RENAL EMERGENCIES

MODERATOR PRESENTOR
Mrs. Ujjwal Dahiya Mr. Shubham Gaur
Associate Professor MSc. Critical Care Nursing
AIIMS AIIMS
OBJECTIVES
At the end of the seminar, you all will be able to understand;
• Acute Kidney Injury
• Chronic Kidney Injury
• Acute Tubular Necrosis
• Bladder Trauma
• Kidney Transplant
ANATOMY
ANATOMY
BLOOD SUPPLY TO KIDNEY
STRUCTURAL & FUNCTIONAL UNIT
WHAT DO YOU UNDERSTAND BY ?
• NORMAL URINE OUTPUT & GFR?

• FREQUENCY, URGENCY, DYSURIA, HESISTANCY, NOCTURIA,

INCONTINENCE, ENURESIS, POLYURIA, OLIGOURIA, ANURIA,
HEMATURIA, PROTIENURIA ?
ACUTE KIDNEY INJURY
DEFINITION OF AKI
• Increase in serum creatinine by ≥0.3 mg/dL (≥26.5 micromol/L) within
48 h, 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/h for 6 h.
STAGES OF AKI
PRESENTATION OF AKI
• May be asymptomatic. • Haematuria (pink, rather than
• Elevated serum creatinine during frank, blood).
biochemical screening. • Drug OD (e.g., paracetamol).
•  Detection of oliguria by nursing • Constitutional symptoms
staff. (arthralgia, rhinitis, respiratory).
•  Malaise, confusion, seizures, or •  Sepsis.
coma. • Vasculitis rash.
• Nausea, anorexia, or vomiting. • MOF.
• Oliguria or abnormal urine colour.
PHASES OF AKI

The The
The oliguria The diuresis
initiation recovery
period period
period period
PHASES OF AKI
The initiation period begins with the initial insult and ends when oliguria
develops.

The oliguria period is accompanied by a rise in the serum concentration of

substances usually excreted by the kidneys . In this phase uremic symptoms
first appear and life-threatening conditions such as hyperkalemia develop.
PHASES OF AKI
In the diuresis period, the third phase, the patient experiences gradually
increasing urine output, which signals that glomerular filtration has
started to recover. Laboratory values stop rising and eventually decrease.
Although the volume of urinary output may reach normal or elevated
levels, renal function may still be markedly abnormal.. The patient must
be observed closely for dehydration during this phase; if dehydration
occurs, the uremic symptoms are likely to increase.

The recovery period signals the improvement of renal function and may
take 3 to 12 months. Laboratory values return to the patient’s normal
level.
DIAGNOSIS OF AKI
Physical examination.
1 Asterixis and myoclonus
2 Peripheral edema (if volume overload is present)
3 Pulmonary rales (if volume overload is present)
4 Elevated right atrial pressure (if volume overload is present)
 Identification of precipitating cause
DIAGNOSIS OF AKI
Serum creatinine and BUN level .(n 7-18mg/dl)
Serum electrolytes.
 Urine analysis.
 Renal bladder ultra sound.
 Renal scan.
 CT scans and MRI scan (to identify lesion and masses)
 The urine will be examined under a microscope.
 Biopsy
NEW DIAGNOSTIC MARKERS
• Neutrophil gelatinase-associated lipocalin (NGAL) rises after poor
perfusion or ischemia. Measurable in both serum or urine, it increases
24 to 48 hrs before S. creatinine rises.
• Cystatin C detected in both the urine and serum. It is early AKI
predictor.
• Tissue inhibitor metalloproteinase-2 (TIMP-2) appears in urine within
12 hrs after renal tubular cells are injured from ischemia or sepsis.
• GFR This biomarker is reflected in urine. GFR is affected by decreased
CO, reduced blood volume or BP.
It’s the best indicators of current kidney function.
COMPLICATIONS
• Uremia
• Hypervolemia And Hypovolemia
• Hyponatremia
• Hyperkalemia
• Acidosis
• Hyperphosphatemia and hypocalcemia
• Bleeding
• Infections
• Cardiac complications
• Malnutrition
MANAGEMENT OF AKI
General Issues
a. Optimization of systemic and renal hemodynamics through volume
resuscitation and judicious use of vasopressors

