64]
Stop/avoid exposure to any nephrotoxins (e.g., non-steroidal anti-inflammatory drugs

[NSAIDs], aminoglycoside antibiotics) and to any other agents that may reduce kidney
function (e.g., ACE inhibitors, angiotensin-II receptor antagonists) . [1]
• Review and adjust dosing of all other medications in line with the degree of kidney injury.
Key Recommendations
Definition and staging of AKI
AKI is diagnosed based on an acutely rising serum creatinine and/or reduction in urine
output.[4] [1]
DIAGNOSIS
• AKI can often be non-oliguric.
AKI is present if any one or more of the following criteria is met:[4] [1] [3]
• A rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours
• A rise in serum creatinine to ≥1.5 times baseline, which is known or presumed to have
occurred within the past 7 days (in practice you can use the lowest value from the past 3 months as
the baseline for the patient)[62]
• Urine volume <0.5 ml/kg/hour for at least 6 hours.
Stage the AKI according to the KDIGO staging criteria.[1]
• A higher stage of AKI is associated with a greater risk of death as well as increased likelihood of
needing renal replacement therapy (RRT).[13]
Clinical presentation
AKI is often asymptomatic so a high index of suspicion is vital for prompt recognition and
treatment.[62]
A relevant history is a key part of the assessment. Check for:
• Risk factors: frail, older people are at particular increased risk, especially those with chronic
kidney disease (CKD), heart failure, liver disease, or cognitive impairment.[3] [9] [64] [65]
• Precipitating insults to the kidney: the most common causes of AKI are sepsis,
nephrotoxins, hypovolaemia, and/or hypotension.[62] [13]
Your examination should prioritise volume statusand a sepsis screen.
• Also look for any symptoms and signs that may suggest a specific underlying cause (e.g., fever,
rash, and/or joint pain suggest small-vessel vasculitis or interstitial nephritis).[9] [64]
Causes of AKI
Establish the underlying cause of AKI as this will determine the correct treatment and the need
for onward referral.[5] [17] [52]
The causes of AKI have traditionally been classified as pre-kidney (pre-renal), intrinsic, and post-
kidney (post-renal):[5] [21]
• Pre-kidney AKI(80% of cases) is usually due to hypovolaemia and/or hypotension:[1] [3] [9]
[62]
• Sepsis (e.g., pneumonia, cellulitis)

• Fluid loss (e.g., vomiting and diarrhoea, or blood loss)
• Reduced fluid intake - a particular problem in frail, elderly patients.
• Intrinsic AKI is due to cellular damage within the kidneys - seek early specialist input if you
suspect an intrinsic cause:[17] [18] [9] [62]
• Prolonged pre-kidney AKI that progresses to overt cellular damage is the most common
DIAGNOSIS
cause.
• Nephrotoxins (e.g., iodinated contrast agents, NSAIDs, aminoglycoside antibiotics).[1] See
our Primary prevention section for information about preventing AKI.
• Rare causes (e.g., vasculitis, glomerulonephritis).
• Post-kidney AKIis due to obstruction:[9] [62]
• Most common in older men with prostatic hyperplasia[4]

• Other causes include kidney stones and tumours.
Investigations
• Bloods
• Urea and electrolytes (including creatinine and bicarbonate) are the key investigations [1]
[62] [13] [64] [65]
11
• Also request liver function tests, C-reactive protein, full blood count, and blood
cultures if infection suspected.
• Urinalysis [3] [9] [62] [64]
• If positive for both protein and blood(in the absence of a urinary tract
infection or catheterisation), consider the possibility of an intrinsic cause (e.g.,
glomerulonephritis).
• Nitrites and leukocytes may indicate infection - send urine culture.
• Routine renal tract ultrasound is not needed if a clear cause has been identified. Only
request it if:[3] [13] [64]
• There is no clear cause of AKI

• Pyelonephritis or pyonephrosis is suspected (if pyonephrosis is suspected, ensure the
patient has an ultrasound within 6 hours because of the risk of septic shock)
• Urinary tract obstruction is suspected (the ultrasound should be performed within 24
hours at the latest).
• Further diagnostic tests (e.g., immunology, kidney biopsy) may be indicated according to the
suspected cause of AKI.[13] [64]
Full Recommendations
When to check for AKI
AKI is a medical emergency. Prompt recognition and treatment are vital to improve patient
outcomes and preserve long-term kidney function. [62]
• Kidney function often does not return to the baseline level after recovery from AKI, especially if the
patient has pre-existing CKD.[66]
AKI is often asymptomatic. Consider the possibility of AKI in any patient who is admit ted as
an emergency or who deteriorates during their hospital stay. [3] [62]
DIAGNOSIS
• AKI occurs in 10% to 20% of emergency admissions and has an inpatient mortality >20%
(>35% in stage 3 AKI).[3] [9] [10]
Measure serum creatinine to check for AKI whenever an acutely ill patient meets one or more
of the following criteria: [3] [9] [62]
• Age ≥ 65 years
• History of any one or more of CKD, heart failure, liver disease, diabetes, dementia
• Previous AKI episode
• Exposure within the previous week to:
• Iodinated contrast agent

• Any other nephrotoxin (e.g., NSAID, aminoglycoside antibiotic)
• Renin-angiotensin-system modifying agent (e.g., ACE inhibitor/angiotensin-II receptor
antagonist)
• Diuretic.
• Symptoms or history of urological obstruction
• Suspected or confirmed sepsis
• Hypovolaemia (with or without hypotension) - may be related to dehydration or over-diuresis
• Hypotension (SBP <90 mmHg or a fall of >40mmHg from baseline BP)
• Oliguria (urine output <0.5ml/kg/hour).
Check for AKI in any patient whose early warning score deteriorates acutely - but never use a
reassuring early warning score to rule out AKI . [1] [3]
• Because AKI is so common in acutely ill patients, the UK Royal College of Physicians recommends
that a NEWS2 score of 5 or above should prompt a check for AKI (kidney function, fluid
balance, and urine output).[62]
• But be aware that some patients with AKI may not have an elevated early warning score.
This is because urine output is not included in commonly used scores such as NEWS2 - so oliguria
(an indicator of possible AKI) will not trigger any increase in the patient’s score.
Practical tip
AKI is often a ‘silent disease’ so a high index of suspicion is important, particularly in

acutely ill patients. [62]
• Most patients with AKI present asymptomatically, with non-specific symptoms or with
• A 2009 report from the UK’s National Confidential Enquiry into Patient Outcome and Death
(NCEPOD) identified an unacceptable delay in post-admission diagnosis of AKI in 43%
of patientswho died in hospital from the condition.[67]
Definition of AKI
AKI is diagnosed based on an acute rise in serum creatinine and/or a sustained reduction in
urine output. [4]
• Acute kidney injury has replaced the term ‘acute renal failure’.
• AKI is a sudden reduction in kidney function that makes it difficult to maintain fluid,
electrolyte, and acid-base balance.[9]
DIAGNOSIS
• The condition covers the f ull spectrum of kidney damage ranging from less severe
kidney injury through to kidney failure requiring RRT.
• Evidence has demonstrated that even a minor increase in serum creatinine is associated with
a significantly increased mortality . [1] [62]
AKI is present if any one or more of the following criteria is met: [4] [1] [3]
• A rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours

• A rise in serum creatinine to ≥1.5 times baseline, which is known or presumed to have
occurred within the past 7 days
• Urine volume <0.5 ml/kg/hour for at least 6 hours (at least 8 hours in children/young people).
• Thesecriteria were defined in the 2012 Kidney Disease: Improving Global Outcomes
(KDIGO) guideline [1]
• One additional criterion for diagnosing AKI applies only to children/young people: a fall in
estimated glomerular filtration rate (eGFR) of ≥25% over the past 7 days.
Baseline serum creatinine is best considered clinically as the lowest value over the previous
3 months. [62]
13
• If no recent creatinine value is available, provided the patient does not have progressive
CKD, it is reasonable to assume that creatinine levels will have been stable for some time, so that a
measurement from 6 months or even 1 year ago can be used as the baseline . [1]
• If there is no previous serum creatinine within the previous year, and AKI is suspected, consider
repeating the creatinine within 12 hours - and certainly within 24 hours.[13]
Practical tip
You may work in an institution with an automatic alert system for AKI that is based on
serum creatinine results.
• The algorithm used in the UK NHS alert system for AKI determines baseline serum creatinine
as the lowest value in the past 7 days. If there is no creatinine value available from that period, it
uses a median value over the previous 12 months.
• In England and Wales a system is mandated across both primary and secondary care, whereby
an AKI alert is triggered by rises in serum creatinine, based on the KDIGO definition and staging
system.
In practice, both the serum creatinine and urine output criteria present diagnostic
challenges. [1]
• Rises in creatinine are delayed for approximately 24 hours following kidney injury.
• A reduction in urine output is an earlier indicator of AKI in some patients but AKI can also
present without oliguria.
• In addition, unless the patient is catheterised, accurate and timely measurement of

urine output is difficult. Routine catheterisation is not recommended [1] [68]
Practical tip
It is important to differentiate AKI from a progression of CKD at initial presentation.

• This can be difficult if there are no recent comparison creatinine values. The clinical context
will be important in helping you assess whether a rise in serum creatinine has been acute or
DIAGNOSIS
occurred over a longer period.

• Features that favour a diagnosis of CKD (although do not exclude AKI) include:[9] [62]
• Hypocalcaemia
• Hyperphosphataemia
• Anaemia
• Small kidneys on ultrasound (sometimes scarred) - suggestive of advanced CKD.
• If the patient is acutely unwell or hypovolaemic, this points towards AKI.[9]

• Remember that pre-existing CKD is a risk factor for AKI.
• Repeat blood testing along with reference to historical creatinine values is the key to confirming
or ruling out AKI.
Practical tip
Beware false positive rises in creatinine, for example: [1] [9]

• Recent use of trimethoprim can lead to a rise in serum creatinine that does not reflect any
change in glomerular filtration rate
• Serum creatinine falls during pregnancy so a rise in creatinine after recent delivery may be a
false positive.
Staging the AKI

Stage the severity of AKI according to KDIGO criteria. [4] [69] [70]
• The stage of AKI is determined by the extent to which serum creatinine rises or urine
output fall s.
• The 2012 KDIGO AKI definition and staging criteria are internationally recognised. They
harmonised the earlier RIFLE (Risk, Injury, Failure, Loss of kidney function, and End stage kidney
disease) and AKIN (Acute Kidney Injury Network) definitions.[69] [70]
Stage the AKI using whichever one of serum creatinine or urine output gives the higher
stage. [1] [13]
A higher stage of AKI is associated with a greater risk of death as well as increased likelihood
of needing RRT. [13]
DIAGNOSIS
15
Serum creatinine (SCr)
AKI Stage [1] [62] criteria* Urine output criteria
Stage 1 • SCr rise of ≥26 • <0.5 mL/kg/h for at least

micromol/L within 48 6 consecutive hours
hours
or
• SCr increase to 1.5 to
1.9 times baseline
Stage#2 • SCr increase to 2 to 2.9 • <0.5 mL/kg/h for at least

times baseline 12 consecutive hours
Stage#3 • SCr increase to ≥3 • <0.3 mL/kg/h for at least

times baseline 24 consecutive hours
or or
• SCr rise to ≥354 • Anuria for 12 hours
micromol/L
or
• Patient initiated on
RRT (irrespective of
AKI stage at time of
initiation)
*Baseline SCr is the lowest level in the last 7 days or, if not available, the lowest within the previous 3
months.
Practical tip
DIAGNOSIS
Even relatively minor changes in serum creatinine levels are associated with a
significant increase in mortality. [62]
• In a person with normal kidney function, a rise of creatinine above the normal range reflects a
loss of more than 50% of function and a significant loss in kidney reserve.
Evidence: AKI stage and mortality
Mortality rises sharply with increasing stage of AKI.
AKI during hospital admission is associated with an overall mortality of greater than 20%
whereas stage 3 AKI is associated with >35% mortality. [3] [9] [10]
• A comparison of the RIFLE, AKIN, and KDIGO staging systems found they were all good
predictors of mortality.[71] Whichever system was used, the key message was that mortality
increases with severity as determined by rising serum creatinine.
• One study of more than 20,000 patients showed a nearly linear increase in in-hospital mortality
with increasing RIFLE stage.[72]
• Patients at Risk (R) had triple the mortality rate of patients without AKI.
• Patients with Injury (I) had close to twice the mortality of R.
• Patients with Failure (F) had 10 times the mortality rate of inpatients without AKI.
• The RIFLE and KDIGO criteria map to each other approximately as:
• R = KDIGO stage 1
• I = KDIGO stage 2
• F = KDIGO stage 3
More info
KDIGO diagnostic and staging criteria
The international KDIGO guideline group harmonised the previous definitions and
staging criteria for AKI to produce a widely accepted consensus. [1]
• Prior to the 2012 KDIGO definitions, there were a large number of different definitions of AKI.
DIAGNOSIS
• The best known were the 2004 RIFLE criteria and the subsequent modification of these to
produce the 2007 AKIN criteria.[70] [69] [73]
• In one study of 50,000 patients that compared the incidence of AKI using the RIFLE, AKIN, and
KDIGO criteria, 11.6% of hospitalised patients were diagnosed as having AKI with the KDIGO
criteria and 11.0% with the RIFLE criteria, whereas only 4.8% were classified as having AKI
under the AKIN criteria.[74] [75]
• A comparison of the RIFLE definition with the modified AKIN definition demonstrated that there
were subsets of patients defined as having AKI by each definition that were not detected by the
other.[75]
• The RIFLE criteria failed to detect 9% of cases that were detected by AKIN criteria.
• The AKIN criteria missed 26.9% of cases detected by RIFLE.
• The advent of agreed AKI definitions has allowed a better understanding of the incidence and
outcomes of patients with AKI. This has in turn stimulated the development of new potential
therapeutic interventions for AKI.[13]
17
Causes of AKI
AKI can be classified as pre-kidney (or pre-renal), intrinsic, or post-kidney (post-renal). [5] [21]
• In practice, AKI is sometimes multi-factorial.[65]
There are many causes of AKI. The most common are: [9] [62]
• Sepsis, hypovolaemia, and/or hypotension (pre-kidney AKI)
• Often due to acute illness in a patient with background risk factors

• In such patients, AKI is a strong indicator of a very sick patient who needs urgent recognition
and management
• Exposure to nephrotoxins (intrinsic AKI).

• If AKI is not secondary to either of these, then consider the possibility of obstruction or a less
common intrinsic cause.
It is essential to take all possible steps to determine and record the cause of the patient’s
AKI, based on the history, examination, and investigations. [5] [17] [1] [52] [13]
• The most appropriate management plan will depend on both the severity of AKI and the underlying
cause.[1]
1. Pre-kidney AKI (80%)

Pre-kidney AKI is caused by reduced kidney perfusion often resulting from sepsis, excessive
fluid loss, and/or hypotension associated with acute illness.
• By definition this is a functional process whereby there is no cellular damage.
Causes of pre-kidney AKI include: [1] [62]
• Hypovolaemia/dehydration. For example, due to:

DIAGNOSIS
• Haemorrhage
• Vomiting and diarrhoea
• Insufficient maintenance or replacement fluids to cover losses[3]
• Acute pancreatitis.
• Sepsis
• Hypotension (SBP <90 mmHg or a drop of >40 mmHg from baseline BP)
• May be related to antihypertensive medications.
• After major surgery

• Ileus (sequestration of fluid)
• High output ileostomy.
2. Intrinsic AKI (10%-20%)

Intrinsic AKI occurs when there is cellular damage within the kidneys.
• If you suspect an intrinsic cause (e.g., vasculitis), seek early specialist input.
Causes of intrinsic AKI include: [9] [62]
• Prolonged pre-kidney AKI leading to acute tubular injury (the most common cause)
• Nephrotoxins (e.g., iodinated contrast agents, aminoglycoside antibiotics, NSAIDs) - see our
Primary prevention section for information on preventing AKI
• Tubulointerstitial nephritis (e.g., triggered by infection or nephrotoxic drugs)
• Acute glomerulonephritis (e.g., post-streptococcal glomerulonephritis)
• Vasculitis (e.g., anti-neutrophil cytoplasmic antibodies [ANCA]-associated vasculitis)
• Haemoglobinuria
• Microangiopathy (e.g., accelerated hypertension, haemolytic uraemic syndrome, thrombotic
thrombocytopenic purpura)
• Rhabdomyolysis.
3. Post-kidney AKI (5%-10%)

Post-kidney AKI is secondary to urinary out flow obstruction. Causes include: [9] [62]
• Prostatic hyperplasia
• Kidney stones (bilateral or in a single kidney)
• Retroperitoneal fibrosis (associated with malignancy, e.g., lymphoma)[76]
• Papillary necrosis (flank pain and haematuria, e.g., associated with NSAIDs)
• Tumour (e.g., cervical, prostate).[65]
Clinical presentation
History
AKI is commonly asymptomatic. A comprehensive history is important to identify risk
DIAGNOSIS
factors or precipitating causes for AKI. You should check for: [17] [18] [67] [9]
• Risk factors [3] [9] [64]
• Age ≥65 years (frail older people are at particular increased risk).[65]
• History of any one or more of CKD, heart failure, liver disease, diabetes, dementia (or any
other neurological/cognitive impairment that may result in limited access to oral fluids).
• Previous AKI.
• Myeloproliferative disorder (e.g., multiple myeloma).[5] [53]
• Precipitating factors [1] [3] [9] [62]
• Suspected or confirmed sepsis.

• Hypovolaemia (with or without hypotension).
• May be related to haemorrhage or dehydration due to poor fluid intake, over-diuresis,

illness (e.g., diarrhoea and vomiting) or insufficient replacement fluids in a hospital
inpatient.
• Hypotension (SBP <90 mmHg or a fall of >40mmHg from baseline BP).
19
• Exposure within the previous week to iodinated contrast.
• Recent surgery (especially cardiac).
• Acute pancreatitis.
• History of urinary tract symptoms that might suggest an obstructive cause.
• Recent vascular intervention - raises the possibility of cholesterol embolisation (livedo
reticularis), contrast-induced AKI.[52] [64] See our Primary prevention section for information
about preventing AKI.
• Medication history [3] [9] [62]
• NSAID or aminoglycoside antibiotic use (nephrotoxic potential - can cause drug-induced

interstitial nephritis).[1]
• ACE inhibitor/angiotensin-II receptor antagonist.
• Renin-angiotensin system modifying agents reduce the kidney’s ability to adapt to

changes in perfusion pressure by lowering efferent glomerular arteriolar tone, making
it more difficult for the kidney to maintain glomerular filtration pressure in the event of
hypovolaemia/hypotension.[9]
• Diuretic or any other antihypertensive - particularly if started (or dose changed) in the last 7
days.
• These medications increase the risk of hypovolaemia and/or hypotension.
• Aciclovir, methotrexate, triamterene, indinavir, or sulfonamides (can cause tubular obstruction

by forming crystals).[77]
• Recreational drug use.
• Over-the-counter drugs and herbal remedies.
If symptoms do occur they may include:
• Dizziness
DIAGNOSIS
• Postural hypotension secondary to hypovolaemia suggests pre-kidney AKI.

• Thirstis another common symptom of hypovolaemia.
• Decreased urine output
• Oliguria is one of the diagnostic criteria for AKI and is an earlier indicator of impaired
kidney function than rising creatinine.
• Urine output <0.5 ml/kg/hour for at least 6 consecutive hours (at least 8 hours in
children/young people) is diagnostic of AKI.[1]
• But be aware that patients with AKI are often not oliguric.
• Anuriasuggests either an obstructive cause or severe AKI from a pre-kidney or intrinsic

cause.
• Nausea/vomiting
• Vomiting may cause pre-kidney AKI or can be a later manifestation of AKI-related

uraemia.[62]
• Lower urinary tract symptoms (urgency, frequency, nocturia, or hesitancy)
• Suggestive of an obstructive cause.[4]
• Altered mental status
• Usually secondary to a primary kidney insult (e.g., sepsis) but may also result fromAKI-
related uraemia.
• Muscle tenderness
• Suspect intrinsic AKI secondary to rhabdomyolysisand tubular toxicity from myoglobin in

the setting of acidosis.
• Haematuria(visible or non-visible)
• May be related to pyelonephritis, kidney stones, papillary necrosis, tumour, or acute

glomerulonephritis.
Less commonly, symptoms of volume overload can be seen at presentation:
• Orthopnoea
• From pulmonary oedema or AKI-related acidaemia.
• Swollen ankles
• Suggests salt/water overload - from an obstructive cause or in patients with nephrotic

syndrome secondary to glomerulonephritis.
In rare causes of AKI, the patient may present with: [9] [64]
• Fever, rash, and/or joint pain
DIAGNOSIS
• Suspect small-vessel vasculitis (e.g., granulomatosis with polyangiitis, microscopic
polyangiitis), or interstitial nephritis.
• Haemoptysis
• Suspect small vessel vasculitis or anti-glomerular basement membrane antibody disease.
• Hypercalcaemia, hyperuricaemia, bone pain, and lytic lesions
• Suspect multiple myeloma.
Examination
Your examination should cover: [9] [64]
• Volume status - signs of hypovolaemia are often present (less commonly, signs of
volume overload are seen at presentation). Check:
21
• Peripheral perfusion (capillary refill)
• Pulse rate
• Blood pressure (BP) - including a check for postural hypotension
• Jugular venous pressure
• Dry axillae/mucous membranes
• Peripheries (oedema)
• Auscultation of lungs (crackles may suggest pulmonary oedema)
• Respiratory rate (tachypnoea suggests fluid overload and/or acidosis).
• Mental status
• May be affected by precipitating illness (e.g., sepsis).

• Confusion can result from encephalopathy in a patient with AKI-related uraemia.
• Any signs of uraemic syndrome (e.g., pericardial rub)[13] [65]
• Acute pericarditis is a complication associated with severe AKI and worsening uraemia.[13]
[65]
• Presence of a pericardial friction rub on clinical examination is an indication for RRT
(although it may be absent if there is a significant effusion).[1] [13]
• Asterixisis another possible symptom of uraemia.
Look for any signs of sepsis and manage promptly. [9] [64]
• Perform aseptic screen and implement your local care bundle (e.g., Sepsis Six) if infection is
suspected. See our Sepsis topic for more information.
Clinical findings that may support a specific underlying diagnosis include: [64]
• Rash- for example, petechiae or purpura (intrinsic AKI, e.g., interstitial nephritis, vasculitis,
glomerulonephritis)
• Jaundice(hepatorenal syndrome)
DIAGNOSIS
• Joint swelling/pain (vasculitis)

• Hypertension, pulmonary oedema, and peripheral oedema (obstructive cause; renal artery
stenosis; acute glomerulonephritis)[18] [78] [79] [9]
• Hypotension(pre-kidney or intrinsic AKI)[9]
• Note that hypotension might be absolute (SBP <90 mmHg) or relative (BP fall of >40 mmHg
from the patient’s baseline).
• May be secondary to sepsis and vasodilation and/or hypovolaemia, resulting in reduced
kidney perfusion and pre-kidney AKI.
• Prolonged hypotension can then cause cell damage and acute tubular injury, resulting in
intrinsic AKI.
• Abdominal bruit (renovascular disease)

• Abdominal distension and/orpalpable bladderand/or enlarged prostate (obstruction).[64]
Investigations
Baseline bloods and urine analysis

The key investigations in suspected or confirmed AKI are baseline bloods and urine
analysis.
Baseline bloods [1] [62] [13] [64] [65]

Urea and electrolytes (including creatinine) are essential.
• The initial serum creatinine level, followed by ongoing serum creatinine monitoring, forms the
basis of diagnosing, staging, and monitoring the progress of any patient with AKI.[1]
• An acutely elevated serum creatinine may be the only sign of AKI.
• Ensure close monitoring of serum potassium. [62] [80]
• Hyperkalaemia is a common complication of AKI.