b. Elimination of nephrotoxic agents (e.g., ACE inhibitors, ARBs, NSAIDs,

aminoglycosides) if possible

c. Initiation of renal replacement therapy when indicated

MANAGEMENT OF AKI
Hyponatremia
a. Restriction of enteral free water intake, minimization of hypotonic
intravenous solutions including those containing dextrose

b. Hypertonic saline is rarely necessary in AKI. Vasopressin antagonists are

generally not needed.
MANAGEMENT OF AKI
Hyperkalemia
a. Restriction of dietary potassium intake
b. Discontinuation of potassium-sparing diuretics, ACE inhibitors, ARBs, NSAIDs
c. Loop diuretics to promote urinary potassium loss
d. Potassium binding ion-exchange resin (sodium polystyrene sulfonate) e.
Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote entry
of potassium intracellularly
f. Inhaled beta-agonist therapy to promote entry of potassium intracellularly
g. Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium
MANAGEMENT OF AKI
Metabolic acidosis
a. Sodium bicarbonate
b. Administration of other bases
c. Renal replacement therapy

Hyperphosphatemia
a. Restriction of dietary phosphate intake
b. Phosphate binding agents (calcium acetate, sevelamer hydrochloride,
aluminum hydroxide—taken with meals)
MANAGEMENT OF AKI
Hypocalcemia
a. Calcium carbonate or calcium gluconate if symptomatic

Hypermagnesemia
a. Discontinue Mg2+ containing antacids

Hyperuricemia
a. Acute treatment is usually not required except in the setting of tumor lysis
syndrome
MANAGEMENT OF AKI
Renal Replacement Therapy
• Volume overload/pulmonary edema.
• Refractory hyperkalemia (>6.5 mEq/L).
• Severe metabolic acidosis (pH<7.1).
• Anuria.
• Uremic encephalopathy.
• Uremic pericarditis.
MANAGEMENT OF AKI
Nutrition
• Dietary proteins 1 gm/kg
• High carbohydrate diet
• Restrict potassium and phosphorus rich food: bananas, citrus fruits and
juices, coffee
• Potassium intake: 40-60 mEq/day
• Sodium intake: 2 g/day
• After the diuretic phase: high-protein & high-caloric diet
NURSING DIAGNOSIS

Excess fluid
volume r/t fluid
retention

Potential for injury

r/t electrolyte
imbalance, uremia
and metabolic
acidosis

Alteration in
nutrition less than
Activity intolerance
body requirements
r/t anemia or
r/t dietary
uremia
restrictions &
uremia
ACUTE ON CHRONIC RENAL
FAILURE
Patients with chronic kidney disease (CKD), as evidenced by a low eGFR
or presence of proteinuria, are at higher risk for developing AKI, a
condition known as acute on chronic renal failure (ACRF).

Diagnosis
• The diagnostic considerations for AKI are the same whether it is acute
on chronic or de novo AKI
ACUTE ON CHRONIC RENAL
FAILURE
The clinical features of ACRF are similar to those in patients with de novo AKI.
• Acidemia
• Hyperkalemia
• Volume/fluid overload
• Hypocalcemia/hyperphosphatemia (as a consequence of secondary
hyperparathyroidism)
• Hyponatremia
• Uremia (elevated BUN, platelet dysfunction, changes in mental status,
pericarditis)
ACUTE ON CHRONIC RENAL
FAILURE
Management
• If the underlying cause of the acute component of ACRF can be ascertained,
it should be treated promptly.

• Hemodynamics and blood pressure should be optimized.

• Manage the sequelae of ACRF (hyperkalemia, uremia and volume overload
can be life-threatening).

• If the sequelae of ACRF cannot be managed medically, prompt consideration

of renal replacement therapy should be done.
RESEARCH INPUT
AKI in Hospitalized Patients with COVID-19
Lili Chan, Kumardeep Chaudhary, Aparna Saha, Kinsuk Chauhan, Akhil
Vaid, Shan Zhao et al

• JASN (Journal of American Society of Nephrology)

• January 2021, 
• DOI: https://doi.org/10.1681/ASN.2020050615
RESEARCH INPUT
• Background Early reports indicate that AKI is common among
patients with coronavirus disease 2019 (COVID-19) and associated
with worse outcomes.