• Urgent treatment is required if potassium >6.0 mmol/L and/or ECG changes are seen.
• For any hospital inpatient with AKI, ensure daily monitoring of urea and electrolytes until the AKI
has resolved (i.e., a return to actual or presumed baseline kidney function or the establishment of
steady state kidney function).[13]
Request bicarbonate if it is not part of the standard panel.
• Alternatively, if previously taken bloods indicate AKI and bicarbonate was not included, request
a venous blood gas.
• Low bicarbonate suggests acidosis.
• Venous blood gases can help with further evaluation of acidosis.
Also request: [13] [64]
• Liver function tests (will aid diagnosis of hepatorenal syndrome)[62]

• CRP(a marker of inflammation; will be elevated in vasculitis)
• FBC
• Leukocytosis may suggest infection.
DIAGNOSIS
• High or low WBC can occur with sepsis.
• If platelets are low, request a blood film and lactate dehydrogenase to check for
rare disorders such as haemolytic uraemic syndrome, thrombotic thrombocytopenic purpura,
cryoglobulinaemia.[1]
• Blood cultures - if infection is suspected[81]

• Serum creatine kinase - if rhabdomyolysis is suspected.
23
Practical tip
Do not use the urea:creatinine ratio as an indicator of the cause of AKI. [82]
• An elevated urea: creatinine ratio can occur in AKI.[13] This is because urea and creatinine are
both freely filtered at the glomerulus, but urea is reabsorbed by the tubules whereas creatinine is
not.
• The urea:creatinine ratio is sometimes suggested as a useful indicator to distinguish pre-kidney
AKI from intrinsic or post-kidney causes, with a higher ratio considered to be suggestive of a pre-
kidney cause.
• However, there is no reliable evidence to support this and there are multiple confounders that
affect the ratio, including gastrointestinal bleeding, drug-induced increases (e.g., corticosteroids)
and a high-protein diet.[81]
Urine analysis [1] [3] [62] [64]

Perform urine dipstick testing for specific gravity, blood, protein, leucocytes, nitrites, and
glucose as soon as AKI is suspected or diagnosed.
• Use a clean-catch specimen.
Consider the possibility of intrinsic AKI if urinalysis is positive for both blood and protein
in the absence of an obvious alternative cause (e.g., urinary tract infection or trauma from
urinary catheterisation). [3] [9] [64]
• Proteinuria together with haematuria may indicate an active urinary sediment due to glomerular
disease.
• Patients with glomerular disease typically present with proteinuria and haematuria with
hypertension and oedema. An early referral to nephrology is indicated.[3]
• However, there remains a wide differential diagnosis for blood and protein on dipstick
(e.g., infection, trauma, papillary necrosis).
• Careful microscopy of freshly collected, freshly spun urine for the presence of red cell casts
DIAGNOSIS
can confirm glomerular origin haematuria. But if this is not available, the absence of catheter
trauma or urinary tract infection should raise concerns about glomerular disease.
• Other causes of an active urinary sediment (dysmorphic red cells and red cell casts) include
infection, tumours, calculi, venous thrombosis, and myoglobinuria (rhabdomyolysis).
Send urine culture if clinical features of urinary tract infection are present and/or urinalysis
is positive for blood, protein, leukocytes, or nitrites. [64]
Start urine output monitoring (hourly if catheterised, 4-hourly if not). [64]
• Routine urinary catheterisation is not appropriate in patients with AKI. Carefully weigh up
the benefits against the risks for the individual patient.[64]
• Potential benefits:
• Oliguria is one of the diagnostic criteria for confirming AKI, but urine output is difficult
to measure accurately without catheterisation
• Urinalysis can be performed on a sample obtained following catheterisation (but
be aware that any proteinuria/haematuria might have resulted from catheter-related
trauma)
• Hourly urinary output monitoring aids assessment of the patient’s response to
treatment
• Catheterisation can be both diagnostic and therapeutic for bladder neck obstruction.
• Potential risks:
• Infection
• Trauma
• Falls risk.
• Catheterisation is indicated:
• In any case where fluid balance management is crucial

• If the patient is too ill to use a bottle or commode
• If bladder neck obstruction is suspected and cannot be quickly ruled out by ultrasound.
Consider requesting urine electrolytes to measure fractional excretion of sodium or urea -

but beware the potential pit falls. [13]
• In principle, calculation of fractional excretion of sodium (FENa) may be helpful in distinguishing

pre-kidney from intrinsic AKI. In practice it is rarely performed and results are often difficult
to interpret, particularly if loop diuretics have been used within the last 24 hours.
• Fractional excretion of sodium (FENa) of <1% suggests pre-kidney AKI but may also be seen
in glomerulonephritis, hepatorenal syndrome, some cases of obstruction, and even acute
tubular necrosis (if tubular function remains intact).
DIAGNOSIS
• Fractional excretion of urea (FEUr) is more useful if the patient has received loop diuretics -
although results are also difficult to interpret so the test is rarely performed in clinical practice.
• Urea excretion is not significantly affected by diuretics.

• A fractional excretion of urea <35% supports a diagnosis of pre-kidney AKI.
• The fractional excretion of urea is calculated as: 100% X (urine urea x plasma creatinine)/
(plasma urea x urine creatinine).
• Urine sodium concentration
• <20 mmol/L (20 mEq/L) suggests pre-kidney AKI with preserved tubule function/sodium
retention.
• Raised levels are seen in intrinsic AKI where there is tubule damage or in response to
diuretics.
Urine osmolality is rarely requested.
25
• Urine osmolality is the number of moles of solute per kg of solvent and it depends on tubule
response to anti-diuretic hormone (ADH).
• High urine osmolality (>500 mOsm/kg) suggests pre-kidney AKI with preservation of tubule function
(assuming no recent administration of iodinated contrast).[1] [83]
• However this should not be interpreted as confirming pre-kidney AKI because intact tubule
function (particularly in the early stages) may be seen in various forms of kidney disease (e.g.,
glomerulonephritis).[1]
• Urine osmolality <300 mOsm/kg suggests tubule damage (intrinsic AKI) as urinary concentration is
impaired.[83]
Urine microscopy can be useful if there is a finding of blood and protein on urinalysis. [13]
• It is not widely used in the UK but is more commonly performed in other countries (e.g., USA,
China).
• It may reveal:
• Granular casts in acute tubular injury

• Red cell casts in glomerulonephritis/vasculitis
• Oxalate crystals - suggestive of ethylene glycol poisoning.[84]
Urinary eosinophil counts may be of some use in patients with pyuria.
• A result above 5% to 7% supports a diagnosis of acute allergic interstitial nephritis but is not
diagnostic because of low sensitivity and specificity.[85] The test is dependent on the expertise of
the microscopist.
• It has a negative predictive value of >90% for patients with AKI and may be useful in excluding the
disease process.[86]
• Eosinophiluria may be seen with atheroembolic disease as well.
Practical tip
• All the urine investigations above, if available, can aid the diagnosis of AKI, but they all have their
own limitations and vary in sensitivity and specificity.
DIAGNOSIS
• A single investigation will not be enough on its own to draw any firm conclusions.[13] [87]
Other initial tests

Request a chest x-ray. [65] It may demonstrate signs of:
• Infection
• Pulmonary oedema
• Haemorrhage (e.g., ANCA-associated vasculitis, Goodpasture syndrome [pulmonary haemorrhage,
rapidly progressive glomerulonephritis, and anti-glomerular basement membrane antibodies])
• Cardiomegaly.
Request an ECG.
• It may demonstrate features consistent with severe hyperkalaemia (peaked T waves, increased PR
interval, widened QRS, atrial arrest, deterioration to a sine wave pattern).
Investigations to consider
Kidney imaging
If pyonephrosis (an infected/obstructed renal tract) is suspected, ensure the patient has an
ultrasound - and if indicated a nephrostomy - within 6 hours, due to the risk of septic shock.
[3] [64]
Renal tract ultrasound is not routinely required. Only request it if no obvious cause for the
AKI can be found or if obstruction, pyelonephritis, or pyonephrosis is suspected. [3] [13]
• The presence of dilated renal calyces suggests obstruction and hydronephrosis.

• Ensure the ultrasound is performed within 24 hours if no obvious cause for the AKI can be
identified or a urinary tract obstruction is suspected.[3] [64]
• Ultrasound has high sensitivity (90%-98%) but lower specificity (65%-84%) for diagnosing upper
tract obstruction, although this may not be the case in the early stages (first 8 hours).[13]
• Repeat the ultrasound after 24 hours if:
• There is a high index of suspicion for hydronephrosis (as it may take several hours for this to
develop due to initial non-compliance of the pelvi-caliceal system)
• The patient has oliguric acute tubular necrosis with superimposed obstruction (because urine
is needed to dilate the kidneys).
If prior creatinine values are not available to give a baseline, ultrasound can sometimes be
helpful in distinguishing AKI from CKD. [62] [13]
• Ultrasound may demonstrate small (sometimes scarred) kidneys consistent with advanced CKD
(such changes are unlikely to be seen in less severe CKD).
• Be aware that an ultrasound finding consistent with CKD does not exclude the possibility of AKI on
a background of CKD.[13]
Consider requesting a CT or MRI if obstruction is suggested on ultrasound (e.g., possible

masses or stones). [13]
DIAGNOSIS
• These are not routinely needed - the decision will depend on the degree of obstruction.
• Be cautious with intravenous iodinated contrast CT scans in patients with AKI. MRI is preferred
(although note that gadolinium may be needed for MRI enhancement).
Nuclear renal flow scans can sometimes be useful to evaluate for obstruction in cases of
mild hydronephrosis, when the diagnosis of mechanical obstruction is uncertain.
• The scan is performed before and after a dose of loop diuretic.
• Impaired tracer excretion is suggestive of acute tubular necrosis.

• Poor blood flow is suggestive of obstructed blood supply.
• Normal blood flow and tracer excretion with tracer accumulation in the collecting system is
suggestive of obstruction of the urine outflow tract.
Other tests
Further diagnostic tests may be determined by the suspected cause of AKI. Examples
include: [13] [64]
27
• Immunological tests
• Anti-nuclear antibodies (ANA) and anti-DNA antibody (lupus nephritis).

• Complement (lupus nephritis, post-infectious glomerulonephritis).
• Anti-glomerular basement membrane antibodies (Goodpasture syndrome, anti-glomerular
basement membrane syndrome).
• Anti-neutrophil cytoplasmic antibodies (ANCA-associated vasculitis).
• Serum/urine electrophoresis and urinary Bence Jones protein (myeloma).
• Myeloma is an important potential cause of AKI and should be considered in a

patient >40 years who presents with hypercalcaemia, hyperuricaemia, or pathological
fracture.[9] [64]
• Serum electrophoresis will show a paraprotein (monoclonal immunoglobulin).
• Urine electrophoresis will detect Bence Jones proteins (free light chains) which are not
detected on urinalysis.
• Acute hepatitis profile: hepatitis B, C, and D (glomerulonephritis).

• HIV test (glomerulonephritis or drug-induced AKI).
• Cryoglobulins (glomerulonephritis).
• Complement mutations (haemolytic uraemic syndrome).
• Anti-streptolysin O titres (post-streptococcal glomerulonephritis).
• Kidney biopsy
• May be performed to diagnose rarer forms of AKI (e.g., interstitial nephritis,

glomerulonephritis, or vasculitis).
• Cystoscopy
• May be requested to identify the cause of obstructive AKI (e.g., ureteric stenosis, bladder
tumour).
DIAGNOSIS
History and exam

Key diagnostic factors
hypotension (common)
Hypotension and/or hypovolaemia is a common cause of reduced kidney perfusion and
resulting pre-kidney AKI . [9] [62]
• Often due to acute illness (e.g., sepsisand vasodilatation; haemorrhage; vomiting and
diarrhoea), particularly in a patient with background risk factors.
• Can also result from dehydration due topoor fluid intake, over-diuresis, or insufficient
replacement fluids in a hospital inpatient.[3]
• Hypovolaemia due to reduced fluid intake is a particular risk for frail, older patients
especially those with cognitive or neurological impairment.[9]
Hypotension may be absolute (SBP <90 mmHg) or relative to the patient’s usual BP (a
drop of >40 mmHg from baseline).
• May be related to antihypertensive medications.
Assessing volume status is a crucial part of your initial examination - signs of

hypovolaemia are often present . [9] [64] Check:
• Peripheral perfusion (capillary refill)

• Pulse rate
• Blood pressure (including a check for postural hypotension)
• Dry axillae/mucous membranes.
Treat hypovolaemia promptly with an immediate bolus of crystalloid intravenous fluid. [1]
[62] [13] [64]
Prolonged hypotension can cause pre-kidney AKI to progress to cell damage and acute
tubular injury (intrinsic AKI).
risk factors (common)

AKI is commonly asymptomatic so is easily missed. Whenever a patient presents with
an acute illness, ensure your history covers characteristics that increase the risk of AKI.
Check for: [17] [18] [67] [9]
• Risk factors [3] [9] [64]
DIAGNOSIS
• Age ≥65 years (frail older people are at particular increased risk).[65]
• History of any one or more of chronic kidney disease (CKD), heart failure, liver disease,
diabetes, dementia (or any other neurological/cognitive impairment that may result in
limited access to oral fluids).
• Previous AKI.
• Myeloproliferative disorder (e.g., multiple myeloma).[5] [53]
Medication history [3] [9] [62]
• Non-steroidal anti-inflammatory drug (NSAID) or aminoglycoside antibiotic use

(nephrotoxic potential - can cause drug-induced interstitial nephritis).
• ACE inhibitor/angiotensin-II receptor antagonist use.
• Renin-angiotensin system modifying agents reduce the kidney’s ability to adapt

to changes in perfusion pressure by lowering efferent glomerular arteriolar tone,
29
making it more difficult for the kidney to maintain glomerular filtration pressure in
the event of hypovolaemia/hypotension.[9]
• Diuretic or any other antihypertensive - particularly if started (or dose changed) in the last
7 days.
• These medications increase the risk of hypovolaemia and/or hypotension.
• Aciclovir, methotrexate, triamterene, indinavir, or sulfonamides (can cause tubular

obstruction by forming crystals).[77]
• Recreational drug use.
• Over-the-counter drugs and herbal remedies.
Practical tip
AKI is often a ‘silent disease’ so a high index of suspicion is important, particularly

in acutely ill patients. [62]
• Most patients with AKI present asymptomatically, with non-specific symptoms or with
• A 2009 report from the UK’s National Confidential Enquiry into Patient Outcome and Death
(NCEPOD) identified an unacceptable delay in post-admission diagnosis of AKI in
43% of patients who died in hospital from the condition.[67]
kidney insults (common)

Many cases of AKI are precipitated by a kidney insult, particularly in patients with
underlying risk factors. Examples include:[1] [3] [9] [62]
• Sepsis or other acute illness (e.g., acute pancreatitis, burns)

DIAGNOSIS
• Perform a septic screen and implement your local care bundle (e.g., Sepsis Six)if
infection is suspected.[9] [63]
• Hypovolaemia (with or without hypotension)

• Nephrotoxins
• Exposure within the previous week to iodinated contrast agent

• Use of an NSAID or aminoglycoside antibiotic[1]
• Recent surgery (especially cardiac)

• Recent vascular intervention - raises the possibility of cholesterol embolisation (livedo
reticularis), contrast-induced AKI.[52] [64]
reduced urine production (common)

Oliguria is one of the diagnostic criteria for AKI and is an earlier indicator of impaired
kidney function than rising creatinine. [1]
• Confirm a diagnosis of AKI if urine output <0.5 ml/kg/hour for at least 6 consecutive
hours (at least 8 hours in children/young people).
• But be aware thatpatients with AKI are often not oliguric.
Anuria suggests either an obstructive cause or severe AKI from a pre-kidney or intrinsic
cause.
AKI can also be staged according to the extent to which urine output falls (or serum
creatinine rises). [1]
• Stage the AKI using whichever one of serum creatinine or urine output gives the higher stage.[1]
[13]
• Stage 1 AKI: urine output <0.5 mL/kg/h for at least 6 consecutive hours
• Stage 2 AKI: urine output <0.5 mL/kg/h for at least 12 consecutive hours
• Stage 3 AKI: urine output <0.3 mL/kg/h for at least 24 consecutive hours or anuria for 12
hours
• A higher stage of AKIis associated with agreater risk of death as well as increased
likelihood of needing renal replacement therapy (RRT).[13]
In practice, accurate and timely measurement of urine output is difficult unless the
patient is catheterised.
• Routine catheterisation is not recommended.[1] [68]
lower urinary tract symptoms (common)

Lower urinary tract symptoms such as urgency, frequency, or hesitancy are suggestive of
a urinary tract obstruction.
DIAGNOSIS
• Prostatic hyperplasia is a common cause of obstructive AKI in older men.[4]
symptoms of volume overload/pulmonary oedema (uncommon)

Symptoms and signs of volume overload may be seen at presentation if the patient has
obstructive AKI or any form of AKI against a background of pre-existing heart failure.
• Otherwise the most common cause of volume overload is overenthusiastic fluid resuscitation.[1]
[13]
Symptoms of volume overload that may be reported at presentation include:
• Orthopnoea
• From pulmonary oedema or AKI-related acidosis
• Swollen ankles/other signs of peripheral oedema
31
• From an obstructive cause or in patients with nephrotic syndrome secondary to
glomerulonephritis.
Examination signs in a patient with volume overload might include:
• Crackleson auscultation of lungs (suggests pulmonary oedema)

• Tachypnoea(suggests fluid overload and/or acidosis).[64]
vomiting/nausea (uncommon)
Vomiting may cause pre-kidney AKI or can be a later manifestation of AKI-related
uraemia. [62]
fever, rash, and/or arthralgia (uncommon)

If present, suspect small-vessel vasculitis (e.g., granulomatosis with polyangiitis,
microscopic polyangiitis), or interstitial nephritis. [64]
haematuria (visible or non-visible) (uncommon)

Can occur with kidney stones, papillary necrosis, infection, tumour, or acute
glomerulonephritis.
palpable bladder and/or enlarged prostate and/or abdominal distension

(uncommon)
Point to an obstructive cause of AKI. [13] [64] [65]
Other diagnostic factors

dizziness and orthostatic symptoms (common)
Orthostatic symptoms and postural hypotension confirmed on blood pressure monitoring are
DIAGNOSIS
consistent with hypovolaemia and suggest pre-kidney AKI.
• Thirstis another common symptom of hypovolaemia.
hypertension (uncommon)
May be seen in AKI secondary to renal artery stenosis or a rapidly progressive
glomerulonephritis. [18] [78] [79] [9]
altered mental status (uncommon)

A change in mental status is usually secondary to a primary kidney insult (e.g., sepsis)
that precipitated AKI.
Confusion can also result from encephalopathy in a patient with AKI-related uraemia. [13]
pericardial/pleural rub (uncommon)

Acute pericarditis is a complication associated with severe AKI and worsening uraemia
(most often on a background of pre-existing CKD). [13] [65]
• The presence of a pericardial friction rub on examination is anindication for renal
replacement therapy (although it may be absent if there is a significant effusion).[1] [13]
• Asterixisis another possible symptom of uraemia.
muscle tenderness (uncommon)

Suspect intrinsic AKI secondary to rhabdomyolysis and tubular toxicity from myoglobin
in the set ting of acidosis.
haemoptysis (uncommon)
Suspect an intrinsic cause of AKI (e.g., small vessel vasculitis or anti-glomerular
basement membrane antibody disease). [64]
abdominal bruit (uncommon)

Suspect renovascular disease.
DIAGNOSIS
33
Investigations
1st test to order
Test Result
basic metabolic profile (including urea and creatinine and liver • acutely elevated serum
function tests)
creatinine, high serum
Creatinine for AKI diagnosis potassium, metabolic
AKI is often asymptomatic so is easily missed. [62] acidosis
• confirm the diagnosis
• An acutely rising creatinine may be the only sign. of AKI if there is:[4] [1]
• Rises in creatinine are delayed for approximately 24 hours [3]
following kidney injury.
• a rise in serum
Measure serum creatinine to check for AKI whenever an creatinine of ≥26

acutely ill patient meets one or more of the following criteria: micromol/L (≥0.3
[3] [9] [62] mg/dL) within 48
hours
• Age ≥65 years
• History of any one or more of chronic kidney disease (CKD), OR
heart failure, liver disease, diabetes, dementia • a rise in serum
• Previous AKI episode creatinine to ≥1.5
• Exposure within the previous week to: times baseline,
which is known
• Iodinated contrast agent
or presumed to
• Any other nephrotoxin (e.g., non-steroidal anti-
have occurred
inflammatory drug [NSAID], aminoglycoside antibiotic)
within the past 7
• Renin-angiotensin-system modifying agent (e.g., ACE
days
inhibitor/angiotensin-II receptor antagonist)
• Diuretic.
• LFTs will be deranged
DIAGNOSIS
in hepatorenal
• Symptoms or history of urological obstruction
syndrome
• Suspected or confirmed sepsis
• Hypovolaemia (with or without hypotension) - may be related to
dehydration or over-diuresis[9]
• Hypotension (SBP <90 mmHg or a fall of >40mmHg from
baseline BP)
• Oliguria (urine output <0.5ml/kg/hour)
• Acute rise in early warning score (e.g., NEWS2 >5).
AKI is diagnosed based on an acute rise in serum creatinine

and/or a sustained reduction in urine output. [1]
Baseline serum creatinine is best considered clinically as

the lowest value over the previous 3 months. [62]
• If no recent creatinine value is available, provided the

patient does not have CKD it is reasonable to assume that
creatinine levels will have been stable for some time, so thata
Test Result
measurement from 6 months or even 1 year ago can be
used as the baseline.[1]
• If there is no previous serum creatinine within the previous
year, and AKI is suspected, consider repeating the creatinine
within 12 hours - and certainly within 24 hours.[13]
Practical tip
It is important to differentiate AKI from a progression of