• Methods This retrospective, observational study involved a review of

data from electronic health records of patients aged ≥18 years with
laboratory-confirmed COVID-19 admitted to the Mount Sinai Health
System from February 27 to May 30, 2020. We describe the frequency
of AKI and dialysis requirement, AKI recovery, and adjusted odds
ratios (aORs) with mortality.
RESEARCH INPUT
Of 3993 hospitalized patients with COVID-19,
• AKI occurred in 1835 (46%) patients;
• 347 (19%) of the patients with AKI required dialysis.
• The proportions with stages 1, 2, or 3 AKI were 39%, 19%, and 42%,
respectively.
• A total of 976 (24%) patients were admitted to intensive care, and 745
(76%) experienced AKI.
• In-hospital mortality was 50% among patients with AKI versus 8%
among those without AKI
• . An additional 28 of 77 (36%) patients who had not recovered kidney
function at discharge did so on posthospital follow-up.
RESEARCH INPUT
• Conclusions AKI is common among patients hospitalized with
COVID-19 and is associated with high mortality.

• Of all patients with AKI, only 30% survived with recovery of kidney
function by the time of discharge.
CHRONIC KIDNEY INJURY
DEFINITION OF CKI
The guidelines define CKI as either kidney damage or a decreased
glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for at
least 3 months. Whatever the underlying etiology, once the loss of
nephrons and reduction of functional renal mass reaches a certain
point, the remaining nephrons begin a process of irreversible sclerosis
that leads to a progressive decline in the GFR.
ETIOLOGY OF CKI
• Diabetic kidney disease
• Hypertension
• Vascular disease
• Glomerular disease (primary or secondary)
• Cystic kidney diseases
• Tubulointerstitial disease
• Urinary tract obstruction or dysfunction
• Recurrent kidney stone disease
• Congenital (birth) defects of the kidney or bladder
• Unrecovered acute kidney injury
CLINICAL MANIFESTATIONS OF CKI
Patients with CKD stages 1-3 are generally asymptomatic. Typically, it is not
until stages 4-5 (GFR < 30 mL/min/1.73 m²) that endocrine/metabolic
derangements or disturbances in water or electrolyte balance become
clinically manifest.

Metabolic changes:Metabolic acidosis is a common disturbance in

advanced CKD. The majority of patients can still acidify the urine, but they
produce less ammonia and, therefore, cannot excrete the normal quantity
of protons in combination with this urinary buffer

Proteinuria ,Hypocalcemia ,Hyponatremia , Hyperphosphatemia

Hyperkalemia
CLINICAL MANIFESTATIONS OF CKI
Failure of kidneys to remove excess fluid may cause:
• Edema of the legs, ankles, feet, face and/or hands
• Shortness of breath due to extra fluid on the lungs
(may also be caused by anemia)
• hypertension and/or congestive heart failure
CLINICAL MANIFESTATIONS OF CKI
Anemia in CKD is associated with the following:
• Fatigue
• Reduced exercise capacity
• Impaired cognitive and immune function
• Reduced quality of life
• Development of cardiovascular disease
• New onset of heart failure or the development of more severe heart
failure
• Increased cardiovascular mortality
CLINICAL MANIFESTATIONS OF CKI
Other manifestations of uremia in ESRD, many of which are more likely
in patients who are being inadequately dialyzed, include the following:

• Pericarditis: Can be complicated by cardiac tamponade, possibly

resulting in death if unrecognized
• Encephalopathy: Can progress to coma and death
• Peripheral neuropathy, usually asymptomatic
• Restless leg syndrome
CLINICAL MANIFESTATIONS OF CKI
• Gastrointestinal symptoms: Anorexia, nausea, vomiting, diarrhea
• Skin manifestations: Dry skin, pruritus, ecchymosis
• Fatigue, increased somnolence, failure to thrive
• Malnutrition
• Erectile dysfunction, decreased libido, amenorrhea
• Platelet dysfunction with tendency to bleed
DIAGNOSIS OF CKI
Laboratory studies
• Laboratory studies used in the diagnosis of CKD can include the
following:
• Complete blood count (CBC)
• Basic metabolic panel
• Urinalysis
• Serum albumin levels: Patients may have hypoalbuminemia due to
malnutrition, urinary protein loss, or chronic inflammation
• Lipid profile: Patients with CKD have an increased risk of
cardiovascular disease
DIAGNOSIS OF CKI
Evidence of renal bone disease can be derived from the following
tests:

• Serum calcium and phosphate

• 25-hydroxyvitamin D
• Alkaline phosphatase
• Intact parathyroid hormone (PTH) levels
DIAGNOSIS OF CKI
Other investigations:

Abdominal ultrasound :Kidneys with CKD are usually smaller (< 9 cm)
than normal kidneys.
Renal Biopsy
Abdominal CT scan
Abdominal MRI
Renal scan & Renal radionuclide scanning
Bone density test
MANAGEMENT OF CKI
The pathologic manifestations of CKD should be treated as follows:

• Anemia: When the hemoglobin level is below 10 g/dL, treat with

erythropoiesis-stimulating agents (ESAs), which include epoetin alfa
and darbepoetin alfa after iron saturation and ferritin levels are at
acceptable levels
• Hyperphosphatemia: Treat with dietary phosphate binders and
dietary phosphate restriction
• Hypocalcemia: Treat with calcium supplements with or without
calcitriol
MANAGEMENT OF CKI
• Hyperparathyroidism: Treat with calcitriol or vitamin D analogues or
calcimimetics
• Volume overload: Treat with loop diuretics or ultrafiltration
• Metabolic acidosis: Treat with oral alkali supplementation
• Uremic manifestations: Treat with long-term renal replacement
therapy (hemodialysis, peritoneal dialysis, or renal transplantation
MANAGEMENT OF CKI
Indications for renal replacement therapy include the following:
• Severe metabolic acidosis
• Hyperkalemia
• Pericarditis
• Encephalopathy
• Intractable volume overload
• Failure to thrive and malnutrition
• Peripheral neuropathy
• Intractable gastrointestinal symptoms
DIETARY MANAGEMENT OF CKI
• Protein restriction: Decreasing protein intake may slow the
progression of chronic kidney disease. Allowed protein of high
biological value.
• Salt restriction: Limit to 4-6 grams a day to avoid fluid retention and
help control high blood pressure.
• Restrict Fluid intake
• Potassium restriction: High levels of potassium can cause abnormal
heart rhythms.
Examples of foods high in potassium include bananas, oranges, nuts,
and potatoes
DIETARY MANAGEMENT OF CKI
• Phosphorus restriction: Decreasing phosphorus intake is
recommended to protect bones.
• Eggs, beans, cola drinks, and dairy products are examples of foods
high in phosphorus.
• High calorie diet
• Vitamin supplements
NURSING DIAGNOSIS
Excess fluid volume r/t decreased urine output & Na+ H20 retention

Imbalanced nutrition less than body req. r/t anorexia, N/V, dietary restrictions

Activity intolerance r/t fatigue, anemia, dialysis procedure

KIDNEY TRANSPLANTATION
DEFINITION
• Kidney transplantation or renal transplantation is the organ
transplant of a kidney into a patient with end-stage renal disease.
• It is a surgical procedure to remove a healthy, functioning kidney
from a donor and implant it into a patient with non-functioning
kidneys
HISTORY
• In 1954, first long-term successful kidney transplantation by Joseph
Murray: the transplantation was done between monozygotic twins;
the organ survived for 8 years.
• In 1962, the first kidney transplantation between genetically
nonrelated patients was done using immunosuppression .
• in India first kidney transplantation was done at the King Edward
Memorial Hospital at Bombay in May 1965, using a cadaver donor in a
non-renal failure patient who had had hypernephroma.
• The first successful Live Donor renal transplant in India was done at
the CMC Hospital, Vellore in January 1971
TYPES OF DONORS

Donor kidneys can be obtained from both deceased and living

donors

heart-beating donors with

loss of brainstem function
(donation after brain death
Deceased donors [DBD]) or
can be classified as
either Non– heart beating donors
(donation after cardiac
death [DCD]).
TYPES OF DONORS
• In DBD, maintenance of adequate blood pressure (BP) and
oxygenation are important to prevent warm ischemic renal injury.