CKD at initial presentation.
• This can be difficult if there are no recent comparison
creatinine values. The clinical context will be important in
helping you assess whether a rise in serum creatinine has
been acute or occurred over a longer period.
• Features that favour a diagnosis of CKD (although do not
exclude AKI) include:[9] [62]
• Hypocalcaemia
• Hyperphosphataemia
• Anaemia
• Small kidneys on ultrasound (sometimes scarred) -
suggestive of advanced CKD.
• If the patient is acutely unwell or hypovolaemic, this points

towards AKI.[9]
• Remember that pre-existing CKD is a risk factor for AKI.
• Repeat blood testing along with reference to historical
creatinine values is the key to confirming or ruling out AKI.
Practical tip
DIAGNOSIS
Beware false positive rises in creatinine, for example: [1]
[9]
• Recent use of trimethoprim can lead to a rise in serum
creatinine that does not reflect any change in glomerular
filtration rate.
• Serum creatinine falls during pregnancy so a rise in
creatinine after recent delivery may be a false positive.
Creatinine for AKI staging

Stage the AKI using whichever one of serum creatinine or
urine output gives the higher stage. [1] [13]
• A higher stage of AKI is associated with a greater risk of death

as well as increased likelihood of needing renal replacement
therapy (RRT).[13]
35
Test Result
For any hospital inpatient with AKI, ensure daily monitoring
of urea and electrolyes until the AKI has resolved, as
indicated by: [13]
• A return to actual or presumed baseline kidney function
or
• The establishment of steady state kidney function.
Serum creatinine (SCr)

AKI Stage [1] [62] criteria*
Stage 1 • SCr rise of ≥26

micromol/L within 48
hours
or
• SCr increase to
1.5 to 1.9 times
baseline
Stage#2 • SCr increase to 2 to

2.9 times baseline
Stage#3 • SCr increase to ≥3

times baseline
or
• SCr rise to ≥354
micromol/L
DIAGNOSIS
or
• Patient initiated on
RRT (irrespective of
AKI stage at time of
initiation)
*Baseline SCr is the lowest level in the last 7 days or, if not
available, the lowest within the previous 3 months.
Practical tip
Even relatively minor changes in serum creatinine

levels are associated with a significant increase in
mortality. [62]
• In a person with normal kidney function, a rise of creatinine
above the normal range reflects a loss of more than 50% of
function and a significant loss in kidney reserve.
Test Result
Evidence: AKI stage and mortality
Mortality rises sharply with increasing stage of AKI
AKI during hospital admission is associated with an

overall mortality of greater than 20%, whereas stage 3 AKI
is associated with >35% mortality. [3] [9] [68]
• A comparison of the RIFLE, AKIN, and KDIGO staging

systems found they were all good predictors of mortality.[71]
Whichever system was used, the key message was that
mortality increases with severity as determined by rising
serum creatinine.
• One study of more than 20,000 patients showed a nearly
linear increase in in-hospital mortality with increasing RIFLE
stage.[72]
• Patients at Risk (R) had triple the mortality rate of

patients without AKI.
• Patients with Injury (I) had close to twice the mortality
of R.
• Patients with Failure (F) had 10 times the mortality
rate of inpatients without AKI.
• The RIFLE and KDIGO criteria map to each other

approximately as:
• R = KDIGO stage 1
• I = KDIGO stage 2
• F = KDIGO stage 3
DIAGNOSIS
More info
KDIGO diagnostic and staging criteria
The international KDIGO guideline group harmonised

the previous definitions and staging criteria for AKI to
produce a widely accepted consensus. [1]
• Prior to the 2012 KDIGO definitions, there were a large

number of different definitions of AKI.
• The best known were the 2004 RIFLE criteria and

the subsequent modification of these to produce the
2007 AKIN criteria.[70] [69] [73]
• In one study of 50,000 patients that compared the incidence

of AKI using the RIFLE, AKIN, and KDIGO criteria, 11.6%
of hospitalised patients were diagnosed as having AKI
37
Test Result
with the KDIGO criteria and 11.0% with the RIFLE criteria,
whereas only 4.8% were classified as having AKI under the
AKIN criteria.[74]
• A comparison of the RIFLE definition with the modified
AKIN definition demonstrated that there were subsets of
patients defined as having AKI by each definition that were
not detected by the other.[75]
• The RIFLE criteria failed to detect 9% of cases that

were detected by AKIN criteria.
• The AKIN criteria missed 26.9% of cases detected by
RIFLE.
• The advent of agreed AKI definitions has allowed a better

understanding of the incidence and outcomes of patients
with AKI. This has in turn stimulated the development of
new potential therapeutic interventions for AKI.[13]
LFTs
Will aid diagnosis of hepatorenal syndrome. [62]
serum potassium elevated in hyperkalaemia
Ensure close monitoring of serum potassium. [62] [80]
• 5.5 to 5.9 mmol/
• Hyperkalaemia is a common complication of AKI. L indicates mild
• Urgent treatment is required if potassium >6.0 mmol/L and/or hyperkalaemia
ECG changes are seen. • 6.0 to 6.4 mmol/L
indicates moderate
hyperkalaemia
• ≥6.5 mmol/L indicates
DIAGNOSIS
severe hyperkalaemia
FBC anaemia, leukocytosis,

Leukocytosis may suggest infection. thrombocytopenia
• High or low WBC can occur with sepsis.
If platelets are low, request a blood film and lactate

dehydrogenase: [62]
• Use to check for rare disorders such as haemolytic

uraemic syndrome, thrombotic thrombocytopenic purpura,
cryoglobulinaemia.[1]
Anaemia can occur in AKI secondary to haemolytic uraemic

syndrome, myeloma, or vasculitis.
Test Result
bicarbonate low bicarbonate suggests
Request bicarbonate if it is not part of the standard panel. acidosis
[62] [64] [65]
• Alternatively, if previously taken bloods indicate AKI and

bicarbonate was not included, request a venous blood gas.
• Venous blood gases can help with further evaluation of
acidosis.
C-reactive protein elevated in infection and also

Request in all patients. [64] [65] in vasculitis
blood culture positive for bacterial pathogen

Request if infection is suspected. [62] [81] [64]
Sepsis is a common cause of AKI. [9] [63]
• Perform a septic screen and implement your local care bundle

(e.g., Sepsis Six) if infection is suspected.
urinalysis RBCs, WBCs, cellular casts,

Perform urine dipstick testing for specific gravity, blood, proteinuria, positive nitrite,
protein, leucocytes, nitrites, and glucose as soon as AKI is and leukocyte esterase
suspected or diagnosed. [3] [62]
• Use a clean-catch specimen.
Consider the possibility of intrinsic AKI if urinalysis is

positive for both blood and protein in the absence of an
obvious alternative cause (e.g., urinary tract infection [UTI]
DIAGNOSIS
or trauma from urinary catheterisation). [3] [9] [64]
• Proteinuria together with haematuria may indicate an active

urinary sediment due to glomerular disease.
• Patients with glomerular disease typically present with

proteinuria and haematuria with hypertension and
oedema. An early referral to nephrology is indicated.[3]
• However, there remains a wide differential

diagnosis for blood and protein on dipstick (e.g.,
infection, trauma, papillary necrosis).
• Careful microscopy of freshly collected, freshly spun

urine for the presence of red cell casts can confirm
glomerular origin haematuria, but if this is not available
then the absence of catheter trauma or UTI should raise
concerns about glomerular disease.
39
Test Result
• Other causes of an active urinary sediment (dysmorphic
red cells and red cell casts) include infection,
tumours, calculi, venous thrombosis, myoglobinuria
(rhabdomyolysis).
urine culture bacterial growth with antibiotic

Send urine culture if clinical features of urinary tract sensitivity
infection are present and/or urinalysis is positive for blood,
protein, leukocytes, or nitrites. [64]
urine output monitoring • confirm a diagnosis of
Start urine output monitoring in any patient diagnosed with AKI if urine output <0.5
AKI (hourly if catheterised, 4-hourly if not). [64] ml/kg/hour for at least
• In practice, accurate monitoring can be difficult if the patient is 6 consecutive hours
(at least 8 hours in
not catheterised.
• Routine urinary catheterisation is not appropriate in children/young people)
patients with AKI. Carefully weigh up the benefits against • if catheterisation is
the risks for the individual patient.[64] considered appropriate:
• Potential benefits: • significant urine

volume released
• A sustained fall in urine output is one of the
diagnostic criteria for confirming AKI, but urine after catheter
output is difficult to measure accurately without placement points
catheterisation[1] to bladder outlet
• Urinalysis can be performed on a sample obtained
obstruction
following catheterisation (but be aware that any • minimal residual
proteinuria/haematuria might have resulted from urine after
catheter-related trauma) catheter
DIAGNOSIS
• Hourly urinary output monitoring aids assessment

placement
of the patient’s response to treatment suggests a
• Catheterisation can be both diagnostic and
non-obstructive
therapeutic for bladder neck obstruction. cause of AKI
or higher level
• Potential risks:
urinary tract
obstruction
• Infection
• Trauma
• Falls risk.
Catheterisation is indicated:
• In any case where fluid balance management is crucial

• If the patient is too ill to use a bottle or commode
Test Result
• If bladder neck obstruction is suspected and cannot be quickly
ruled out by ultrasound.
fluid challenge kidney function improves

A good response to a fluid challenge supports a diagnosis of rapidly in pre-kidney AKI
pre-kidney AKI.
venous blood gases an anion gap acidosis occurs
Can be requested to assess acid/base status. [64] in a number of different
scenarios
• An anion gap acidosis is seen in AKI due to impaired excretion
of non-volatile acids.
CXR may show signs of infection,

Request a chest x-ray. [65] It may demonstrate signs of: fluid, cardiomegaly, or
haemorrhage
• Infection
• Pulmonary oedema
• Haemorrhage (e.g., ANCA-associated vasculitis, Goodpasture
syndrome [pulmonary haemorrhage, rapidly progressive
glomerulonephritis, and anti-glomerular basement membrane
antibodies])
• Cardiomegaly.
ECG ECG changes associated

An ECG is important to assess for hyperkalaemia. with hyperkalaemia: peaked T
waves, increased PR interval,
• Hyperkalaemia is a common complication of AKI.
widened QRS, atrial arrest,
DIAGNOSIS
and deterioration to a sine
wave pattern
41
Other tests to consider
Test Result
renal tract ultrasound • presence of dilated
If pyonephrosis (an infected/obstructed renal tract) is renal calyces suggests
suspected, ensure the patient has an ultrasound - and if obstruction and
indicated a nephrostomy - within 6 hours due to the risk of
hydronephrosis
septic shock. [3] [13] [64]
• normal kidney size
Renal tract ultrasound is not routinely required. Only in the setting of AKI
request it if no obvious cause for the AKI can be found or if
and unclear cause
obstruction, pyelonephritis, or pyonephrosis is suspected.
[3] [13] and positive serology
suggests a rarer cause
• Ensure the ultrasound is performed within 24 hours if no • reduced
obvious cause for the AKI can be identified or a urinary tract
corticomedullary
obstruction is suspected.[3] [64]
• Ultrasound has high sensitivity (90%-98%) but lower specificity differentiation and/
(65%-84%) for diagnosing upper tract obstruction, although or small and scarred
this may not be the case in the early stages (first 8 hours).[13] kidneys is consistent
• Repeat the ultrasound after 24 hours if:
with CKD
• There is a high index of suspicion for hydronephrosis (as
it may take several hours for this to develop due to initial
non-compliance of the pelvi-caliceal system)
• The patient has oliguric acute tubular necrosis with
superimposed obstruction (because urine is needed to
dilate the kidneys).
If prior creatinine values are not available to give a baseline,

ultrasound can sometimes be helpful in distinguishing AKI from
CKD.[62] [13]
DIAGNOSIS
• Ultrasound may demonstrate small (sometimes scarred)

kidneys consistent with advanced CKD (such changes are
unlikely to be seen in less severe CKD).
• Be aware that an ultrasound finding consistent with CKD does
not exclude the possibility of AKI on a background of CKD.[13]
abdominal CT or MRI scan image of mass or stone may

Consider requesting a CT or MRI If obstruction is suggested be present
on ultrasound (e.g., possible masses or stones). [13]
• These are not routinely needed - the decision will depend on

the degree of obstruction.
• Be cautious with intravenous iodinated contrast CT scans
in patients with AKI. MRI is preferred (although note that
gadolinium may be needed for MRI enhancement).
Test Result
nuclear renal flow scan normal scan reveals
Nuclear renal flow scans can sometimes be useful to appropriate kidney perfusion,
evaluate for obstruction in cases of mild hydronephrosis, tracer uptake, and excretion
when the diagnosis of mechanical obstruction is uncertain.
[13] abnormal scan may
• The scan is performed before and after a dose of loop diuretic. demonstrate:
• impaired tracer
excretion (supportive of
acute tubular necrosis)
• poor blood flow
(supportive of
obstruction of blood
supply)
• normal blood flow and
tracer excretion with
tracer accumulation
in the collecting
system (supportive of
obstruction of the urine
outflow tract)
urine osmolality • urine osmolality >500

Urine osmolality is rarely requested. [13] mOsm/kg (in the
absence of recent
• Urine osmolality is the number of moles of solute per kg of
administration of
solvent and it depends on tubule response to anti-diuretic
iodinated contrast)
hormone (ADH).
DIAGNOSIS
suggests pre-kidney
• High urine osmolality suggests pre-kidney AKI with
preservation of tubule function (assuming no recent AKI with preservation
administration of iodinated contrast).[1] [83] of tubule function
• urine osmolality <300
• However this should not be interpreted as confirming
mOsm/kg suggests
pre-kidney AKI because intact tubule function
(particularly in the early stages) may be seen in various tubule damage
forms of kidney disease (e.g., glomerulonephritis).[1]
• Low urine osmolality suggests tubule damage (intrinsic AKI) as

urinary concentration is impaired.[83]
urine sodium concentration urinary sodium <20 mmol/

In pre-kidney AKI the urinary sodium is typically low (<20 L suggests avid sodium
mmol/L). [13] retention in pre-kidney AKI
• This is dependent on preserved tubule function.
Urinary sodium is raised in intrinsic AKI when there is

tubule damage, or in response to diuretics.
43
Test Result
fractional excretion of sodium/urea • a fractional excretion of
sodium (FENa ) of <1%
supports pre-kidney
AKI, as long as tubular
function remains intact
• invalid if the
patient has
received
diuretics
• a fractional excretion of
urea of <35% supports
a diagnosis of pre-
kidney AKI
• may be helpful
if the patient
has had diuretic
exposure
urinary eosinophil count • >5% to 7% supports

Urinary eosinophil counts may be of some use in patients a diagnosis of
with pyuria. [85] [13] [64] acute interstitial
nephritis but is not
• A result above 5% to 7% supports a diagnosis of acute allergic diagnostic because
interstitial nephritis but is not diagnostic because of low of low sensitivity and
sensitivity and specificity.[85] The test is dependent on the specificity[85]
• has a negative
DIAGNOSIS
expertise of the microscopist.

• It has a negative predictive value of >90% among patients with predictive value of
AKI and may be useful in excluding the disease process.[86] >90% for patients
• Eosinophiluria may be seen with atheroembolic disease as with AKI and may be
useful in excluding the
well. disease process[86]
serum creatine kinase markedly elevated in

Request if rhabdomyolysis is suspected. [62] [13] [64] rhabdomyolysis
ANA (anti-nuclear antibodies) normal or elevated

A broad screening test for a range of autoimmune
diseases (e.g., kidney manifestations of systemic lupus
erythematosus [SLE]).[13] [64] [65]
anti-dsDNA normal or elevated
Elevated titre supports the diagnosis of SLE, which often
includes the kidney. [13] [64] [65]
Test Result
complement (C3, C4, CH50) normal or depressed
Low complement levels support an active disease process
such as SLE. [13] [64] [65]
• Reduced levels are also seen in infectious endocarditis.
anti-glomerular basement membrane antibody normal or elevated

Elevated in anti-glomerular basement membrane antibody
disease and Goodpasture syndrome. [13] [64] [65]
anti-neutrophil cytoplasmic antibodies (ANCA) normal or elevated titres
Elevated titres are seen in small vessel vasculitic syndromes
such as: [13] [64] [65]
• Granulomatosis with polyangiitis

• Eosinophilic polyangiitis
• Microscopic polyangiitis.
acute hepatitis profile positive or negative serology

Positive serology in active hepatitis B or C is associated
with kidney conditions such as membranoproliferative
glomerulonephritis and cryoglobulinaemia.
HIV serology positive or negative
Relevant with regard to HIV-associated nephropathy and
nephrotoxicity of some of the medications used to manage
HIV.
cryoglobulins positive or negative serology
The presence of cryoglobulins in a patient with AKI
supports a diagnosis of cryoglobulin-associated
DIAGNOSIS
glomerulonephritis.
anti-streptolysin-O antibody normal or elevated
An elevated titre supports but is not diagnostic of post-
streptococcal glomerulonephritis as the cause of AKI.[13]
serum/urine electrophoresis • paraprotein
Myeloma is an important potential cause of AKI and should identified on serum
be considered in a patient aged >40 years who presents with electrophoresis
hypercalcaemia, hyperuricaemia, or pathological fracture. [9] • Bence Jones protein
[64] [65]
detected on urine
• Serum electrophoresis will show a paraprotein (monoclonal electrophoresis
immunoglobulin).
• Urine electrophoresis will detect Bence Jones proteins (free
light chains) which are not detected on urinalysis.
45
Test Result
cystoscopy direct visualisation and
May be requested to identify cause of obstruction (e.g., treatment of ureteral stenosis
ureteric stenosis, bladder tumour). if present
kidney biopsy changes associated with rarer

Kidney biopsy may be required to further investigate positive forms of intrinsic AKI
serological studies and confirm the cause of AKI. [13]
Emerging tests
Test Result
novel serum and urinary biomarkers not in current clinical use
Various novel serum and urinary biomarkers have been studied in
the earlier diagnosis of AKI[88] and as predictors of mortality after
AKI.[89] [90] More robust studies are required to determine the role of
the biomarkers.[91] [92] [93] [94] [95]
DIAGNOSIS
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Chronic kidney disease • Reduced kidney function • An acutely elevated serum
with elevation of creatinine creatinine is diagnostic
is chronic (>3 months), of AKI and indicative of
although there may be acute reduced clearance. The
on chronic kidney disease. clinical context is important
in differentiating AKI from
a progression of CKD at
initial presentation if there
are no recent comparison
creatinine values available
for the patient. Features that
favour a diagnosis of CKD
(although do not exclude
AKI) include hypocalcaemia,
hyperphosphataemia,
anaemia, and small kidneys
(sometimes scarred) on
ultrasound.[9] [62]
• There are no causes of
chronically elevated serum
creatinine other than
reduced glomerular filtration
(except for minor elevations
in subjects with increased
muscle mass and from
certain medications).
• Creatinine elevation over
time provides a chronological
perspective and assists in
differentiating acute from
DIAGNOSIS
chronic kidney disease.
• Twenty-four-hour urine study
for creatinine clearance
demonstrates the level of
kidney function; the use
of 131-I iothalamate is
the definitive test for this
purpose.
Increased muscle mass • Any elevation of creatinine • Acutely elevated serum

is minor and typically non- creatinine is diagnostic of
acute. AKI.
• Minor elevations in creatinine
from increased muscle mass
may rarely be seen.
• Twenty-four-hour urine study
for creatinine clearance
demonstrates normal kidney
function.
47
Condition Differentiating signs / Differentiating tests

symptoms
Drug side effect • Certain medicines such as • Discontinuing the medicine
cimetidine or trimethoprim should result in normalising
may lead to an elevation of of the serum creatinine.
creatinine that is minor and • Twenty-four-hour urine study
non-acute. for creatinine clearance
should demonstrate normal
function.
Criteria
Kidney Disease: Improving Global Outcomes (KDIGO) - definition
criteria[1]
Any of the following:
• Increase in serum creatinine by ≥26 micromol/L (≥0.3 mg/dL) within 48 hours; or

• Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred
within the prior 7 days; or
• Urine volume <0.5 mL/kg/hour for 6 hours.
Kidney Disease: Improving Global Outcomes (KDIGO) - severity

criteria[1]
• Stage 1
• Serum creatinine 1.5 to 1.9 times baseline; or

• ≥26 micromol/L (≥0.3 mg/dL) increase in serum creatinine; or
DIAGNOSIS
• Urine output <0.5 mL/kg/hour body weight for 6 to 12 hours
• Stage 2
• Creatinine increased 2.0 to 2.9 times; or

• Urine output <0.5 mL/kg/hour for 12 hours or longer
• Stage 3
• Creatinine increased ≥3.0 times; or

• Increase in creatinine to ≥354 micromol/L (≥4.0 mg/dL); or
• Initiation of renal replacement therapy; or
• Urine output <0.3 mL/kg/hour for 24 hours OR anuria for 12 hours.
RIFLE (Risk, Injury, Failure, Loss of kidney function, and Endstage

kidney disease) consensus criteria[69]
Laboratory test indicates reduced kidney clearance.
Severity groups are as follows.
• Indicates risk:
• Serum creatinine increased 1.5 times; or

• Urine production of <0.5 mL/kg body weight for 6 hours.
• Indicates injury:
• Creatinine increased 2.0 times; or

• Urine production of <0.5 mL/kg for 12 hours.
• Indicates failure:
• Creatinine increased 3.0 times; or