• In DCD either rapid surgical exposure of the great vessels with cooling
of the organs followed by prompt retrieval is required, or,
Alternatively, the kidneys are cooled in situ by insertion of perfusion
catheters through the femoral vessels
INDICATIONS OF KIDNEY
TRANSPLANTATION
• End Stage Kidney Disease (ESRD)

• Irreversible GFR of less than 15ml/min.

C/I OF KIDNEY TRANSPLANTATION
Absolute Contraindications to Transplantation
• Active sepsis
• Current uncontrolled malignancy
• Uncontrolled psychosis
• Active drug dependence
• Any medical condition with a severely shortened life expectancy (<1
to 2 years)
• Positive T cell CDC crossmatch
INITIAL DIAGNOSTIC TESTS FOR
TRANSPLANT CANDIDATES
• Complete blood count, Blood group, PT/PTT/INR
• Human leukocyte antigen (HLA typing) and panel reactive antibody
testing (PRA)
• Blood chemistry & metabolic profile: BUN, creatinine, uric acid,
electrolytes, calcium, phosphate, liver function test, albumin,
globulin,
• parathyroid hormone (PTH), lipid profile
• Urinalysis
• Serology: hepatitis B and C, human immunodeficiency virus (HIV),
cytomegalovirus (CMV), EpsteinBarr virus (EBV), varicella virus,
INITIAL DIAGNOSTIC TESTS FOR
TRANSPLANT CANDIDATES
• Pregnancy test for fertile women
• Chest X-ray
• Electrocardiogram
• Prostatic specific antigen in elderly men
• Pap smear (all women), mammography (elderly women)
• Screening colonoscopy (elderly patients)
POP CARE
• Depending on its quality, the new kidney usually begins functioning
immediately.
• Living donor kidneys normally require 3–5 days to reach normal
functioning levels.
• cadaveric donations stretch that interval to 7–15 days.
• If complications arise, additional medications (diuretics) may be
administered to help the kidney produce urine.
POP COMPLICATIONS
• Post operative complications, such as bleeding, infection, vascular
thrombosis and urinary complications.
• Transplant rejection (hyperacute, acute or chronic)
• Infections and sepsis due to the immunosuppressant drugs that are
required to decrease risk of rejection
• Malignancies
• Reoccurrence of renal disease
• Corticosteroid related complications
IMMUNOSUPPRESANTS
INDUCTION THERAPY
1)monoclonal antibodies:
• Muromonab-cd3,
• Basiliximab
• Daclizumab
• Alemtuzumab

2) polyclonal antibodies:
• Antithymocyte globulin
• Antithymocyte globulin
IMMUNOSUPPRESANTS
MAINTENANENCE THERAPY-
1) Calcineurin inhibitors :
• Cyclosporine
• Tacrolimus
2) Purine synthesis inhibitors/APA
• Azathioprine
• Mycophenolate mofetil
3) steroids
• Prednisone
TRANSPLANT PROGNOSIS
• Currently, deceased-donor grafts have a 92% 1-year survival and
living-donor grafts have a 96% 1-year survival.

• currently the “average” (t 1/2) life expectancy of a living-donor graft is

around 20 years and that of a deceased-donor graft is close to 14
years
 TRANSPLANT REJECTION

4) A mixture of
acute rejection
1) Hyperacute 2) Acute 3) Chronic
superimposed
rejection rejection) rejection
on chronic
rejection

Antibody- B) Acute T-cell

mediated mediated
rejection rejection
EPIDEMIOLOGY OF TRANSPLANT
REJECTION
• The incidence of acute rejection within the first year is around
7.9%. Overall, the rate of acute rejection is lower in living-donor than
deceased-donor kidney transplants; this is likely related to better
matching and less cold ischemia time
ETIOLOGY OF TRANSPLANT
REJECTION
• Prior sensitization - high panel reactive antibodies
• Type of transplant: Deceased donor has a higher rejection than a
living transplant
• Advanced age of the donor
• Prolonged cold ischemia time
• HLA mismatch
• Positive B cell crossmatch
• ABO incompatibility
ETIOLOGY OF TRANSPLANT
REJECTION
• Recipient’s age: Younger recipients have more rejection than older
ones
• Recipient’s race: Black race greater than White race
• Delayed graft function
• Therapy non-compliance
• Previous episodes of rejections
• Inadequate immunosuppression
S/S OF TRANSPLANT REJECTION
• Most patients who have acute rejection episodes are asymptomatic
and have abnormal allograft dysfunction as evidence by the routine
blood workups.
• Sometimes a rejecting graft may present with