• Urine output <0.3 mL/kg for 24 hours or anuria for 12 hours.
• Indicates loss:
• Persistent AKI for more than 4 weeks; complete loss of kidney function.
• Indicates ESRD:
• ESRD (loss >3 months).
DIAGNOSIS
National Institute for Health and Care Excellence: detecting acute
kidney injury[3]
Detect AKI, in line with the RIFLE, Acute Kidney Injury Network (AKIN), or KDIGO definitions, by using any of
the following criteria:
• A rise in serum creatinine of 26 micromol/L (0.3 mg/dL) or greater within 48 hours; or
• A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days;
or
• A fall in urine output to <0.5 mL/kg/hour for more than 6 hours in adults and more than 8 hours in
children and young people; or
• A 25% or greater fall in estimated GFR in children and young people within the past 7 days.
49
Acute kidney injury Management
Recommendations
Urgent
Immediate management is supportiveand guided by the cause.
• In most patients with AKI, the priority is to treat hypovolaemia and correct electrolyte
imbalances.[13]
Use a simple care bundle - STOP AKI is a good option although others are available:[62] [64]
• Sepsis - perform an urgent septic screen and implement your local care bundle (e.g., Sepsis Six)
within 1 hour if infection is suspected. See our Sepsis in adults topic for more information.
• Toxins - identify and stop (or avoid exposure to):[1] [13]
• Nephrotoxic drugs (e.g., non-steroidal anti-inflammatory drugs [NSAIDs],

aminoglycoside antibiotics, iodinated contrast agents)[1]
• Nephrotoxins (a contributor in 20%-30% of cases of AKI).[1]
• Optimise volume status and blood pressure (BP).
• If hypovolaemic, give an immediate intravenous bolus of crystalloid (choose a balanced

crystalloid unless hyperkalaemia is confirmed or suspected, in which case use normal
saline).[62] [65]
• Withhold drugs that may exacerbate AKI, particularly ACE inhibitors or angiotensin-II
receptor antagonists.
• Consider withholding diuretics and other antihypertensive medications.
• Escalate to critical carefor consideration of vasopressors if the patient remains severely
hypotensive despite adequate volume resuscitation.
• Prevent harm
• Identify and treat reversible causes (e.g., relief of any urinary tract obstruction).
• Treat life-threatening complications (e.g., hyperkalaemia and acidosis).
• Review and modify doses of all medications in line with the degree of kidney injury.[13]
[64]
Refer the following life-threatening complications for emergency renal replacement therapy
(RRT): [13] [64]
• Refractory hyperkalaemia (potassium >6.5 mmol/L)

• Refractory metabolic acidosis (pH <7.15)
MANAGEMENT
• Refractory volume overload with or without pulmonary oedema

• End-organ complications of uraemia (e.g., pericarditis, encephalopathy, uraemic bleeding) or
other end-organ involvement (e.g., neuropathy, myopathy)
• Severe AKI and poisoning/drug overdose (e.g., ethylene glycol, lithium).
Key Recommendations
It is crucial to identify the cause and severity of the AKI when formulating your management plan for
the patient.[1] [62]
In most patients, successful management consists of:[1] [62] [13] [64] [65]
• Supportive therapy with close ongoing monitoring of volume status and electrolytes
• Prompt identification and management of the underlying cause (e.g., sepsis, nephrotoxic
medication, urinary tract obstruction)
• Early recognition and correction of life-threatening complications (e.g., hyperkalaemia,
acidosis, volume overload).
Most patients with AKI do not need referral to nephrology. [62] Do referif there is:[3] [64]
• Uncertainty about the cause or apoor response to treatment or complications that fail to
respond to medical management
• A specific diagnosis that might need specialist treatment (e.g., vasculitis, glomerulonephritis,
myeloma)
• Stage 3 AKIor AKI in a patient with pre-existingCKD stage 4 or 5
• A history of kidney transplant.
Management of volume status

Prompt correction of volume depletion or volume overloadcan often reverse or improve AKI.
Hypovolaemia is common at presentation.
• Start immediate intravenous fluid resuscitation to improve kidney perfusion but take care to
use close monitoring to avoid volume overload.[1] [62] [13] [64]
• Give a 500 mL intravenous bolus of crystalloid over 15 minutesand then continue with goal-
directed fluid therapy.
• Escalate for senior reviewif no improvement after two boluses.[62] [96]
If the patient is volume overloaded, consider the need for a loop diuretic or RRT - consult the
nephrology team.[1] [13]
• Never use loop diuretics in AKI without specialist supervision.
Specific treatment of the underlying cause

No specific treatment has been shown to be effective in pre-kidney AKIthat is secondary to
hypovolaemia and/or sepsis.[13]
• A key principle is to correct the haemodynamic status of the patient to improve kidney
MANAGEMENT
perfusion.[62] [64]
Specific management of intrinsic AKIdepends on the aetiology and is led by the nephrology team
so early referral is important.[62] For example:
51
• Interstitial nephritis - stop causative drugs and manage with a corticosteroid.
• Acute glomerulonephritis/vasculitis - managed with a cytotoxic or immunomodulating agent.
In obstructive AKI relief of the obstruction is key.[9] [64]
• Insert a bladder catheterif obstruction is suspected clinically and cannot be quickly ruled out by
ultrasound. Input from the urology and/or radiology team will be needed.
• Refer immediately to urology and/or radiology if the patient has pyonephrosis (ensure an
ultrasound within 6 hours), an obstructed single kidney, bilateral upper urinary tract obstruction, or
complications secondary to obstruction.[3]
Management of complications
Hyperkalaemia - management depends on the severity but may include:
• Immediate cardiac protection with intravenous calcium chloride or calcium gluconate -

ensure ongoing ECG monitoring
• Adjunctive therapy to drive potassium intracellularly with intravenous insulin/glucose (beware
the risk of hypoglycaemia) and nebulised salbutamol
• Treatment to remove potassium from the body with a cation-exchange resin (e.g., calcium
polystyrene sulfonate)
• Withholding culprit medications (e.g., ACE inhibitor, angiotensin-II receptor antagonist,
potassium-sparing diuretics)
• RRT is indicated for severe refractory hyperkalaemia.
Acidosis - severe metabolic acidosis may need treatment with intravenous sodium bicarbonate
(only under expert supervision due to the risk of volume overload and/or hypernatraemia).
• RRT is indicated for refractory acidosis.
Pulmonary oedema - often results from overzealous fluid resuscitation in a patient who presented with
hypovolaemic AKI. For immediate management:[62] [64]
• Sit the patient upright

• Give high-flow ox ygen and intravenous glyceryl trinitrate
• Seek senior support
• A loop diuretic may be used to manage associated volume overload but only with specialist
supervision
• Never allow these holding measures to delay initiation of RRT if indicated.[13]
Full Recommendations
Principles for managing AKI
MANAGEMENT
Determine the cause and severity of AKI when formulating your management plan for the
patient. [1] [62]
• Monitor electrolytes and acid-base balance and correct any abnormalities. Tailor the frequency of
monitoring to individual patient risk factors and the severity (stage) of AKI.
In most patients, successful management of AKI consists of: [1] [62] [13] [64] [65]
• Supportive therapyand close ongoing monitoringof volume status and electrolytes.
• Focus in particular on giving adequate intravenous fluids to ensure rapid correction of

hypovolaemia if present (e.g., from haemorrhage, gastrointestinal losses, inadequate fluid
intake) - but take care to avoid volume overload.
• Prompt identification and treatment of any reversible underlying cause, for example:
• Sepsis - perform an urgent septic screen and implement your local care bundle
(e.g., Sepsis Six) within one hour if infection is suspected. See our Sepsis in adults topic for
more information.
• Discontinuation/avoidance of nephrotoxic medicationsor any other drugs that might
cause indirect harm to kidney function.
• Relief of any urinary tract obstruction - refer urgently to urology and/or radiology as
appropriate.[3]
• Recognition and management of life-threatening complications (e.g., hyperkalaemia,

acidosis, pulmonary oedema, uraemia).
RRT is indicated in patients who have refractory volume overload or other complications
that fail to improve with medical management. [1] [3] [13] [64]
In rarer forms of intrinsic AKI, more specific management interventions will be needed. [13]
Practical tip
The UK Royal College of Physicians suggests the use of the STOP AKI acronym as an
aide-memoire to recall the immediate steps needed for management of AKI: [62]
• Sepsis - implement the your local care bundle (e.g., Sepsis Six) within 1 hour if sepsis is
suspected or confirmed. Identify and treat the source of infection.
• Toxins - stop/avoid nephrotoxins (e.g., NSAIDs, aminoglycoside antibiotics, iodinated contrast
agents).[1]
• Optimise volume status/BP - assess volume status and give intravenous fluids as needed;
hold antihypertensive medication and diuretics; consider vasopressors if patient does not
respond.[3]
• Prevent harm - treat complications; identify and treat the cause of AKI; review all medications
and adjust doses appropriately; closely monitor intravenous fluid therapy.
MANAGEMENT
Specialist referral
Most patients with AKI do not need referral to nephrology. [62]
• Do not refer if there is a clear cause and the AKI is responding to medical management.[3] [97] [98]
53
Refer immediately to critical care and/or nephrology if:
• The patient meets (or is anticipated to meet) the criteria for RRT[3] [64]
• There are severe complications that cannot be managed medically (such as hyperkalaemia,
pulmonary oedema, acidosis, or uraemia)[64]
• The patient remains haemodynamically unstable after appropriate supportive care and/or there are
signs of multi-organ failure.[64]
Check local protocols for referral criteria and pathways.
Refer for urgent discussion with nephrology (as soon as possible and within 24 hours at the
latest) if any one or more of the following is present: [3] [64]
• Uncertainty about the cause of AKI or a poor responseto treatment

• A possible diagnosis that may need specialist treatment (e.g., vasculitis,
glomerulonephritis, tubulointerstitial nephritis, myeloma)
• Complications associated with AKI that are not responding to medical treatment
• Stage 3AKI
• AKI in a patient with pre-existing chronic kidney disease (CKD) stage 4 or 5
• The patient has a kidney transplant.
Refer to urology and/or radiology if the patient has an upper urological tract obstruction. [3]
• Refer immediately in any case of pyonephrosis, an obstructed solitary kidney, bilateral upper
urinary tract obstruction, or complications of AKI associated with obstruction.
After recovery from an episode of AKI, consider referral to nephrology if: [3]
• 2
Estimated glomerular filtration rate (eGFR) is ≤30 mL/min/1.73 m
• There is hypertension or proteinuria (1+) on an early morning urine dipstick (particularly in a child or
young person).
MANAGEMENT
Evidence: Speed of referral to nephrology
There is little evidence available to support routine referral to the nephrology team for every
patient with stage 2 AKI.
Evidence is lacking on whether outcomes are improved by routine rapid referral to

nephrology (within 12 hours) for all patients with stage 2 or 3 AKI that does not need
critical care input. [3]
• The large number of AKI cases among patients admitted acutely to hospital makes it impractical
to refer every patient with suspected or confirmed AKI to nephrology.
• Initial management for most patients encompasses identification and treatment of sepsis,
avoidance of nephrotoxins, fluid replacement, and correction of hypotension. These steps can
be commenced by any medical or surgical team.
• Potential benefits of routine nephrology referral include a faster diagnosis in patients with
primary kidney disease, prevention of progressive AKI and the potential need for RRT,
avoidance of a delayed transfer to critical care, improved chances of kidney recovery, and a
shorter hospital stay.
• However, there is very little evidence to support routine nephrology referral for all patients with
stage 2 or 3 AKI.[3]
• Very low quality evidence from one large retrospective study suggested that for non-
critically ill patients with AKI, early compared with delayed referral to nephrology may
reduce in-hospital mortality, the number of patients needing RRT, and length of hospital
stay.[99]
Volume status monitoring and management

An assessment of the patient’s volume status is a crucial part of your initial examination. [1]
[62] [13] [64]
• Prompt correction of volume depletion or volume overload (especially if associated with worsening
cardiac output) can reverse or improve AKI.
• Both hypovolaemia and volume overload are associated with worse outcomes, so careful
management of fluid balance is vital.[1]
Pre-kidney AKI (80% of all cases) is most often caused by hypovolaemia and/or hypotension
• A key principle is to improve the haemodynamic status of the patient and restore kidney
perfusion.[62] [64]
Look for signs of hypovolaemia. Your assessment should cover: [62] [13]
MANAGEMENT
• Peripheral perfusion (capillary refill time)

• Pulse rate
• BP (including a check for postural hypotension) - taking into account the patient’s baseline BP
55
• Dry axillae/mucous membranes
• Skin turgor.
Practical tip
An early fluid challenge can be both diagnostic and therapeutic for pre-kidney AKI.
• In AKI that is secondary to hypovolaemia, kidney function may improve rapidly in response to
administration of intravenous fluids.
Signs of volume overload are less common at presentation; for example: [64]
• Respiratory rate - tachypnoea suggests fluid overload and/or acidosis

• Crackles on auscultation of lungs may suggest pulmonary oedema
• Peripheral oedema.
Ensure at least daily ongoing monitoring of volume status for any patient with established
AKI or at risk of AKI, via: [13] [64]
• Review of haemodynamic status, including postural BP

• Weight monitoring
• Fluid input/output chart
• Routine urinary catheterisation is not appropriate, so weigh up the benefits and risks (in
particular, infection and trauma) for the individual patient.[64] Catheterisation is indicated if
fluid balance management is crucial in an acutely unwell patient (e.g., hourly monitoring of
fluid balance is needed) or if the patient is too ill or frail to use a bottle or commode
• Urea and electrolytes.
Management of hypovolaemia
Fluid resuscitation
If the patient is hypovolaemic, start immediate intravenous fluid resuscitation to improve
kidney perfusion - but take care to avoid volume overload. [1] [62] [13] [64]
• Give a 500 mL intravenous bolus of fluid over 15 minutes.

• Use a wide bore cannula to allow adequate fluid resuscitation.
• A crystalloid fluid is preferred.[1] [62] [13] [64]
• A smaller bolus (e.g., 250 mL) may be more appropriate if the patient has a history of cardiac
failure.[65]
Use a balanced crystalloid unless hyperkalaemia is suspected or confirmed. [62] [65]

MANAGEMENT
• Balanced crystalloid options include Hartmann’s solution, Ringer’s acetate, or Plasma-

Lyte 148® (a solution of sodium chloride, sodium gluconate, sodium acetate trihydrate, potassium
chloride, and magnesium chloride hexahydrate).
• Use normal saline(0.9% sodium chloride) instead if hyperkalaemia is present (potassium
>5.5 mmol/L) or suspected (e.g., rhabdomyolysis). This is because balanced crystalloids all
contain potassium.
• Once hyperkalaemia has been treated and resolved, switch to a balanced crystalloid due
to the risk of hyperchloraemic metabolic acidosis associated with excessive use of normal
saline.[62]
Reassess haemodynamic status after the initial fluid bolus and consider whether further 250
to 500 mL boluses are required.
• Goal-directed fluid therapy is recommended.[13]

• Reassess the patient’s response to each fluid challenge through careful clinical examination
(ABCDE approach) and monitoring of:[96]
• BP
• Pulse rate
• Capillary refill time
• Signs of pulmonary oedema
• Urine output.
• If no improvement is seen after two fluid challenges, escalate the patient for senior
review. [62] [96]
• If the patient has already had ≥2 L of fluid, or is in shock, seek immediate senior help
so that critical care involvement for vasopressor support can be considered.[62]
• In a patient with profound sepsis it can take >24 hours for antibiotics to act and the
vascular permeability to reverse and BP to respond to intravenous fluids.
As soon as haemodynamic stability is restored and the patient is euvolaemic, review and
adjust the intravenous fluid prescription to match the patient’s ongoing fluid requirements.
[62] [96]
• It is vital to recognise when to de-escalate intravenous fluid therapy. Failure to do so can result in
volume overloadand precipitate pulmonary oedema.
• There is a particular risk from over-aggressive fluid resuscitation if the patient is oliguric/
anuric or has a history of heart failure.[13] [96]
MANAGEMENT
57
Practical tip
Passive leg raising can help predict fluid responsiveness in critically ill patients. [62]
[13]
• In the context of acute hypovolaemia, passive leg raising can improve the venous return and the
response in BP can be recorded.
• A rise in BP confirms hypovolaemia and the need for further fluid resuscitation.[62]
• Passive leg raising is most commonly practised on critical care units.
Practical tip
Always be clear about the purpose of the intravenous fluid therapy you are prescribing.
• The UK National Institute for Health and Care Excellence (NICE) has categorised these as
Resuscitation, Replacement, or Routine maintenance:[100]
• Resuscitation fluid therapy is aimed at re-establishing haemodynamic stability by

restoring intravascular volume.
• Replacement fluid therapy provides daily maintenance water and electrolyte
requirements and replaces any ongoing abnormal fluid losses.
• Maintenance fluid therapy must provide daily ongoing water and electrolyte
requirements (i.e., sodium 1 mmol/kg, potassium 1 mmol/kg, and water 25-35 mL/kg)
• Never give maintenance fluids at a rate of >100 mL/hour.
Never prescribe intravenous fluid therapy for more than 24 hours at once due to the risk
of causing volume overload.
Blood transfusion will be indicated if hypovolaemia is secondary to significant blood loss.
• This is generally not given unless more than one unit is anticipated, based on local guidelines and
the clinical assessment of the patient.[5]
• Note that this may worsen hyperkalaemia.
Vasoactive drugs
Vasopressor support is recommended if the patient remains severely hypotensive despite
adequate volume resuscitation (e.g., in septic/hypovolaemic shock). [1] [62] [13] [96]
• Escalate to critical care. Vasopressors should only be used with continuous haemodynamic
monitoring in place.
• A reasonable goal is to maintain mean arterial pressure (MAP) ≥65 mmHg, but this target may
MANAGEMENT
need adjusting according to the patient’s baseline BP.[1] [13] [64]
• In the setting of vasomotor shock where the patient has persistent hypotension despite
optimisation of intravascular volume through aggressive fluid resuscitation, preservation and
improvement of kidney perfusion can only be achieved by the use of systemic vasopressors.[1]
Noradrenaline (norepinephrine) is the usual vasopressor of choice, with the addition of

vasopressin if needed.
• There is little good evidence available to guide the choice of vasopressor in patients with AKI and
septic shock.[1] [13]
• Do not use low-dose dopamine to treat AKI.[1] [3] [13]
• There is no evidence to support its use and it can worsen kidney perfusion in patients
with AKI.
Consider the potential need for an inotrope (e.g., dobutamine) to optimise cardiac output
if kidney hypoperfusion is caused by impaired cardiac function due to poor left ventricular
systolic function. [13]
MANAGEMENT
59
Evidence: Evidence is scarce to guide the choice of vasopressor
It is not known which vasopressor agent is most effective for prevention or treatment of AKI
and septic shock.
There is insufficient evidence to say that one vasoactive agent is bet ter than another in
preventing or treating AKI. [1]
• Small open-label studies have shown improvement in creatinine clearance after a 6- to 8-hour
infusion of noradrenaline.[101]
• Vasopressin, when compared with noradrenaline in one RCT, was found to increase BP and
enhance diuresis, but has not yet been proven to enhance survival or reduce the need for
RRT.[102]
• A post-hoc analysis of the same RCT used the RIFLE criteria for AKI to compare the
effects of vasopressin versus noradrenaline.[103] Vasopressin was associated with a
trend to a lower rate of progression of the AKI, and a lower rate of use of RRT.
• According to the Kidney Disease: Improving Global Outcomes (KDIGO) guideline group,
this study suggests that vasopressin may reduce progression to kidney failure and
mortality in patients with septic shock who have or are at risk of AKI.[1]
• Dopamine has no significant clinical benefits in patients with AKI. [13]
• A large randomised controlled trial (RCT) comparing dopamine with noradrenaline as

the initial vasopressor in patients with shock showed no significant differences between
groups with regard to kidney function or mortality.[104]
• However, there were more arrhythmic events among the patients treated with
dopamine than among those treated with noradrenaline, and dopamine was
associated with an increased rate of death at 28 days among the patients with
cardiogenic shock.
• Both the NICE and KDIGO guidelines include a recommendation not to offer low-dose
dopamine to treat AKI.[1] [3]
Management of volume overload

Volume overload in a patient with AKI can occur as a result of:
• Overaggressive fluid resuscitation in a patient who initially presented with hypovolaemic pre-
kidney AKI. This is most commonly seen in patients with sepsis.
• Oliguria in intrinsic or post-kidney AKI.
MANAGEMENT
If the patient is volume overloaded, consider the potential need for a diuretic or RRT. Discuss
with the nephrology team.
• Patients with volume overload need careful monitoring and management to reduce the risk of a
poor outcome.
• Failure to manage volume overload can lead to complications including pulmonary oedema.[62]
In critically ill patients, a positive fluid balance (>5% body weight) has been found to be associated
with an increase in mortality at up to 1 year follow-up when compared to neutral or negative (<5%)
fluid balance.[13]
• Management of volume overload may include:
• Sodium restriction
• Cautious use of a loop diuretic under specialist supervision[1] [13]
• RRT -immediate RRT is indicated for refractory volume overload or volume overload
associated with severe complications of AKI.[62] [13] [64] For more details, see the section
further down on Indications for RRT.
Consider a loop diuretic (under specialist supervision) to treat volume overload.[1] [13]
• A loop diuretic such as furosemide may be useful in achieving euvolaemia in a patient

with fluid overload (with or without pulmonary oedema).[1] This must be done with caution and
under the supervision of the nephrology team.
• Note that there is no evidence to support the routine use of loop diuretics for
management of AKI in the absence of volume overload.[1] [3] [13]
• Never use a loop diuretic if the patient is hypovolaemic or hypotensive. The diuretic will
exacerbate the haemodynamic instability.
• Do not allow the use of loop diuretics to delay more definitive management of volume
overload.
• Careful monitoring of response is important (e.g., urine output). Stop the diuretic if there is no
response.
• Proceed without delay to more definitive management with RR T if the response to
diuretics is unsuccessful.[64]
MANAGEMENT
61
Evidence: The role of loop diuretics in patients with AKI
Loop diuretics have no routine role in the management of AKI. They should be reserved for
specific indications (such as volume overload) and only used under specialist supervision.
There is no evidence for any benefits from the routine use of loop diuretics in patients
with AKI - but there is some evidence to suggest harm.
• The theoretical rationale for the use of loop diuretics to treat AKI is based on their potential to
reduce oxygen consumption in the ascending loop of Henle, thereby reducing any ischaemic
damage to the kidneys. They may also be used to convert oliguric AKI to non-oliguric AKI.[1]
[13]
• However, diuretics can also excessively reduce circulating volume and so cause a pre-
kidney insult that could worsen established AKI. Hence an evaluation of the available
evidence is vital to determine their appropriate role.
• There is no evidence to support the use of loop diuretics in routine treatment of AKI.
• One RCT found furosemide to be ineffective in treating AKI and epidemiological data
suggest the use of loop diuretics may increase mortality in patients with critical illness and
AKI.[105] [106]
• Two systematic reviews on the use of furosemide to prevent or treat AKI found no
significant effect on in-hospital mortality, risk for requiring RRT, the number of dialysis
sessions needed, or even the proportion of patients with persistent oliguria.[107] [108]
• Prophylactic furosemide has been shown to increase the risk of AKI when given to
prevent AKI in patients having cardiac surgery.[109]
• There is no evidence to support the use of loop diuretics for managing AKI-associated
hyperkalaemia.[110]
• However, in practice their use may be considered (with specialist supervision) as an

adjunct to other therapies provided the patient is fluid replete.
Medication review
Whenever AKI is suspected or confirmed, review all medications and stop/avoid any
nephrotoxic drugs and other drugs that may affect kidney function. [13] [64] [65]
• Common nephrotoxic drugs include aminoglycoside antibiotics, NSAIDs, and iodinated

contrast agents.[1] Consult a pharmacist for a full list of nephrotoxic drugs.
• ACE inhibitors, angiotensin-II receptor antagonists, and other renin-angiotensin modifying
MANAGEMENT
agents can exacerbate AKI by reducing the kidney’s ability to adapt to changes in perfusion
pressure.[9]
• Diuretics or other antihypertensives increase the risk of hypovolaemia/hypotension.
• If there are overriding reasons why a potentially harmful drug must be continued, seek specialist
pharmacist advice to minimise negative effects (e.g., dose adjustment, keep the treatment
course as short as possible, monitor blood levels of the drug if feasible).
Review and adjust doses of all other medications in line with the patient’s degree of kidney
injury. [13] [64]
• Any medication that is cleared via the kidneys has the potential to accumulate during an episode of
AKI. Dose adjustment is therefore important to prevent toxicity and patient harm.
• Inappropriate drug dosing in patients with AKI is an important cause of adverse drug events.[13]
When restarting drugs after an episode of AKI, ensure:
• Any medications that were used for the treatment of pre-existing heart failure are re-started as
soon as clinically reasonable and re-titrated to achieve the best control of fluid balance and blood
pressure[13]
• All medications are reviewed before discharge and a plan is put in place to reintroduce any
medications that have been withheld, at an appropriate time, with re-titration to the optimum dose
continued in primary care as appropriate[96]
• Ensure a process is in place for measurement of serum creatinine and potassium 1 to

2 weeks later. This may need to be part of discharge planning.[13]
Specific treatment for the underlying cause of AKI

Alongside supportive therapy and management of any complications, it is important to identify and treat
the specific underlying cause of AKI.
Pre-kidney AKI
No specific pharmacological treatment has been proven to treat AKI that is secondary to
hypovolaemia and/or sepsis. [13]
• Pre-kidney AKI is most often caused by hypovolaemia and/or hypotension.

• A key principle is to improve the haemodynamic statusof the patient and restore kidney
perfusion through careful administration of intravenous fluid resuscitation (plus vasopressor
therapy if needed).[62] [64]
Intrinsic AKI
Specific management of intrinsic AKI depends on the aetiology and is led by the nephrology
team. [62]
MANAGEMENT
• Immunological tests and kidney biopsy are needed to confirm acute glomerulonephritis,
ANCA-associated vasculitis, anti–glomerular basement membrane (anti-GBM)
antibody disease (Goodpasture syndrome if associated with pulmonary hypertension),
and lupus nephritis.
63
• Treatment will require corticosteroids, cytotoxic agents, immunomodulating drugs, and/or
plasma exchange.
• Atypical haemolytic uraemic syndrome (HUS)is treated with the monoclonal antibody
eculizumab or plasma exchange.[111]
• Thrombotic thrombocytopenic purpura (TTP)is treated with plasma exchange.[112]
• Acute allergic interstitial nephritis is treated with a corticosteroid (after excluding
infection) and stopping potential causative medications (e.g., proton-pump inhibitors, NSAIDs,
antibiotics).[113]
Obstructive AKI
Relief of the obstruction is key in the management of obstructive AKI. [9] [64]
• Insert a bladder catheter in any case of AKI when bladder outlet obstruction is suspected
clinically and cannot be quickly ruled out by ultrasound.
• Refer to urology within 24 hours if obstruction is confirmed on ultrasound.[3] [64]
Refer immediately to urology and/or radiology if one of more of the following is present: [3]
• Pyonephrosis - if pyonephrosis is suspected, ensure the patient has an ultrasound within 6 hours
(because of the risk of septic shock)[3]
• Obstructed single kidney
• Bilateral upper urinary tract obstruction
• Complications of AKI secondary to urological obstruction.
Refer to urology and/or radiology for ureteral stenting, urinary diversion, debulking
procedures, or other case-specific requirements. [64]
• Nephrostomy or ureteral stenting must be undertaken as quickly as possible and at the latest
within 12 hoursof diagnosis.[3]
• Ureteral stenting may be indicated if there is a ureteral stricture, stone, or extrinsically obstructing
mass.
• Lithotripsy or surgical removal may be needed if obstruction is caused by stones at the
ureteropelvic junction.
• Exploratory laparotomy may be indicated if a compressing tumour is suspected that may require
surgical removal; this may be done following ureteral stenting.
• Percutaneous nephrostomy (placement of a catheter into the renal pelvis percutaneously for
drainage of urine from a distal obstruction) may be undertaken by a urologist, surgeon, or
interventional radiologist.
MANAGEMENT
RRT may be needed while the underlying obstruction is being addressed if there is severe
acidosis, volume overload, or electrolyte or uraemic complications.
Management of complications of AKI
Hyperkalaemia [62]
Hyperkalaemia is a common complication of AKI. It can lead to:
• Muscle weakness
• Cardiac arrhythmias (e.g., bradycardia, bundle branch block, ventricular tachycardia, ventricular
fibrillation, asystole).
Treatment depends on the severity and presence of muscular and/or cardiac complications.
The principles of treatment are: [110]
• Immediate cardiac protection with intravenous calcium chloride or calcium gluconate

• Adjunctive therapy to drive potassium intracellularly
• Intravenous insulin/glucose
• Nebulised salbutamol
• Removal of potassium from the body
• Cation-exchange resin (e.g., calcium polystyrene sulfonate)
• Correction of exacerbating factors:
• Manage the AKI

• Withhold culprit medications (e.g., ACE inhibitor, angiotensin-II receptor antagonist,
potassium-sparing diuretics)
• Restrict dietary intake - avoid potassium-rich foods and fluids[80]
• Close ongoing monitoring of potassium and glucose.
Refer for RRT if the patient has moderate or severe hyperkalaemia that fails to respond to
medical management. [13] [64]
Check your local protocols - many hospitals have institutional guidelines for managing
hyperkalaemia.
Management of mild hyperkalaemia (potassium 5.5 to 5.9 mmol/L) [62] [80]

In mild hyperkalaemia, always look for and treat the underlying cause.
• Review medications that might be responsible (e.g., ACE inhibitor, angiotensin-II receptor
antagonist, potassium-sparing diuretics).
• Treatment of hyperkalaemia only results in a temporary intracellular shift of potassium so the

cause of hyperkalaemia must be identified and corrected.[62]
• Consult a pharmacist for a full list of medications that can cause hyperkalaemia.
MANAGEMENT
A cation-exchange resin can be considered. [110]
• This will help remove potassium from the body.[80]
65
• Do not use if the patient has obstructive bowel disease.
Management of moderate hyperkalaemia (potassium 6.0 to 6.4 mmol/L) [62] [80]

Check for any acute ECG changes:
• Features of hyperkalaemia include peaked t waves, flattened p waves, broad QRS complexes.
If there are ECG changes consistent with hyperkalaemia, treat in the same way as severe
hyperkalaemia (see below).
If there are no acute ECG changes consistent with hyperkalaemia:
• Give an infusion of insulin/glucose to push potassium intracellularly [62] [80]
• Give over 15 minutes

• Acts within 10 to 20 minutes
• Lasts 4 to 6 hours
• Monitor hourly for hypoglycaemia
• Consider further adjunctive treatment with nebulised salbutamol if necessary
• Decide whether this is needed based on the ECG and the rate of rise of serum
potassium[80]
• Use caution if there is a history of ischaemic heart disease and avoid if there is a history of
tachyarrhythmias.[62] [80]
Always look for and treat the underlying cause.
Management of severe hyperkalaemia (potassium ≥6.5 mmol/L) [62] [80]

Check for any acute ECG changes.
If the patient has severe hyperkalaemia or moderate hyperkalaemia with associated ECG
changes: [80]
• Seek expert advice from the nephrology or ICU team to consider whether immediate RRT may be
needed
• RRT is indicated if severe hyperkalaemia (potassium ≥6.5 mmol/L) fails to respond

quickly to medical management [13]
• Monitor the patient in a high-dependency area. [62]

MANAGEMENT
Give immediate intravenous calcium for cardiac protection. [62] [80]
• Give over 5 to 10 minutes, then repeat the ECG and consider a further dose if ECG changes
persist.[80]
• Use a wide bore cannula and avoid extravasation.
• Ensure cardiac monitoring.
• Intravenous calcium antagonises the cardiac membrane excitability and so protects the heart
against arrhythmias.[110]
• Effective within 3 minutes and lasts 30 to 60 minutes.
• Seek senior advice if the ECG fails to normalise after one dose.[62]
Give an immediate infusion of insulin/glucose to push potassium intracellularly: [62] [80]

• Lasts 4 to 6 hours
• Monitor hourly for hypoglycaemia.
Give further adjunctive treatment with nebulised salbutamol. [80]
• Use caution if there is a history of ischaemic heart disease and avoid if there is a history of
tachyarrhythmias.[62]
Always look for and treat the underlying cause.
Routine use of sodium bicarbonate is not recommended.
• Sodium bicarbonate is often used to treat acute hyperkalaemia in clinical practice although there is
lit tle evidence to support its use.[110]
• It can be considered in the setting of hyperkalaemia with hypovolaemia and acidosis.
• Use only with expert supervision due to the risk of causing volume overload and/or
hypernatraemia.
There is no evidence to support the use of loop diuretics for managing AKI-associated
hyperkalaemia. [110]
• However, in practice their use may sometimes be considered as an adjunct to other therapies,
provided the patient is fluid replete (but only with supervision from the nephrology team). MANAGEMENT
67
Debate: Loop diuretics
The role of loop diuretics in the management of AKI-associated hyperkalaemia remains

controversial.
• Loop diuretics may be used under specialist supervision for volume management in patients
with AKI and there is a theoretical rationale to suggest they could be beneficial in managing
hyperkalaemia.[1]
• Loop diuretics promote potassium excretion in the urine through their action in inhibiting
the Na+-K+-2Cl co-transporter on the ascending limb of Henle, thereby reducing uptake
of potassium (as well as sodium and chloride).
• However, the 2014 UK Renal Association guideline on acute hyperkalaemia concluded that
there is no evidence to support the use of diuretics in the management of AKI-associated
hyperkalaemia.[110]
• Both the NICE and KDIGO guidelines are clear that loop diuretics should not be used routinely
to manage AKI.[1] [3] The use of loop diuretics is indicated (under specialist supervision) only
if a patient with AKI-associated hyperkalaemia also has volume overload (which is a clear
indication for their use).[3]
Acidosis (pH <7.25) [62] [64]

Metabolic acidosis is a common metabolic disturbance in AKI.
• It occurs primarily due to impaired excretion of the normal load of metabolic acid in the setting of a
low glomerular filtration rate (GFR).
• Other factors may also contribute (e.g., increased production of lactic acid in patients with sepsis).
• Note that there will be relative resistance to vasopressors in the presence of severe metabolic
acidosis.
If the patient has severe acidosis, seek expert supervision as intravenous sodium
bicarbonate may be needed. [64]
• Severe metabolic acidosis (pH <7.2) is an indication for intravenous sodium bicarbonate.
• This should only be given under expert supervision due to the risk of causing volume
overload and/or hypernatraemia.
• Consider referring to ICU.
• Sodium bicarbonate should only be used if venous bicarbonate is <16 mmol/L with no signs
of volume overload.[64]
MANAGEMENT
• 2+
Ionised Ca falls with rapid correction and this can trigger tetany, seizures and cardiac
2+
instability. Prior to administration of sodium bicarbonate, correct low ionised Ca via
a different intravenous route due to the incompatibility of bicarbonate and calcium
solutions.[64]
Refer for RRT if the patient has: [13] [64]
• Refractory acidosis (pH <7.15) that is not responding to initial management

• Severe acidosis in the setting of volume overload (hence sodium bicarbonate must not be
given).
Pulmonary oedema [62] [64]

Pulmonary oedema may occur:
• As a result of overzealous intravenous fluid resuscitation in a patient who presented with

hypovolaemic pre-kidney AKI[96]
• At presentation in some types of AKI, for example:
• Renal artery stenosis - flash pulmonary oedema

• Renal tract obstruction - salt and water retention
• Cardiac failure with AKI.
Mortality is high in acute pulmonary oedema so emergency management is vital.
For immediate management of pulmonary oedema: [62] [64]
• Sit the patient upright

• Give high-flow ox ygen(15 L/minute via a reservoir mask) and, if available, consider continuous
positive airway pressure ventilation
• Give intravenous glyceryl trinitrate - titrate the dose upwards, aiming to maintain systolic BP
(SBP) >95mmHg
• Consider a loop diuretic (under specialist supervision) provided the patient is
haemodynamically stable and well filled intravascularly [1] [62] [13]
• For more details, see the section on Management of volume overload above
• Seek senior support.
Refractory pulmonary oedema is an indication for emergency RRT. [13] [64]
• The use of an intravenous nitrate and a loop diuretic such as furosemide can be a useful holding
measure but do not delay proceeding to definitive management with kidney support if
needed.
MANAGEMENT
Renal replacement therapy
69
Indications for RRT
Renal replacement therapy (RRT) is the cornerstone for treatment of severe AKI with
complications that are not responding to medical management.
• It can be used to manage refractory hyperkalaemia, restore metabolic homeostasis, and correct
volume overload.[3]
Refer immediately to the nephrology team for consideration of RRT if a patient with AKI has
any one or more of the following indications for emergency kidney support: [13] [64]
• Refractory hyperkalaemia (potassium >6.5 mmol/L)

• Refractory metabolic acidosis(pH <7.15)
• Refractory volume overloadwith or without pulmonary oedema
• End-organ complications of uraemia (e.g., pericarditis, encephalopathy, uraemic bleeding) or
other end-organ involvement (e.g., neuropathy, myopathy)
• Severe AKI and poisoning/drug overdose (e.g., ethylene glycol, lithium).
The decision to start RRT must be based on the patient’s overall condition and not on any
isolated urea, creatinine, or potassium value.[1] [3]
• The potential metabolic and fluid benefits of earlier initiationof RRT must be balanced
with the potential harm for the individual patient (e.g., complications related to line insertion,
anticoagulation).[13]
• In the absence of any of the emergency indications for RRT listed above, there islit tle clear
evidence available to guide decisions on whether and when to start RRT, with individual
studies reaching conflicting findings and meta-analyses hampered by varied definitions of ‘early’
and ‘late’ initiation.[13]
• In practice, the decision to start RRT is based on a combination of clinical, physiological, and
laboratory parameters used to assess the patient’s fluid, electrolyte, and metabolic status.[1]
[13]
• Factors to consider include: [13]
• The trend as well as the absolute values of biochemical parameters (e.g., potassium, pH,
urea)
• The uraemic solute burden (which is increased in tumour lysis syndrome, rhabdomyolysis,
and hypercatabolic states)
• The need for intravascular space to allow administration of therapeutic interventions such as
blood products or nutrition
• The degree and duration of oliguria
• Whether or not the underlying kidney insult has resolved
• Any signs of organ dysfunction (which will affect the patient’s ability to tolerate uraemic
complications)
• The presence of any other electrolyte disturbances that may be corrected by RRT (e.g.,
MANAGEMENT
hypercalcaemia).
There may be some patients with pre-existing comorbidities for whom RRT will not offer any
realistic benefits. [114] [13]
• This needs to be a shared decision between the patient and their family members/carers after
discussion with the multidisciplinary team.
Pre-assessment for RRT requires careful consideration and must include: [114]
• Clinical preparation
• Discussion with the patient around the types of RRT that are available and the acute process (it
must be made clear that RRT is supportive treatment that is doing the work of the kidneys)
• If it is unclear whether the patient has a reversible form of AKI, discussion about the longer term
options and the impact they may have on the patient’s life
• Psychological assessment and support.
Choice of RRT modality

The nephrology team will select the best modality of RRT after assessment of the patient's
overall medical condition and comorbidities. [63]
• Various options exist for supporting kidney function.

• There isno evidence that one modality is bet terthan another in terms of outcomesamong
patients with AKI.[115]
• If your patient is in a non-renal centre and is too unwell to transfer, the critical care team will lead
the decision-making.
The choice of RRT modality depends on several factors, including:[63]
• Individual patient factors:
• Haemodynamic stability (and hence the patient’s physiologic reserve to tolerate

metabolic shifts and fluctuations in fluid status) is a key determinant of the most appropriate
RRT modality[13]
• Severity of electrolyte and acid base balance disorders
• Risk of ongoing catabolism with cellular breakdown and acidosis.
• Any need for rapid poison removal (e.g., lithium or ethylene glycol)
• Availability of modality and staff skill mix.
The options for RRT include: [115] [13]
• Intermit tent haemodialysis (IHD) - usually the preferred option in haemodynamically

stable AKI patients, but generally avoided in haemodynamically unstable patients, as it often
precipitates hypotensive events.[1]
• Duration up to 4 hoursso the patient can participate in active rehabilitation.

• Fast removal of toxins (e.g., urea, ethylene glycol). In the case of lithium, rebound can
MANAGEMENT
occur after IHD as the drug redistributes from the intracellular to extracellular compartment.
• May risk dialysis disequilibrium syndrome through over-rapid solute removal and
attendant osmolar shifts.
• Fast correction of acidosis/hyperkalaemiawith risk of rebound following the treatment.
71
• Hybrid versions of IHD include:
• Sustained low-efficiency dialysis (SLED)

• Extended daily dialysis (EDD)[116]
• Prolonged intermittent renal replacement therapy (PIRRT).
• Continuous renal replacement therapy (CRRT) - preferred in haemodynamically

unstable patients. [117] [118] [119]
• Duration 24 to 72 hours, depending on blood circuit clotting.

• Slower blood flow.
• Slower but continual removal of toxins allowing more gradual restoration of metabolic
homeostasis and avoidance of rebound (e.g., lithium toxicity).
• Slows patient rehabilitation when recovering.
• There are several different types of CRRT but no evidence to support one form over another
in terms of better outcomes:
• Continuous venovenous haemofiltration (CVVH)[120] [121] [122]

• Continuous venovenous haemodialysis (CVVHD)
• Continuous venovenous haemodiafiltration (CVVHDF).[116] [117] [118] [119]
• Peritoneal dialysis - rarely used in the developed world except in paediatric patients.
RRT (whether IHD or CRRT) is performed through a large double lumen catheter placed into
the central venous system, such as the internal jugular or femoral vein.
MANAGEMENT
Evidence: Choice of RRT modality
CRRT and IHD have similar outcomes in AKI.
Mortality outcomes are similar in critically ill AKI patients treated with CRRT and IHD.
• Several RCTs have compared CRRT to IHD in AKI patients, including the Hemodiafe study, the
SHARF study, the CONVINT study and the OUTCOMEREA study. None has found any survival
advantage from one modality over the other.[13]
• A Cochrane systematic review that analysed 15 RCTs in 1550 AKI patients concluded that
outcomes were similar in the CRRT and IHD groups in terms of hospital mortality, ICU mortality,
length of hospitalisation, and kidney recovery.[123]
Peritoneal dialysis has generally been thought ineffective in adults with AKI and
hypercatabolic states, although some studies now suggest equal effectiveness in
appropriate subjects. [124] [125]
• However, one study was stopped early because there was a significant benefit to patients being
on CRRT rather than PD.[126]
• In practice, PD is rarely used in adult patients in high-income countries although it is an option
for children with AKI.[13]
MANAGEMENT
73
Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Acute ( summary )
hypovolaemic
1st fluid resuscitation
plus review medications and stop nephrotoxins
plus identify and treat underlying cause of AKI
consider vasoactive drug
consider blood transfusion
consider specialist referral
with mild hyperkalaemia plus identify and treat underlying cause of

(potassium 5.5 to 5.9 hyperkalaemia
mmol/L)
consider cation-exchange resin
with moderate plus identify and treat underlying cause of

hyperkalaemia hyperkalaemia
(potassium 6.0 to
6.4 mmol/L) and no
associated ECG changes
plus insulin/glucose
consider salbutamol
with severe plus calcium

hyperkalaemia
(potassium ≥6.5 mmol/
L) OR moderate
hyperkalaemia
(potassium 6.0 to 6.4
mmol/L) and associated
ECG changes
plus salbutamol
plus identify and treat underlying cause of

hyperkalaemia
with metabolic acidosis consider sodium bicarbonate

MANAGEMENT
with uraemia, refractory consider renal replacement therapy

severe hyperkalaemia,
or refractory metabolic
acidosis
hypervolaemic
Acute ( summary )
1st loop diuretic (only under specialist
supervision) and sodium restriction
plus identify and treat the underlying cause of

AKI
consider renal replacement therapy
with pulmonary oedema plus upright positioning
plus high-flow ox ygen
plus glyceryl trinitrate

mmol/L)

(potassium 6.0 to
6.4 mmol/L) and no
consider salbutamol

hyperkalaemia
L) OR moderate
hyperkalaemia
ECG changes
plus salbutamol

hyperkalaemia
with metabolic acidosis plus seek specialist advice from the renal team
MANAGEMENT
75
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
Acute
hypovolaemic
1st fluid resuscitation
» Pre-kidney AKI (80% of all cases) is most

often caused by hypovolaemia and/or
hypotension.
• A key principle is to improve the

haemodynamic status of the patient.[62]
[64]
• Prompt correction of volume depletion can
reverse or improve AKI.
» If the patient is hypovolaemic, start

immediate intravenous fluid resuscitation
to improve kidney perfusion - but take care
to avoid volume overload . [1] [62] [13] [64]
• Give a 500 mL bolus of intravenous fluid

over 15 minutes.
• Use a wide bore cannula to allow
adequate fluid resuscitation.
• A crystalloid fluid is preferred . [1] [62]
[13] [64]
• A smaller bolus (e.g., 250 mL) may be
more appropriate if the patient has a
history of cardiac failure.[65]
» Use a balanced crystalloid unless

hyperkalaemia is suspected or confirmed.
[62] [65]
• Balanced crystalloid options include

Hartmann’s solution, Ringer’s
acetate, or Plasma-Lyte 148® (a
solution of sodium chloride, sodium
gluconate, sodium acetate trihydrate,
potassium chloride, and magnesium
chloride hexahydrate).
» Use normal saline (0.9% sodium

chloride) instead if hyperkalaemia is
present (potassium >5.5 mmol/L) or
MANAGEMENT
suspected (e.g., rhabdomyolysis).
• This is because balanced crystalloids all

contain potassium.
• Once hyperkalaemia has been
treated and resolved, switch to a
Acute
balanced crystalloid due to the risk of
hyperchloraemic metabolic acidosis
associated with excessive use of normal
saline.[62]
» Reassess haemodynamic status after

the initial fluid bolus and consider
whether further 250 to 500 mL boluses are
required.
• Goal-directedfluid therapy is
recommended.[13]
• Reassess the patient’s response to each
fluid challenge through careful clinical
examination (ABCDE approach) and
monitoring of:[96]
• Capillary refill time

• Pulse rate
• Blood pressure (BP)
• Signs of pulmonary oedema
• Urine output.
• If no improvement is seen after two

fluid challenges, escalate the patient
for senior review. [62] [96]
• If the patient has already had

≥2 L of fluid, or is in shock,
seek immediate senior help
so that critical care involvement
for vasopressor support can be
considered.[62]
• In a patient with profound sepsis
it can take >24 hours for antibiotics
to act and the vascular permeability
to reverse and BP to respond to
intravenous fluids.
Practical tip
An early fluid challenge can be both

diagnostic and therapeutic for pre-
kidney AKI.
• In AKI that is secondary to
hypovolaemia, kidney function
MANAGEMENT
may improve rapidly in response to

administration of intravenous fluids.
77
Acute
Practical tip
Passive leg raising can help predict

fluid responsiveness in critically ill
patients. [62] [13]
• In the context of acute hypovolaemia,
passive leg raising can improve the
venous return and the response in
blood pressure can be recorded.
• A rise in blood pressure confirms
hypovolaemia and the need for further
fluid resuscitation.[62]
• Passive leg raising is most commonly
practised on critical care units.
» As soon as haemodynamic stability is

restored and the patient is euvolaemic,
review and adjust the intravenous fluid
prescription to match the patient’s
ongoing fluid requirements. [62] [96]
• It is vital to recognise when to de-escalate

intravenous fluid therapy. Failure to do
so can result in volume overload and
precipitate pulmonary oedema.
• There is a particular risk from over-

aggressive fluid resuscitation if the
patient is oliguric/anuric or has a
history of heart failure.[13] [96]
MANAGEMENT
Acute
Practical tip
Always be clear about the purpose of

the intravenous fluid therapy you are
prescribing.
• The UK National Institute for Health
and Care Excellence (NICE) has
categorised these as Resuscitation,
Replacement or Routine
maintenance. [100]
• Resuscitation fluid therapy

is aimed at re-establishing
haemodynamic stability by
restoring intravascular volume.
• Replacement fluid therapy
provides daily maintenance water
and electrolyte requirements and
replaces any ongoing abnormal
fluid losses.
• Maintenance fluid therapy
must provide daily ongoing water
and electrolyte requirements (i.e.,
sodium 1 mmol/kg, potassium 1
mmol/kg, and water 25-35 mL/
kg)
• Never give maintenance

fluids at a rate of >100 mL/
hour.
Never prescribe intravenous fluid

therapy for more than 24 hours at
once due to the risk of causing
volume overload.
» Ensure at least daily ongoing

monitoring of volume status for any
patient with established AKI or at risk of
AKI, via: [13] [64]
• Review of haemodynamic status,

including postural BP
• Weight monitoring
• Fluid input/output chart
• Routine urinary catheterisation

MANAGEMENT
is not appropriate, so weigh

up the benefits and risks
(in particular, infection and
trauma) for the individual
patient.[64] Catheterisation
79
Acute
is indicated if fluid balance
management is crucial in an
acutely unwell patient (e.g., hourly
monitoring of fluid balance is
needed) or if the patient is too ill or
frail to use a bottle or commode
• Urea and electrolytes.
plus review medications and stop nephrotoxins

Treatment recommended for ALL patients in
selected patient group
» Whenever AKI is suspected or
confirmed, review all medications and
stop/avoid any nephrotoxic drugs and
other drugs that may affect kidney
function. [13] [64] [65]
• Common nephrotoxic drugs include

aminoglycoside antibiotics, non-
steroidal anti-inflammatory drugs
(NSAIDs), and iodinated contrast
agents.[1] Consult a pharmacist for a full
list of nephrotoxic drugs.
• ACE inhibitors, angiotensin-II
receptor antagonists, and other
renin-angiotensin modifying agents can
exacerbate AKI by reducing the kidney’s
ability to adapt to changes in perfusion
pressure.[9]
• Diuretics or other antihypertensives
increase the risk of hypovolaemia/
hypotension.
• If there are overriding reasons why
a potentially harmful drug must be
continued, seek specialist pharmacist
advice on steps to minimise negative
effects (e.g., dose adjustment, keep the
treatment course as short as possible,
monitor blood levels of the drug if
feasible).
» Review and adjust doses of all other

medications in line with the patient’s
degree of kidney injury . [13] [64]
• Any medication that is cleared via the

kidneys has the potential to accumulate
MANAGEMENT
during an episode of AKI. Dose

adjustment is therefore important to
prevent toxicity and patient harm.
Acute
• Inappropriate drug dosing in patients with
AKI is an important cause of adverse drug
events.[13]
» When restarting drugs after an episode

of AKI, ensure:
• Any medications that were used for the

treatment of pre-existing heart failureare
re-started as soon as clinically reasonable
and re-titrated to achieve the best control
of fluid balance and blood pressure[13]
• All medications are reviewed before
discharge and a plan is put in place to
reintroduce any medications that have
been withheld, at an appropriate time, with
re-titration to the optimum dose continued
in primary care as appropriate[96]
• Ensure a process is in place

for measurement of serum
creatinine and potassium 1
to 2 weeks after restarting. This
may need to be part of discharge
planning.[13]
plus identify and treat underlying cause of AKI

» Determine the cause and severity of AKI
when formulating your management plan
for the patient. [1] [62]
» Pre-kidney AKI (80% of cases) is usually

due to hypovolaemia and/or hypotension
and is often associated with acute illness,
particularly in a patient with background
risk factors. Common causes are: [1] [3] [9]
[62]
• Sepsis (e.g., pneumonia, cellulitis) -

perform a septic screen and implement
your local care bundle (e.g., Sepsis Six) if
infection is suspected[9] [63]
• See our Sepsis in adults topic for

more information
MANAGEMENT
• Fluid loss(e.g., vomiting and diarrhoea,

or blood loss)
• Reduced fluid intake - a particular
problem in frail, elderly patients in the
community. May also be due to insufficient
81
Acute
maintenance or replacement fluids to
replace losses in a hospital inpatient.
» In acutely ill patients, AKI is astrong

indicator of a very sick patientwho needs
urgent recognition and management.
Practical tip
The UK Royal College of Physicians

suggests the use of the STOP AKI
acronym as an aide-memoire to
recall the immediate steps needed for
management of AKI: [62]
• Sepsis - implement your local care
bundle (e.g., Sepsis Six) within 1 hour
if sepsis is suspected or confirmed.
Identify and treat the source of
infection.
• Toxins - stop/avoid nephrotoxins (e.g.,
NSAIDs, aminoglycoside antibiotics,
iodinated contrast agents). These are
a contributory cause in 20% to 30% of
patients with AKI.[1]
• Optimise volume status/BP- assess
volume status and give intravenous
fluids as needed; hold antihypertensive
medication and diuretics; consider
vasopressors if patient does not
respond.[3]
• Prevent harm - treat complications;
identify and treat the cause of AKI;
review all medications and adjust
doses appropriately; closely monitor
intravenous fluid therapy.
consider vasoactive drug

Treatment recommended for SOME patients in
Primary options
» noradrenaline (norepinephrine): 0.4 to 0.8

mg/hour intravenous infusion initially, adjust
dose according to response
Dose refers to noradrenaline base.
OR
MANAGEMENT
» noradrenaline (norepinephrine): 0.4 to 0.8

mg/hour intravenous infusion initially, adjust
dose according to response
Dose refers to noradrenaline base.
-and-
Acute
» vasopressin: 0.01 units/minute intravenous
infusion initially, adjust dose according to
response, maximum 0.03 units/minute
OR
» dobutamine: 2.5 to 10 micrograms/kg/

minute intravenous infusion initially, adjust
dose according to response, maximum 40
micrograms/kg/minute
» Vasopressor support is recommended if

the patient remains severely hypotensive
despite adequate volume resuscitation
(e.g., in septic/hypovolaemic shock). [1] [62]
[13] [96]
• Escalate to critical care. Vasopressors

should only be used with continuous
haemodynamic monitoring in place.
• A reasonable goal is to maintain mean
arterial pressure (MAP) ≥65 mmHg,
but this target may need adjusting
according to the patient’s baseline BP.[1]
[13] [64]
• In the setting of vasomotor shock
where the patient has persistent
hypotension despite optimisation of
intravascular volume through aggressive
fluid resuscitation, preservation and
improvement of kidney perfusion can
only be achieved by the use of systemic
vasopressors.[1]
» Noradrenaline (norepinephrine) is the

usual vasopressor of choice, with the
addition of vasopressin if needed.
• There is little good evidence available

to guide the choice of vasopressor in
patients with AKI and septic shock.[1] [13]
• Do not use low-dose dopamineto treat
AKI.[1] [3] [13]
• There is no evidence to support

its use and it can worsen kidney
perfusion in patients with AKI.
Evidence: Evidence is scarce to guide

MANAGEMENT
the choice of vasopressor
It is not known which vasopressor

agent is most effective for prevention or
treatment of AKI and septic shock.
83
Acute
There is insufficient evidence to say
that one vasoactive agent is bet ter than
another in preventing or treating AKI.
[1]
• Small open-label studies have

shown improvement in creatinine
clearance after a 6- to 8-hour infusion
of noradrenaline.[101]
• Vasopressin, when compared with
noradrenaline in one RCT, was found
to increase blood pressure and
enhance diuresis, but has not yet been
proven to enhance survival or reduce
the need for RRT.[102]
• A post-hoc analysis of the

same RCT used the RIFLE
criteria for AKI to compare the
effects of vasopressin versus
noradrenaline.[103] Vasopressin
was associated with a trend to a
lower rate of progression of the
AKI, and a lower rate of use of
RRT.
• According to the Kidney
Disease: Improving Global
Outcomes (KDIGO) guideline
group, this study suggests
that vasopressin may reduce
progression to kidney failure and
mortality in patients with septic
shock who have or are at risk of
AKI.[1]
Dopamine has no significant clinical

benefits in patients with AKI. [13]
• A large RCT comparing dopamine with

noradrenaline as the initial vasopressor
in patients with shock showed no
significant differences between groups
with regard to kidney function or
mortality.[104]
• However, there were more

arrhythmic events among
the patients treated with
dopamine than among those
MANAGEMENT
treated with noradrenaline, and

dopamine was associated with
an increased rate of death at 28
Acute
days among the patients with
cardiogenic shock.
• Both the NICE and KDIGO guidelines

include a recommendation not to offer
low-dose dopamine to treat AKI.[1] [3]
» Consider the need for an inotrope (e.g.,

dobutamine) to optimise cardiac output
if kidney hypoperfusion is caused by
impaired cardiac function due to poor left
ventricular systolic function. [13]
consider blood transfusion
» Blood transfusion is indicated if
hypovolaemia is secondary to significant
blood loss.
• This is generally not given unless more

than one unit is anticipated, based
on local guidelines and the clinical
assessment of the patient.[5]
• Note that this may worsen hyperkalaemia.
consider specialist referral

» Most patients with AKI do not need
referral to nephrology. [62]
• Do not refer if there is a clear cause

and the AKI is responding to medical
management.[3] [97] [98]
» Refer immediately to critical care and/or

nephrology if:
• The patient meets (or is anticipated to

meet) the criteria for RRT[3] [64]
• There are severe complications that
cannot be managed medically (such
as hyperkalaemia, pulmonary oedema,
acidosis, or uraemia)[64]
• The patient remains haemodynamically
unstable after appropriate supportive
MANAGEMENT
care and/or there are signs of multi-organ

failure.[64]
85
Acute
Check local protocols for referral criteria
and pathways.
» Refer for urgent discussion with

nephrology (as soon as possible and
within 24 hours at the latest) if any one or
more of the following is present: [3] [64]
• Uncertainty about the cause of AKI or

a poor response to treatment
• A possible diagnosis that may need
specialist treatment (e.g., vasculitis,
glomerulonephritis, tubulointerstitial
nephritis, myeloma)
• Complications associated with AKI
that are not responding to medical
treatment
• Stage 3 AKI
• AKI in a patient with pre-existing
chronic kidney disease (CKD) stage 4
or 5
• The patient has a kidney transplant.
Evidence: Speed of referral to

nephrology
There is little evidence available to

support routine referral to the nephrology
team for every patient with stage 2 AKI.
Evidence is lacking on whether

outcomes are improved by routine rapid
referral to nephrology (within 12 hours)
for all patients with stage 2 or 3 AKI that
does not need critical care input. [3]
• The large number of AKI cases among

patients admitted acutely to hospital
makes it impractical to refer every
patient with suspected or confirmed
AKI to nephrology.
• Initial management for most patients
encompasses identification and
treatment of sepsis, avoidance of
nephrotoxins, fluid replacement, and
correction of hypotension. These steps
can be commenced by any medical or
MANAGEMENT
surgical team.
• Potential benefits of routine nephrology
referral include a faster diagnosis in
patients with primary kidney disease,
Acute
prevention of progressive AKI and the
potential need for renal replacement
therapy, avoidance of a delayed
transfer to critical care, improved
chances of kidney recovery, and a
shorter hospital stay.
• However, there is very little evidence to
support routine nephrology referral for
all patients with stage 2 or 3 AKI.[3]
• Very low quality evidence from

one large retrospective study
suggested that for non-critically
ill patients with AKI, early
compared with delayed referral
to nephrology may reduce in-
hospital mortality, the number
of patients needing RRT, and
length of hospital stay.[99]

mmol/L)
» Always look for the underlying cause of
hyperkalaemia and treat it. [62]
• Review medications that might

be responsible (e.g., ACE inhibitors,
angiotensin-II receptor antagonists,
potassium-sparing diuretics).
• Treatment of hyperkalaemia only

results in a temporary intracellular
shift of potassium so the cause of
hyperkalaemia must be identified
and corrected.[62]
• Consult a pharmacist for a full list
of medications that can cause
hyperkalaemia.
• Restrict dietary intake - avoid

potassium-rich foods and fluids. [80]
• Ensure close ongoing monitoring of
MANAGEMENT
potassium and glucose.
» Hyperkalaemia is a common
complication of AKI. It can lead to:
87
Acute
• Muscle weakness
• Cardiac arrhythmias (e.g., bradycardia,
bundle branch block, ventricular
tachycardia, ventricular fibrillation,
asystole).
» Check your local protocols - many

hospitals have institutional guidelines for
managing hyperkalaemia.
Primary options
» calcium polystyrene sulfonate: 15 g orally

three to four times daily; 30 g rectally once
daily (as a retention enema retained for 9
hours followed by irrigation to remove resin
from colon)
Guidelines recommend twice daily
administration of the rectal formulation; UK
Renal Association. Emergency management
of hyperkalaemia in adults. March 2014
[internet publication]. https://renal.org/wp-
content/uploads/2017/10/HYPERKALAEMIA-
ALGORITHM-MARCH-2014.pdf however,
the manufacturer only recommends once
daily administration. Adjust dose according to
serum electrolyte levels.
» A cation-exchange resin (e.g., calcium

polystyrene sulfonate) can be considered .
[110]
• This will help remove potassium from the

body.[80]
• Do not use if the patient has obstructive
bowel disease.
• Can be administered orally or rectally.
The rectal route should be reserved for
patients who are vomiting or have upper
gastrointestinal conditions (e.g., paralytic
ileus).
• Administer the oral formulation 3 hours
before or after other oral medications
(consider a 6-hour separation in patients
MANAGEMENT
with gastroparesis). Check potential

drug-drug interactions before use (e.g.,
digoxin).
• May cause constipation. Administer a
suitable laxative during treatment.[80]
Acute
Magnesium-containing laxatives and
sorbitol are not recommended due to the
risk of alkalosis and intestinal necrosis,
respectively.
• Monitor serum electrolyte levels during
treatment and stop once potassium levels
fall to 5 mmol/L.

(potassium 6.0 to
6.4 mmol/L) and no
» Look for the underlying cause of
• Review medicationsthat might


and corrected.[62]
hyperkalaemia.
• Restrict dietary intake - avoid

» Check for any acute ECG changes.
• Features of hyperkalaemia include

peaked t waves, flat tened p waves,
broad QRS complexes.
• If there are ECG changes consistent with
hyperkalaemia, treat in the same way
as severe hyperkalaemia.
• Muscle weakness
MANAGEMENT

asystole).
89
Acute
Primary options
» insulin neutral: 10 units by intravenous

infusion over 15 minutes
-and-
» glucose: 25 g (50 mL of a 50% solution or
125 mL of a 20% solution) by intravenous
» Give an infusion of soluble (neutral)

insulin and glucose to push potassium
intracellularly: [62] [80]

• Lasts 4 to 6 hours.
» Monitor hourly for hypoglycaemia.

consider salbutamol
Primary options
» salbutamol inhaled: 10-20 mg inhaled via

nebuliser as a single dose
A lower dose of 10 mg is recommended in
patients with ischaemic heart disease. UK
ALGORITHM-MARCH-2014.pdf
» Consider further adjunctive treatment

with nebulised salbutamol to drive
potassium intracellularly if necessary. [62]
• Decide whether this is needed based on

the ECG and the rate of rise of serum
potassium.[80]
• Use with caution if there is a history of
ischaemic heart disease (a lower dose
MANAGEMENT
is recommended), and avoid if there is a

history of tachyarrhythmias.[62] [80]

hyperkalaemia
Acute
(potassium ≥6.5 mmol/ Treatment recommended for ALL patients in
L) OR moderate selected patient group
hyperkalaemia
Primary options
» calcium chloride: 6.8 mmol (10 mL of
ECG changes
a 10% solution) intravenously over 5-10
minutes; may repeat if ECG changes persist;
consult local protocols for further guidance on
dose
OR
» calcium gluconate: 6.8 mmol (30 mL of

dose
» Give immediate intravenous calcium for

cardiac protection. [62] [80]
• Give over 5 to 10 minutes, then repeat

the ECG and consider a further dose if
ECG changes persist.[80]
• Use a wide bore cannula and avoid

extravasation.
• Intravenous calcium antagonises

the cardiac membrane excitability
and so protects the heart against
arrhythmias.[110]
• Effective within 3 minutes and lasts

30 to 60 minutes.
• Seek senior advice if the ECG fails to

normalise after one dose.[62]
Primary options

MANAGEMENT
-and-
91
Acute
intracellularly: [62] [80]


plus salbutamol
Primary options



potassium.[80]

hyperkalaemia

MANAGEMENT

and corrected.[62]
Acute
hyperkalaemia.
• Muscle weakness
asystole).

» There is no evidence to support the

use of loop diuretics for managing AKI-
associated hyperkalaemia. [110]
• However, in practice their use may

sometimes be considered by the
nephrology team as an adjunct to other
therapies provided the patient is fluid
replete (but only with close specialist
supervision).
The role of loop diuretics in the

management of AKI-associated
hyperkalaemia remains controversial.
• Loop diuretics may be used under

specialist supervision for volume
management in patients with AKI
and there is a theoretical rationale to
suggest they could be beneficial in
managing hyperkalaemia.[1]
• Loop diuretics promote

potassium excretion in the urine
through their action in inhibiting
the Na+-K+-2Cl co-transporter
MANAGEMENT
on the ascending limb of Henle,

thereby reducing uptake of
93
Acute
potassium (as well as sodium
and chloride).
• However, the 2014 UK Renal

Association guideline on acute
hyperkalaemia concluded that there
is no evidence to support the use of
diuretics in the management of AKI-
associated hyperkalaemia.[110]
are clear that loop diuretics should
not be used routinely to manage
AKI.[1] [3] The use of loop diuretics is
indicated (under specialist supervision)
only if a patient with AKI-associated
hyperkalaemia also has volume
overload (which is a clear indication for
their use).[3]
with metabolic acidosis consider sodium bicarbonate

Primary options
» sodium bicarbonate: consult local protocols

for guidance on dose
» If the patient has severe acidosis,

seek senior input as intravenous sodium
bicarbonate may be needed. [64]
• Severe metabolic acidosis (pH <7.2)

is an indication for intravenous sodium
bicarbonate.
• This should only be given under
expert supervision due to the risk
of causing volume overload and/or
hypernatraemia.
• Consider referring to ICU.
• Sodium bicarbonate should only be used

if venous bicarbonate is <16 mmol/L
with no signs of volume overload.[64]
• 2+
Ionised Ca falls with rapid
correction and this can trigger
tetany, seizures, and cardiac
MANAGEMENT
instability. Prior to administration

of sodium bicarbonate, correct
2+
low ionised Ca with intravenous
calcium via a different intravenous
route due to the incompatibility
Acute
of bicarbonate and calcium
solutions.[64]
» Metabolic acidosis is a common

metabolic disturbance in AKI.
• It occurs primarily due to impaired

excretion of the normal load of metabolic
acid in the setting of a low glomerular
filtration rate (GFR).
• Other factors may also contribute (e.g.,
increased production of lactic acid in
patients with sepsis).
• Note that there will be relative resistance
to vasopressors in the presence of severe
metabolic acidosis.
» Sodium bicarbonate can also be considered

in the setting of hyperkalaemia with
hypovolaemia and acidosis.
• Use only with expert supervisiondue

to the risk of causing volume overload
and/or hypernatraemia.
with uraemia, refractory consider renal replacement therapy

severe hyperkalaemia,
or refractory metabolic
acidosis
» Refer immediately to the renal team for
emergency initiation of RRT if the patient
has: [13] [64]
• End-organ complications of uraemia

(e.g., pericarditis, encephalopathy,
uraemic bleeding)
• Severe hyperkalaemia
(potassium≥6.5 mmol/L) that fails
to respond quickly to medical
management
• If the patient has severe

hyperkalaemia (or moderate
hyperkalaemia with associated
ECG changes), seek expert
advice from the nephrology or
MANAGEMENT
ICU team to consider whether RRT

may be needed[80]
95
Acute
• Refractory acidosis (pH <7.15)
that is not responding to initial
management.
» RRT is the cornerstone for treatment of

severe AKI with complications that are not
responding to medical management.
» There may be some patients with pre-

existing comorbidities for whom RRT will
not offer any realistic benefits. [114] [13]
• This needs to be a shared decision

between the patient and their family
members/carers after discussion with the
multidisciplinary team.
» Pre-assessment for RRT requires careful

consideration and must include: [114]
• Discussion with the patient around the
types of RRT that are available and the
acute process (it must be made clear that
RRT is supportive treatment that is doing
the work of the kidneys)
• If it is unclear whether the patient has a
reversible form of AKI, discussion about
the longer term options and the impact
they may have on the patient’s life

The renal team will select the best
modality of RRT after assessment of the
patient's overall medical condition and
comorbidities. [63]
• Various options exist for supporting kidney

function.
• There is no evidence that one
modality is bet ter than another in
terms of outcomes among patients with
AKI.[115]
• If your patient is in a non-renal centre and
MANAGEMENT
is too unwell to transfer, the critical care

team will lead the decision-making.
Acute
The choice of RRT modality depends on
several factors, including: [63]
• Haemodynamic stability(and
hence the patient’s physiologic
reserve to tolerate metabolic shifts
and fluctuations in fluid status)
is a key determinant of the most
appropriate RRT modality[13]
• Severity of electrolyte and acid base
balance disorders
• Risk of ongoing catabolism with
cellular breakdown and acidosis
• Any need for rapid poison removal
(e.g., lithium or ethylene glycol)
• Availability of modality and staff

skill mix.
• Intermit tent haemodialysis (IHD)-

usually the preferred option in
haemodynamically stable AKI
patients, but generally avoided in
haemodynamically unstable patients, as it
often precipitates hypotensive events.[1]
• Duration up to4 hours so the

patient can participate in active
rehabilitation.
• Fast removal of toxins (e.g.,
urea, ethylene glycol). In the case
of lithium, rebound can occur
after IHD as the drug redistributes
from the intracellular to extracellular
compartment.
• May risk dialysis disequilibrium
syndrome through over-rapid
solute removal and attendant
osmolar shifts.
• Fast correction of acidosis/
hyperkalaemia with risk of
rebound following the treatment.
• Sustained low-efficiency
MANAGEMENT
dialysis (SLED)
• Extended daily dialysis
(EDD)[116]
97
Acute
• Prolonged intermittent
renal replacement therapy
(PIRRT).
• Continuous renal replacement

therapy (CRRT) - preferred in
haemodynamically unstable
patients. [117] [118] [119]
• Duration 24 to 72 hours,
depending on blood circuit clotting.
• Slower but continual removal
of toxins allowing more
gradual restoration of metabolic
homeostasis and avoidance of
rebound (e.g., lithium toxicity).
• Slows patient rehabilitation when
recovering.
• There are several different types of
CRRT but no evidence to support
one form over another in terms of
better outcomes:
• Continuous venovenous
haemofiltration (CVVH)[120]
[121] [122]
haemodialysis (CVVHD)
haemodiafiltration(CVVHDF).[116]
[117] [118] [119]
• Peritoneal dialysis - rarely used in

the developed world except in paediatric
patients.
RRT (whether IHD or CRRT) is performed

through a large double lumen catheter
placed into the central venous system,
such as the internal jugular or femoral
vein.

MANAGEMENT
CRRT and IHD have similar outcomes in

AKI.
Mortality outcomes are similar in

critically ill AKI patients treated with
CRRT and IHD.
Acute
• Several RCTs have compared CRRT
to IHD in AKI patients, including
the Hemodiafe study, the SHARF
study, the CONVINT study and the
OUTCOMEREA study. None has
found any survival advantage from one
modality over the other.[13]
• A Cochrane systematic review that
analysed 15 RCTs in 1550 AKI patients
concluded that outcomes were similar
in the CRRT and IHD groups in terms
of hospital mortality, ICU mortality,
length of hospitalisation, and kidney
recovery.[123]
Peritoneal dialysis has generally been

thought ineffective in adults with AKI
and hypercatabolic states, although
some studies now suggest equal
effectiveness in appropriate subjects.
[124] [125]
• However, one study was stopped early

because there was a significant benefit
to patients being on CRRT rather than
PD.[126]
• In practice, PD is rarely used in adult
patients in high-income countries
although it is an option for children with
AKI.[13]
hypervolaemic
1st loop diuretic (only under specialist

supervision) and sodium restriction
Primary options
» furosemide: consult specialist for guidance

on dose
» Volume overload in a patient with AKI

can occur as a result of:
• Overaggressive fluid resuscitation

in a patient who initially presented with
hypovolaemic pre-kidney AKI. This is most
commonly seen in patients with sepsis.
• Oliguria in intrinsic or post-kidney AKI.
MANAGEMENT
» Consider a loop diuretic (under

specialist supervision) to treat volume
overload. [1] [13]
• A loop diuretic such as furosemide may

be useful in achieving euvolaemia
99
Acute
in a patient with fluid overload (with
or without pulmonary oedema).[1] This
must be done with caution and under the
supervision of the nephrology team.
• Note that there is no evidence

to support the routine use of
loop diuretics for management
of AKI in the absence of volume
overload.[1] [3] [13]
• Never use a loop diuretic if
the patient is hypovolaemic
or hypotensive.The diuretic will
exacerbate the haemodynamic
instability,
• Do not allow the use of loop diuretics

to delay more definitive management
of volume overload.
• Careful monitoring of response is

important (e.g,. urine output). Stop
the diuretic if there is no response.
• Proceed without delay to more
definitive management with
RRT if the response to diuretics is
unsuccessful.[64]
» Sodium restriction may also be required.
» Patients with volume overload need

careful monitoring and management to
reduce the risk of a poor outcome.
• Failure to manage volume overload

can lead to complications including
pulmonary oedema.[62] In critically
ill patients, a positive fluid balance
(>5% body weight) has been found
to be associated with an increase in
mortality at up to 1 year follow-up when
compared to neutral or negative (<5%)
fluid balance.[13]
Evidence: The role of loop diuretics in

patients with AKI
Loop diuretics have no routine role in

MANAGEMENT
the management of AKI. They should be

reserved for specific indications (such
as volume overload) and only used under
specialist supervision.
Acute
There is no evidence for any benefits
from the routine use of loop diuretics
in patients with AKI - but there is some
evidence to suggest harm.
• The theoretical rationale for the use

of loop diuretics to treat AKI is based
on their potential to reduce oxygen
consumption in the ascending loop of
Henle, thereby reducing any ischaemic
damage to the kidneys. They may also
be used to convert oliguric AKI to non-
oliguric AKI.[1] [13]
• However, diuretics can also

excessively reduce circulating
volume and so cause a pre-
kidney insult that could worsen
established AKI. Hence an
evaluation of the available
evidence is vital to determine
their appropriate role.
• There is no evidence to support

the use of loop diuretics in routine
treatment of AKI.
• One RCT found furosemide to

be ineffective in treating AKI and
epidemiological data suggest
the use of loop diuretics may
increase mortality in patients
with critical illness and AKI.[105]
[106]
• Two systematic reviews on the
use of furosemide to prevent or
treat AKI found no significant
effect on in-hospital mortality,
risk for requiring RRT, the
number of dialysis sessions
needed, or even the proportion
of patients with persistent
oliguria.[107] [108]
• Prophylactic furosemide has
been shown to increase the risk
of AKI when given to prevent
AKI in patients having cardiac
surgery.[109]
MANAGEMENT
There is no evidence to support the

101
Acute
• However, in practice their
use may be considered (with
specialist supervision) as an
adjunct to other therapies
provided the patient is fluid
replete.
plus identify and treat the underlying cause of

AKI
Obstructive AKI
Relief of the obstruction is key in the
management of obstructive AKI. [9] [64]
• Insert a bladder catheter in any case

of AKI when bladder outlet obstruction is
suspected clinically and cannot be quickly
ruled out by ultrasound.
• Refer to urology within 24 hours

if urinary tract obstruction is
confirmed on ultrasound.[3] [64]
Refer immediately to urology and/or

radiology if one of more of the following is
present:[3]
• Pyonephrosis - if pyonephrosis is
suspected, ensure the patient has an
ultrasound within 6 hours (because of the
risk of septic shock)[3]
• Obstructed single kidney
• Bilateral upper urinary tract
obstruction
• Complications of AKI secondary to
urological obstruction.
Arrangements for ureteral stenting,

urinary diversion, debulking procedures,
or other case-specific requirements will
be made by the specialist urology or
MANAGEMENT
radiology team. [64]
• Nephrostomy or ureteral stenting must

be undertaken as quickly as possible
Acute
and at the latest within 12 hoursof
diagnosis.[3]
• Ureteral stenting is indicated if there is a
ureteral stricture, stone, or extrinsically
obstructing mass.
• Lithotripsy or surgical removal may be
needed if obstruction is caused by stones
at the ureteropelvic junction.
• Exploratory laparotomy may be indicated
if a compressing tumour is suspected that
may require surgical removal; this may be
done following ureteral stenting.
• Percutaneous nephrostomy (placement
of a catheter into the renal pelvis
percutaneously for drainage of urine from
a distal obstruction) may be undertaken
by a urologist, surgeon, or interventional
radiologist.
Renal replacement therapy may be needed

while the underlying obstruction is being
addressed if there is severe acidosis,
volume overload, or electrolyte or uraemic
complications.
Intrinsic AKI
Intrinsic AKI is due to cellular damage
within the kidneys – seek early specialist
input from nephrology if you suspect an
intrinsic cause (e.g., vasculitis). Causes
include:[9] [17] [18] [62]
• Prolonged pre-kidney AKI that

progresses to overt cellular damage (the
most common cause of intrinsic AKI)
• Nephrotoxins (e.g,. iodinated contrast
agents, non-steroidal anti-inflammatory
drugs [NSAIDs], aminoglycoside
antibiotics)[1]
• Rare causes (e.g., vasculitis,
glomerulonephritis).
Consider the possibility of intrinsic AKI

if urinalysis is positive for both blood
and protein in the absence of an obvious
alternative cause for this (e.g., urinary
MANAGEMENT
tract infection or trauma from urinary

catheterisation). [3] [9] [64]
Specific management of intrinsic AKI

depends on the aetiology and is led by the
nephrology team. [62]
103
Acute
• Immunological tests and kidney
biopsy are needed to confirm
acute glomerulonephritis, anti-
neutrophil cytoplasmic antibodies
[ANCA]-associated vasculitis,
anti–glomerular basement
membrane (anti-GBM) antibody
disease (Goodpasture syndrome
if associated with pulmonary
hypertension) and lupus nephritis.
• Treatment will require

corticosteroids, cytotoxic agents,
immunomodulating drugs, and/or
plasma exchange.
• Atypical haemolytic uraemic

syndrome (HUS) is treated with the
monoclonal antibody eculizumab or
plasma exchange.[111]
• Thrombotic thrombocytopenic
purpura (TTP) is treated with plasma
exchange.[112]
• Acute allergic interstitial nephritis
is treated with a corticosteroid (after
excluding infection) and stopping potential
causative medications (e.g., proton-pump
inhibitors, NSAIDs, antibiotics).[113]
Medication review
Whenever AKI is suspected or confirmed,
review all medications and stop/avoid any
nephrotoxic drugs and other drugs that
may affect kidney function. [13] [64] [65]
• Common nephrotoxic drugs include

aminoglycoside antibiotics, NSAIDs,
and iodinated contrast agents.[1]
Consult a pharmacist for a full list of
nephrotoxic drugs.
• ACE inhibitors, angiotensin-II
receptor antagonists, and other
renin-angiotensin modifying agents can
exacerbate AKI by reducing the kidney’s
ability to adapt to changes in perfusion
pressure.[9]
• Diuretics or other antihypertensives
increase the risk of hypovolaemia/
MANAGEMENT
hypotension.
• If there are overriding reasons why
a potentially harmful drug must be
continued, seek specialist pharmacist
advice to minimise negative effects (e.g.,
dose adjustment, keep the treatment
Acute
course as short as possible, monitor blood
levels of the drug if feasible).
Review and adjust doses of all other

medications in line with the patient’s
degree of kidney injury. [13] [64]
• Any medication that is cleared via the

kidneys has the potential to accumulate
during an episode of AKI. Dose
adjustment is therefore important to
prevent toxicity and patient harm.
• Inappropriate drug dosing in patients with
AKI is an important cause of adverse drug
events.[13]
consider renal replacement therapy

» Immediate RRT is indicated for
refractory volume overload or volume
overload associated with severe
complications of AKI. [62] [13] [64]
• Refractory volume overload typically

includes pulmonary oedema.
• However, RRT may also be needed in
a patient with gross peripheral oedema
(without pulmonary oedema) that fails to
respond to a loop diuretic. Such patients
will usually have oliguric AKI.
» The decision to start RRT must be based

on the patient’s overall condition and not
on any isolated urea or creatinine value.[1]
[3]
• The potential metabolic and fluid benefits

of earlier initiation of RRT must
be balanced with the potential
harm for the individual patient (e.g.,
complications related to line insertion,
anticoagulation).[13]
• In the absence of an emergency
indication for RRT (e.g., severe refractory
hyperkalaemia, acidosis or volume
MANAGEMENT
overload, or end-organ complications of

uraemia), there is lit tle clear evidence
available to guide decisions on
whether and when to start RRT.
105
Acute
• Individual studies have reached
conflicting findings and meta-
analyses have been hampered by
varied definitions of ‘early’ and ‘late’
initiation of RRT.[13]
• In practice, the decision to start RRT

is based on a combination of clinical,
physiological, and laboratory parameters
used to assess the patient’s fluid,
electrolyte, and metabolic status.[1]
[13]
• Factors to consider include: [13]
• The trend as well as the absolute

values of biochemical parameters
(e.g., potassium, pH, urea)
• The uraemic solute burden (which
is increased in tumour lysis
syndrome, rhabdomyolysis, and
hypercatabolic states)
• The need for intravascular space to
allow administration of therapeutic
interventions such as blood
products or nutrition
• The degree and duration of oliguria
• Whether or not the underlying
kidney insult has resolved
• Any signs of organ dysfunction
(which will affect the patient’s ability
to tolerate uraemic complications)
• The presence of any other
electrolyte disturbances that
may be corrected by RRT (e.g.,
hypercalcaemia).
» There may be some patients with pre-

existing comorbidities for whom RRT will
not offer any realistic benefits. [114] [13]
• This needs to be a shared decision

between the patient and their family
members/carers after discussion with the
MANAGEMENT
multidisciplinary team.
» Pre-assessment for RRT requires careful

consideration and must include: [114]
Acute
• Discussion with the patient around the
types of RRT that are available and the
acute process (it must be made clear that
RRT is supportive treatment that is doing
the work of the kidneys)
• If it is unclear whether the patient has a
reversible form of AKI, discussion about
the longer term options and the impact
they may have on the patient’s life

The nephrology team will select the best
modality of RRT after assessment of the
patient's overall medical condition and
comorbidities . [63]
• Various options exist for supporting kidney

function.
• There is no evidence that one
modality is bet ter than another in
terms of outcomes among patients with
AKI.[115]
• If your patient is in a non-renal centre and
is too unwell to transfer, the critical care
team will lead the decision-making.
The choice of RRT modality depends on

several factors, including: [63]
• Haemodynamic stability(and
hence the patient’s physiologic
reserve to tolerate metabolic shifts
and fluctuations in fluid status)
is a key determinant of the most
appropriate RRT modality[13]
• Severity of electrolyte and acid base
balance disorders
• Risk of ongoing catabolism with
cellular breakdown and acidosis
• Any need for rapid poison removal
MANAGEMENT
(e.g., lithium or ethylene glycol)
• Availability of modality and staff

skill mix.
107
Acute
• Intermit tent haemodialysis (IHD)-

usually the preferred option in
haemodynamically stable AKI
patients, but generally avoided in
haemodynamically unstable patients, as it
often precipitates hypotensive events.[1]
• Duration up to4 hours so the

patient can participate in active
rehabilitation.
• Fast removal of toxins (e.g.,
urea, ethylene glycol). In the case
of lithium, rebound can occur
after IHD as the drug redistributes
from the intracellular to extracellular
compartment.
• May risk dialysis disequilibrium
syndrome through over-rapid
solute removal and attendant
osmolar shifts.
• Fast correction of acidosis/
hyperkalaemia with risk of
rebound following the treatment.
• Sustained low-efficiency
dialysis (SLED)
• Extended daily dialysis
(EDD)[116]
• Prolonged intermittent
renal replacement therapy
(PIRRT).
• Continuous renal replacement

therapy (CRRT) - preferred in
haemodynamically unstable
patients. [117] [118] [119]
• Duration 24 to 72 hours,
depending on blood circuit clotting.
• Slower but continual removal
of toxins allowing more
gradual restoration of metabolic
homeostasis and avoidance of
rebound (e.g., lithium toxicity).
MANAGEMENT
• Slows patient rehabilitation when

recovering.
• There are several different types of
CRRT but no evidence to support
Acute
one form over another in terms of
better outcomes:
haemofiltration (CVVH)[120]
[121] [122]
haemodialysis (CVVHD)
haemodiafiltration
(CVVHDF).[116] [117] [118]
[119]
• Peritoneal dialysis - rarely used in

the developed world except in paediatric
patients.
RRT (whether IHD or CRRT) is performed

through a large double lumen catheter
placed into the central venous system,
such as the internal jugular or femoral
vein.
CRRT and IHD have similar outcomes in

AKI.
Mortality outcomes are similar in

critically ill AKI patients treated with
CRRT and IHD.
• Several RCTs have compared CRRT

to IHD in AKI patients, including
the Hemodiafe study, the SHARF
study, the CONVINT study and the
OUTCOMEREA study. None has
found any survival advantage from one
modality over the other.[13]
• A Cochrane systematic review that
analysed 15 RCTs in 1550 AKI patients
concluded that outcomes were similar
in the CRRT and IHD groups in terms
of hospital mortality, ICU mortality,
length of hospitalisation, and kidney
recovery.[123]
Peritoneal dialysis has generally been

MANAGEMENT
thought ineffective in adults with AKI

and hypercatabolic states, although
some studies now suggest equal
effectiveness in appropriate subjects.
[124] [125]
109
Acute
• However, one study was stopped early
because there was a significant benefit
to patients being on CRRT rather than
PD.[126]
• In practice, PD is rarely used in adult
patients in high-income countries
although it is an option for children with
AKI.[13]
with pulmonary oedema plus upright positioning

» Sit the patient upright. [62] [64]
» Pulmonary oedema may occur:
• As a result of overzealous
intravenous fluid resuscitation in a
patient who presented with hypovolaemic
pre-kidney AKI[96]
• At presentation in some types of AKI,
for example:
• Renal artery stenosis - flash

pulmonary oedema
• Renal tract obstruction - salt and
water retention
• Cardiac failure with AKI.
» Mortality is high in acute pulmonary

oedema so emergency management is
vital.
plus high-flow ox ygen
» Give high-flow ox ygen: [62]
• 15 L/minute via a reservoir mask.
» If available, consider continuous

positive airway pressure ventilation. [64]
plus glyceryl trinitrate
MANAGEMENT

Primary options
Acute
» glyceryl trinitrate: 10 micrograms/minute
intravenous infusion initially, increase
gradually according to response, maximum
400 micrograms/minute
An alternative regimen recommended
by the Royal College of Physicians in
the UK is 2 mg/hour initially, titrated up
to 20 mg/hour according to response
maintaining systolic BP >95 mmHg. Royal
College of Physicians. Acute care toolkit 12:
acute kidney injury and intravenous fluid
therapy. October 2015 [internet publication].
https://www.rcplondon.ac.uk/guidelines-
policy/acute-care-toolkit-12-acute-kidney-
injury-and-intravenous-fluid-therapy
» Give intravenous glyceryl trinitrate. [62]

[64]
• Titrate the dose upwards, aiming to

maintain systolic BP >95 mmHg.[62]

mmol/L)
» Always look for the underlying cause of


and corrected.[62]
hyperkalaemia.
• Restrict dietary intake – avoid

MANAGEMENT
• Muscle weakness
111
Acute
asystole).

Primary options
» calcium polystyrene sulfonate: 15 g orally

three to four times daily; 30 g rectally once
daily (as a retention enema retained for 9
hours followed by irrigation to remove resin
from colon)
Guidelines recommend twice daily
administration of the rectal formulation; UK
ALGORITHM-MARCH-2014.pdf however,
the manufacturer only recommends once
daily administration. Adjust dose according to
serum electrolyte levels.
» A cation-exchange resin (e.g., calcium

polystyrene sulfonate) can be considered.
[110]
• This will help remove potassium from the

body.[80]
• Do not use if the patient has obstructive
bowel disease.
• Can be administered orally or rectally.
The rectal route should be reserved for
patients who are vomiting or have upper
gastrointestinal conditions (e.g., paralytic
ileus).
• Administer the oral formulation 3 hours
before or after other oral medications
(consider a 6-hour separation in patients
with gastroparesis). Check potential
drug-drug interactions before use (e.g.,
digoxin).
MANAGEMENT
• May cause constipation. Administer

a suitable laxative during
treatment.[80] Magnesium-containing
laxatives and sorbitol are not
recommended due to the risk of alkalosis
and intestinal necrosis, respectively.
Acute
• Monitor serum electrolyte levels during
treatment and stop once potassium levels
fall to 5 mmol/L.

(potassium 6.0 to
6.4 mmol/L) and no


and corrected.[62]
hyperkalaemia.
• R estrict dietary intake – avoid

» Check for any acute ECG changes.
• Features of hyperkalaemia include

peaked t waves, flat tened p waves,
broad QRS complexes.
• If there are ECG changes consistent with
hyperkalaemia, treat in the same way
as severe hyperkalaemia.
• Muscle weakness
MANAGEMENT
asystole).
» Check your local protocols – many

113
Acute
Primary options

-and-

intracellularly:[62] [80]


consider salbutamol
Primary options



potassium.[80]
MANAGEMENT

hyperkalaemia
L) OR moderate
hyperkalaemia
Acute
Primary options
ECG changes
» calcium chloride: 6.8 mmol (10 mL of
dose
OR
» calcium gluconate: 6.8 mmol (30 mL of

dose
» Give immediate intravenous calcium for

cardiac protection. [62] [80]
• Give over 5 to 10 minutes, then repeat

the ECG and consider a further dose if
ECG changes persist.[80]
• Use a wide bore cannula and avoid

extravasation.
• Intravenous calcium antagonises

the cardiac membrane excitability
and so protects the heart against
arrhythmias.[110]
• Effective within 3 minutes and lasts

30 to 60 minutes.
• Seek senior advice if the ECG fails to

normalise after one dose.[62]
Primary options

-and-
MANAGEMENT


intracellularly:[62] [80]
115
Acute

plus salbutamol
Primary options



potassium.[80]

hyperkalaemia


MANAGEMENT

and corrected.[62]
Acute
hyperkalaemia.
• Muscle weakness
asystole).
» Check your local protocols – many

» There is no evidence to support the

associated hyperkalaemia. [110]
• However, in practice their use may

sometimes be considered by the
nephrology team as an adjunct to other
therapies provided the patient is fluid
replete (but only with close specialist
supervision).
The role of loop diuretics in the

management of AKI-associated
hyperkalaemia remains controversial.
• Loop diuretics may be used under

specialist supervision for volume
management in patients with AKI
and there is a theoretical rationale to
suggest they could be beneficial in
managing hyperkalaemia.[1]
• Loop diuretics promote

potassium excretion in the urine
through their action in inhibiting
the Na+-K+-2Cl co-transporter
MANAGEMENT
on the ascending limb of Henle,

thereby reducing uptake of
117
Acute
potassium (as well as sodium
and chloride).
• However, the 2014 UK Renal

Association guideline on acute
hyperkalaemia concluded that there
is no evidence to support the use of
diuretics in the management of AKI-
are clear that loop diuretics should
not be used routinely to manage
AKI.[1] [3] The use of loop diuretics is
indicated (under specialist supervision)
only if a patient with AKI-associated
hyperkalaemia also has volume
overload (which is a clear indication for
their use).[3]
with metabolic acidosis plus seek specialist advice from the renal team
» Once any obstruction has been relieved
and diuresis is progressing satisfactorily,
the renal team will decide whether or not
sodium bicarbonate is indicated, based on an
assessment of benefits and risks.
MANAGEMENT
Emerging
Novel therapeutic agents
The use of novel therapeutic agents, including atrial natriuretic peptide, theophylline, insulin-like growth
factor, epidermal growth factor, free radical oxygen scavengers, antibodies to adhesion molecules, and
prostaglandins, has been reviewed. None have been shown to be beneficial in human AKI.[21] The protective
effect of statins (administered either pre-intervention or chronically) is debated,[95] [220] [221] but results
from recent studies are disappointing.[222] [223] [224] Controlled hypothermia and recombinant alkaline
phosphatase infusion may be of benefit.[225] [226] Erythropoietin does not appear to exert nephroprotective
effects,[227] and treatment with thyroid hormone has been associated with worse outcomes than other
possible treatments for patients with established AKI; its role in preventing AKI was not adequately
investigated.[228] Remote ischaemic pre-conditioning appeared to hold promise to prevent AKI, but two
systematic reviews (including more than 28 randomised controlled trials) cast doubt on the value of the
treatment.[229] [230] [231]
Primary prevention
Prevention of contrast-induced AKI
Intravenous iodinated contrast has previously been reported to cause contrast-induced AKI (CI-
AKI).[5] However, the association has been questioned more recently by large population studies that have
failed to demonstrate this risk.[40] [41] [42] The evidence regarding the prevention of CI-AKI is weak, and
often conflicting.[57] [58]
The patient’s’ kidney function must be measured within 3 months of offering iodinated contrast for non-
emergency imaging.
In 2019, the UK National Institute for Health and Care Excellence (NICE) recommendations on preventing CI-
AKI were updated.[3]
• The updated guidance now recommends that you should encourage oral hydration, rather than
previously recommended intravenous volume expansion, before and after procedures using
intravenous iodinated contrast agents in adults at increased risk of contrast-induced AKI.
Patients at increased risk of CI-AKI include those people with:
• 2
Chronic kidney disease (eGFR <40 mL/min/1.73 m ). Consider temporarily stopping ACE inhibitors
2
and angiotensin-II receptor antagonists if the patient has an eGFR <40 mL/min/1.73 m
• 2
Diabetes, but only if the patient has concomitant chronic kidney disease (eGFR <40 mL/min/1.73 m )
• Heart failure
• Kidney transplant
• Age ≥75 years
• Hypovolaemia
• Increasing volume of iodinated contrast agent
• Intra-arterial administration of contrast agent with first pass kidney exposure (e.g., contrast injected
into the left side of the heart or directly into the renal arteries).
MANAGEMENT
However, it is important to stress that risk assessment should not delay emergency imaging. Consider
intravenous volume expansion with either isotonic sodium bicarbonate or normal saline (0.9% sodium
chloride) for inpatients having iodinated contrast agents if they have particularly high risk factors,
including:[Evidence C]
119
• 2
eGFR <30 mL/min/1.73 m
• Kidney transplant
• Large volume of contrast agent
• Intra-arterial administration of contrast agent.
Discuss patients on renal replacement therapy or with a kidney transplant with the renal team before offering
iodinated contrast but do not delay emergency imaging.
Do not use N-acetylcysteine to prevent contrast-induced AKI.[59] [60] [61]
Prevention of perioperative AKI

Identify patient risk factors for AKI prior to surgery, including:
• Sepsis
• Hypovolaemia
• Intraperitoneal surgery
• 2
Chronic kidney disease (eGFR <60 ml/min/1.73 m )
• Diabetes
• Heart failure
• Age ≥65 years
• Liver disease
• Nephrotoxins (e.g., NSAIDs, aminoglycoside antibiotics such as gentamicin).
Secondary prevention
Patient discussions
Inform the patient if they have an episode of AKI; give information on what the cause was and what
measures they can take to avoid a further episode (e.g., avoiding getting dehydrated during an
intercurrent illness).
The UK National Institute for Health and Care Excellence (NICE) recommends:[3]
• Involving parents and carers in the discussion if appropriate

• Discussing immediate treatment options, monitoring, and prognosis; and long#term treatment
options, monitoring, self#management, and support in collaboration with a multidisciplinary team
appropriate to the person's individual needs
• Providing information to people needing renal replacement therapy after discharge, including what
preparation might be needed (such as having a fistula or peritoneal catheter) and the frequency
and length of dialysis sessions
• Discussing the risk of developing future AKI, particularly with people who have chronic kidney
MANAGEMENT
2
disease with an eGFR <60 ml/min/1.73 m , or neurological or cognitive impairment or disability,
and who may have limited access to fluids.
• Emphasise the risk associated with conditions leading to dehydration (for example, diarrhoea
and vomiting) and drugs that can cause or worsen kidney injury (including over#the#counter
NSAIDs).
MANAGEMENT
121
Acute kidney injury Follow up
Monitoring
Monitoring
FOLLOW UP
If recovery of function is complete and a normal glomerular filtration rate is re-established with no
evidence of residual kidney injury, no kidney follow-up is required.
If the patient is left with residual chronic kidney disease (CKD) after AKI, a nephrologist follow-up is
recommended with interventions based on stage of CKD.[245]
The National Kidney Foundation KDOQI guidelines include recommendations regarding the management
of patients who have developed CKD subsequent to AKI.[246] Management of chronic intrinsic kidney
diseases (e.g., glomerulonephritis and vasculitis) requires nephrologist intervention to manage therapies
including corticosteroids, cytotoxic drugs, and immune-modifying drugs. Adverse effects and toxicities
require close observation.
Complications
Complications Timeframe Likelihood
FOLLOW UP
hyperphosphataemia long term high
A late complication usually arising several days after glomerular filtration falls.
Treatment includes dietary restriction and the administration of phosphate binders, such as calcium
acetate, calcium carbonate, sevelamer, or lanthanum carbonate.
Haemodialysis is effective in phosphorus reduction. In patients in whom intense renal replacement

is undertaken, such as those on continuous renal replacement therapies or daily dialysis regimens,
phosphorus replacement may be required.
uraemia long term medium
Uraemic toxins accumulate with severe and untreated kidney failure, resulting in lethargy, confusion, and
obtundation.
Dialysis is required for management of uraemia.
hyperkalaemia variable high
Results from impaired excretion of potassium, cell lysis, or tissue breakdown.
Severe hyperkalaemia may result in muscle weakness and classic ECG findings of peaked T waves,
increased PR interval, widened QRS, atrial arrest, and deterioration to a sine wave pattern.
If hyperkalaemia is confirmed or suspected, use normal saline (0.9% sodium chloride) rather than a
balanced crystalloid for fluid balance.[241] [63]
Treatment depends on the severity and presence of muscular and/or cardiac complications. Check your
local protocols - many hospitals have institutional guidelines for managing hyperkalaemia.
See the Treatment algorithm section of this topic for information on managing mild, moderate and severe
hyperkalaemia.
chronic progressive kidney disease variable medium
AKI may leave the patient with prolonged kidney damage, and functional recovery may not return to the
baseline.
Recovery is dependent on the mechanism and severity of the injury and the underlying comorbid medical
conditions.
AKI in children may be associated with chronic kidney disease that may progress to end-stage kidney
disease.[242] [243]
Patients with partial or no recovery from AKI are at increased risk for congestive heart failure and acute
myocardial infarction.[244]
123
Complications Timeframe Likelihood

end-stage kidney disease variable medium
FOLLOW UP
Some patients may not recover from severe kidney injury, especially those with underlying kidney disease
or other comorbid medical conditions. Chronic renal replacement therapy may be required.[237]
Prognosis
Recovery for AKI is variable and depends on cause of injury and the severity and duration of AKI.[232]
There is an independent association of AKI with a higher risk of death.[233] [232] [234] In-hospital mortality
rates associated with AKI vary from 6% to 80%, and there is increased long-term mortality in those with AKI
surviving hospitalisation.[234]
Up to 6% of patients admitted to the intensive care unit have AKI requiring renal replacement therapy.[20]
[232] [235] In hospital, when AKI requires dialysis, mortality exceeds 50%; those with multi-organ failure
are at greatest risk.[17] [20] [235] Mortality rates are high due to death from underlying disease and
complications, not just the AKI.
Five-year survival rates in patients with AKI requiring renal replacement therapy range from 15% to 35%
(less than 10% of those patients are dialysis-dependent).[236]
AKI is irreversible in approximately 5% to 7% of adults and as many as 16% of older adult patients.[237]
There is controversy as to whether prior AKI is a major risk factor leading to future chronic kidney disease,
but increasing evidence of strong association mounts.[238] [239] [240]
Acute kidney injury Guidelines
Diagnostic guidelines
United Kingdom
Acute kidney injury (AKI)

Published by: The Renal Association Last published: 2019
Acute kidney injury: prevention, detection and management

Published by: National Institute for Health and Care Excellence Last published: 2019
International
Kidney disease: improving global outcomes (KDIGO) clinical practice

guideline for acute kidney injury
GUIDELINES
Published by: International Society of Nephrology Last published: 2012
North America
Management of acute kidney injury: core curriculum 2018

Published by: American Journal of Kidney Diseases Last published: 2018
ACR appropriateness criteria: renal failure

Published by: American College of Radiology Last published: 2013
Treatment guidelines
United Kingdom
Acute kidney injury: prevention, detection and management

Published by: National Institute for Health and Care Excellence Last published: 2019
Acute kidney injury (AKI)

Published by: The Renal Association Last published: 2019
British consensus guidelines on intravenous fluid therapy for adult surgical

patients
Published by: BAPEN; Association for Clinical Biochemistry; Last published: 2011
Association of Surgeons of Great Britain and Ireland; Society of Academic
and Research Surgery; Renal Association/Intensive Care Society
125
Acute kidney injury Guidelines
Europe
ESPEN guidelines on parenteral nutrition: adult renal failure

Published by: European Society for Clinical Nutrition and Metabolism Last published: 2009
International
Kidney disease: improving global outcomes (KDIGO) clinical practice

guideline for acute kidney injury
Published by: International Society of Nephrology Last published: 2012
North America
Management of acute kidney injury: core curriculum 2018

GUIDELINES
Published by: American Journal of Kidney Diseases Last published: 2018
KDOQI US commentary on the 2012 KDIGO clinical practice guideline for

acute kidney injury
Published by: The National Kidney Foundation Last published: 2013
Acute kidney injury Evidence tables
Evidence tables
What are the effects of sodium chloride 0.9% (normal saline) in preventing
EVIDENCE TABLES
contrast-induced acute kidney injury (CI-AKI) in at risk adults?[3]
This table is a summary of the analysis reported in a guideline (underpinned by a systematic review)
that focuses on the above important clinical question.
View the full source guideline
Evidence C * Confidence in the evidence is very low or low where GRADE has been performed
and there may be no difference in effectiveness between the intervention and
comparison for key outcomes. However, this is uncertain and new evidence could
change this in the future.
Population: Adults who are at risk of CI-AKI

Intervention: Sodium chloride 0.9%
Comparison: No intravenous hydration, oral fluids, sodium chloride 0.45%, sodium bicarbonate, oral
sodium bicarbonate plus oral fluids
† ‡
Outcome Effectiveness (BMJ rating) Confidence in evidence (GRADE)
Sodium chloride 0.9% versus no intravenous hydration
CI-AKI No statistically significant Low

difference
In-hospital mortality No statistically significant Very Low

difference
All-cause mortality No statistically significant Low

difference
Need for renal replacement No statistically significant Low

therapy: dialysis difference
Adverse events No statistically significant Very Low

difference
Sodium chloride 0.9% versus oral fluids
CI-AKI No statistically significant Very Low

difference
All-cause mortality No statistically significant Very Low

difference
127
† ‡
Outcome Effectiveness (BMJ rating) Confidence in evidence (GRADE)
Need for renal replacement No statistically significant Very Low

EVIDENCE TABLES
Sodium chloride 0.9% versus sodium chloride 0.45%

difference
Mortality No statistically significant Very Low

difference
Need for renal replacement No statistically significant Very Low

Adverse events No statistically significant Very Low

difference
Sodium chloride 0.9% versus sodium bicarbonate
CI-AKI No statistically significant Moderate

difference
All-cause mortality (30 days) No statistically significant Very Low

difference
All-cause mortality (>30 days) No statistically significant Very Low

difference
In-hospital mortality No statistically significant Very Low

difference
Need for renal replacement No statistically significant Low

therapy difference
Adverse events No statistically significant Low

difference
Adverse events: heart failure No statistically significant Very Low

difference
Sodium chloride 0.9% versus oral sodium bicarbonate plus oral fluids

difference
Recommendations as stated in the source guideline

For inpatients having iodine-based contrast media, consider intravenous volume expansion with either
isotonic sodium bicarbonate or 0.9% sodium chloride if they are at particularly high risk, for example, if:
• They have an eGFR less than 30 ml/min/1.73 m2
• They have had a renal transplant
EVIDENCE TABLES
• A large volume of contrast medium is being used (for example, higher than the standard diagnostic
dose or repeat administration within 24 hours)
• Intra-arterial administration of contrast medium with first-pass renal exposure is being used.
Note
The guideline committee undertook both network and pairwise meta-analyses. The results in this table are
for the pairwise meta-analysis.
The guideline committee noted that evidence from the network meta-analysis showed that sodium chloride
0.9% and sodium bicarbonate appear to be equivalent for preventing CI-AKI. They also noted there was
limited evidence on subgroup analyses and that none of those identified showed evidence of an effect from
any of the interventions on the incidence of CI-AKI.
The guideline committee stated that the primary outcomes for the pairwise analysis were: CI-AKI, CKD
progression at 3 months following CI-AKI diagnosis, mortality up to 12 months, need for renal replacement
therapy, and adverse events. Other outcomes of interest were: length of hospital stay, readmission for AKI,
and health-related quality of life. See the full guideline for details of these additional outcomes.
* Evidence levels
The Evidence level is an internal rating applied by BMJ Best Practice. See the EBM Toolkit for details.
Confidence in evidence
A - High or moderate to high

B - Moderate or low to moderate
C - Very low or low
† Effectiveness (BMJ rating)

Based on statistical significance, which demonstrates that the results are unlikely to be due to chance, but
which does not necessarily translate to a clinical significance.
129
‡ Grade certainty ratings
High The authors are very confident that the true

effect is similar to the estimated effect.
EVIDENCE TABLES
Moderate The authors are moderately confident that

the true effect is likely to be close to the
estimated effect.
Low The authors have limited confidence in the
effect estimate and the true effect may be
substantially different.
Very Low The authors have very little confidence in
the effect estimate and the true effect is
likely to be substantially different.
BMJ Best Practice EBM Toolkit: What is GRADE?
Acute kidney injury References
Key articles
• Kidney disease: improving global outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical
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practice guideline for acute kidney injury. Kidney Int Suppl. 2012 Mar;2(1):1-138. Full text
• National Institute for Health and Care Excellence. Acute kidney injury: prevention, detection and
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• Kanagasundaram S, Ashley C, Bhojani S, et al. Renal Association clinical practice guideline acute
kidney injury (AKI). August 2019 [internet publication]. Full text
• Royal College of Physicians. Acute care toolkit 12: acute kidney injury and intravenous fluid
therapy. October 2015 [internet publication]. Full text
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Contributors:
// Peer Reviewers:
Suren Kanagasundaram,
Consultant Nephrologist
Newcastle upon Tyne Hospitals NHS Trust, Clinical Lead , Newcastle Hospitals Haemodialysis Service ,
Honorary Clinical Senior Lecturer , Newcastle University, Newcastle, UK
DISCLOSURES: SK was an expert adviser to the National Confidential Enquiry into Patient Outcome and
Death (NCEPOD) report into AKI and is lead author of the UK Renal Association clinical practice guideline
on AKI.
// Expert Advisers:
Andrew Lewington, BSc (Hons), MBBS,#MEd, MD, FRCP

Consultant Renal Physician
Honorary Associate Professor, Nephrology Department, Leeds Teaching Hospitals NHS Trust, Head of
MBChB, School of Medicine, University of Leeds, Leeds, UK
DISCLOSURES: AL has been the principal applicant/co-applicant for a number of grants including:
Engineering and Physical Sciences Research Council Research - Multiplexed AKI biomarker detection with
a single molecule biosensor; Leeds Cares - A novel, non-invasive diagnostic approach to assess kidney
transplant health through the targeted measurement of biomarkers of kidney injury and immune response
in kidney transplant recipients at the Leeds Teaching Hospitals NHS Trust; Kidney Research Yorkshire -
Use of enhanced technology to characterise haemodialysis treatment for acute kidney injury (AKI); Bringing
It Home - Validation of a micro-sampling technique for measuring tacrolimus and creatinine remotely; and
to fund a research nurse; British Renal Society - Renal function assessment with point of care creatinine
in diverse populations (RAPID), and several NIHR grants including on a) Improving the quality of post-
discharge care following AKI b) An investigation into the use of remote blood sample collection to reduce
health inequalities in patients with mental health disorders c) A comparison of remote blood collection
devices: a human factor use study d) Defining the characteristics for a novel automatic device to monitor
urine output in catheterized patients e) Leeds Medtech and In-vitro Diagnostic Cooperative Grant Extension
f) Surgical MedTech Co-operative for the 2019/20 proof-of-principle funding stream g) A pilot investigation
into the use of beta-trace protein for residual renal function estimation in haemodialysis h) Application of
functional MRI to improve assessment of chronic kidney disease (AFiRM study) i) SuperResPath-Renal:
Quantitative super-resolution technology for a fast, decentralised clinical diagnosis of renal pathologies. AL
is the co-author of a number of manuscripts including on extracorporeal treatments, AKI, kidney function
testing prior to contrast-enhanced CT, plasma exchange and glucocorticoids in severe ANCA-associated
vasculitis, COVID-19 rapid diagnostics, multimodal image-guided ablation on management of renal cancer
in Von-Hippel-Lindau syndrome, and on a summary of NICE guidance on CKD. AL is the author of several
book chapters on nephrology and AKI. AL has received expenses for accommodation and travel for
conferences at which he has given lectures, other than those delivered virtually. AL was a member of the
AKI Scientific Program Committee for the ISN World Congress of Nephrology 2020-2021 and Chair of this
same committee in 2021-2022.
Acknowledgements,
BMJ Best Practice would like to gratefully acknowledge the previous expert contributor, whose work has
been retained in parts of the content:
Richard A. Lafayette MD, Professor of Medicine, Nephrology Division, Stanford University Medical Center,
Stanford, CA
Contributors:
DISCLOSURES: RAL works as a consultant and researcher for Relypsa, Inc. Although unrelated to this
topic area, RAL also works as a consultant for Fibrogen, Inc.; Mallinckrodt, Inc.; and Omeros, Inc.; and as
a researcher for Genentech, Inc.; Mallinckrodt, Inc.; GlaxoSmithKline, Inc.; Rigel, Inc.; Aurinia, Inc.; and the
NIH.
// Editors:
Tessa Davis,
Section Editor, BMJ Best Practice
Consultant in Paediatric Emergency Medicine, Royal London Hospital, London, UK
DISCLOSURES: TD declares that she has no competing interests.
Jo Haynes,
Head of Editorial, BMJ Knowledge Centre
DISCLOSURES: JH declares that she has no competing interests.
Julie Costello,
Comorbidities Editor, BMJ Best Practice
DISCLOSURES: JC declares that she has no competing interests.
Adam Mitchell,
Drug Editor, BMJ Best Practice
DISCLOSURES: AM declares that he has no competing interests.

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Acute kidney injury

Straight to the point of care

Last updated: Mar 05, 2020

Evidence tables 127

underlying kidney disease

exposure to nephrotoxins (e.g., aminoglycosides, vancomycin + piperacillin-

excessive fluid loss

recent vascular intervention

myeloproliferative disorders, such as multiple myeloma

sodium-retaining states (e.g., congestive heart failure, cirrhosis, nephrotic

recent blood transfusion

use of renin-angiotensin system inhibitors

• Increase in serum creatinine by ≥26 micromol/L (≥0.3 mg/dL) within 48 hours; or

Classification based on pathophysiology[5]

• AKI secondary to abdominal masses or an enlarged bladder may be found on examination or

Look for signs of sepsis and manage promptly. [9] [63]

Recognise and treat hypovolaemia promptly with an immediate bolus of crystalloid

Stop/avoid exposure to any nephrotoxins (e.g., non-steroidal anti-inflammatory drugs

• AKI can often be non-oliguric.

• A rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours

Stage the AKI according to the KDIGO staging criteria.[1]

A relevant history is a key part of the assessment. Check for:

Your examination should prioritise volume statusand a sepsis screen.

• Sepsis (e.g., pneumonia, cellulitis)

• Post-kidney AKIis due to obstruction:[9] [62]

• Most common in older men with prostatic hyperplasia[4]

• Urinalysis [3] [9] [62] [64]

• There is no clear cause of AKI

• Iodinated contrast agent

• Symptoms or history of urological obstruction

AKI is often a ‘silent disease’ so a high index of suspicion is important, particularly in

• A rise in serum creatinine of ≥26 micromol/L (≥0.3 mg/dL) within 48 hours

• In addition, unless the patient is catheterised, accurate and timely measurement of

It is important to differentiate AKI from a progression of CKD at initial presentation.

occurred over a longer period.

• If the patient is acutely unwell or hypovolaemic, this points towards AKI.[9]

Beware false positive rises in creatinine, for example: [1] [9]

Staging the AKI

Stage 1 • SCr rise of ≥26 • <0.5 mL/kg/h for at least

Stage#2 • SCr increase to 2 to 2.9 • <0.5 mL/kg/h for at least

Stage#3 • SCr increase to ≥3 • <0.3 mL/kg/h for at least

Evidence: AKI stage and mortality

Mortality rises sharply with increasing stage of AKI.

KDIGO diagnostic and staging criteria

• In practice, AKI is sometimes multi-factorial.[65]

• Sepsis, hypovolaemia, and/or hypotension (pre-kidney AKI)

• Often due to acute illness in a patient with background risk factors

• Exposure to nephrotoxins (intrinsic AKI).

1. Pre-kidney AKI (80%)

• By definition this is a functional process whereby there is no cellular damage.

Causes of pre-kidney AKI include: [1] [62]

• Hypovolaemia/dehydration. For example, due to:

• May be related to antihypertensive medications.

• After major surgery

2. Intrinsic AKI (10%-20%)

Causes of intrinsic AKI include: [9] [62]

3. Post-kidney AKI (5%-10%)

• Risk factors [3] [9] [64]

• Precipitating factors [1] [3] [9] [62]

• Suspected or confirmed sepsis.