Fever,
Pain At The Graft Site,
Hematuria,
Dysuria,
Hypertension,
Fluid Retention, And Decreased Urine
Output
MANAGEMENT OF TRANSPLANT
REJECTION
1. HYPERACUTE REACTION
No effective therapy usually leads to early allograft nephrectomy, and
so prevention is the key by assuring the following:
• ABO-compatibility between donor and recipient
• Pre-transplant cross-match
MANAGEMENT OF TRANSPLANT
REJECTION
2. ANTIBODY MEDIATED REJECTION
The treatment of acute antibody-mediated rejection also depends on the
level of the antibody levels. Higher antibody levels need plasma exchange
for the removal of the antibodies.
• Plasma exchange
• IVIG
• Rituximab
• Bortezomib
• Splenectomy
• Optimize the dose and the level of the maintenance immunosuppressive
drugs.
MANAGEMENT OF TRANSPLANT
REJECTION
3. T CELL MEDIATED REJECTION
They receive treatment with the following agents based on the severity
of the lesion.
• Methyl prednisone IV (250 to 1000 mg daily) targeting T cells, B cells,
and macrophages; given for 3 to 5 days
• rATG - rabbit anti-thymocyte globulin IV (1 to 1.5 mg/kg) targeting T
cell receptors. The duration varies among different transplant centers,
but in general, it is for 7 to 14 doses based on the response and Cd3
level.
• Optimize the dose and the level of the maintenance
immunosuppressive drugs. 
MANAGEMENT OF TRANSPLANT
REJECTION
3. CHRONIC REJECTION
Since the antibody-mediated rejection mechanism is a major cause of
chronic rejection, the same therapy as ABMR has been used, but
generally, these measures are ineffective when serum creatinine is over
3 mg/dl and/or heavy proteinuria is present.
NATIONAL ORGAN & TISSUE TRANSPLANT
ORGANISATION
• It is a national level organization set up under Directorate
General of Health Services, Ministry of Health
th
andth Family
Welfare, Government of India located at 4 and 5 floor of
Institute of Pathology Building in Safdarjung Hospital, New
Delhi.

• It functions as the apex body for activities of relating to

procurement, allotment and distribution of organs in the
country.
NURSING DIAGNOSIS
• Ineffective airway clearance related to pain of high abdominal or flank
incision, abdominal discomfort, and immobility; risk for ineffective
breathing pattern related to high abdominal incision.
• Acute pain and discomfort related to surgical incision, positioning,
and stretching of muscles during kidney surgery.
• Risk for Infection related to inadequate secondary
defences (Immunosuppression)
• Risk for Fluid Volume Excess related to renal insufficiency, steroid
therapy or decreased cardiac output
• Fear and anxiety related to diagnosis, outcome of surgery, and
alteration in urinary function
BLADDER TRAUMA
INTRODUCTION OF TRAUMA
BLADDER
• Traumatic injury to bladder and urethra is caused by outside force
• 8-10 % pelvic injury cause bladder trauma

Causes:
 Road traffic accidents
 Kick
 Gunshot
 Endoscopic trauma
 Diathermy
 Hysterectomy/LSCS
TYPES OF BLADDER INJURY
CLINICAL MANIFESTATIONS OF
BLADDER TRAUMA
• Sudden pain in suprapubic region
• Syncope
• Diffuse abdominal pain
• Abdominal distension
• Peritonitis> guarding and rigidity
• Gross hematuria
• Others: inability to void, bruises over suprapubic region
DIAGNOSIS
• Plain xray (ground glass appearance)
• Peritoneal tap- urine
• Retrograde cystography
• CT scan / renal ultrasound
MANAGEMENT OF TRAUMA
BLADDER
Goals of treatment:
• Control symptoms
• Repair the injury
• Prevent complications  Intraperitoneal rupture- surgical repair
 Extraperitoneal- catheter drainage
 antibiotics
COMPLICATIONS OF TRAUMA
BLADDER
• Peritonitis
• Pelvic abscess
• Cystitis
• Pyelonephritis
• Vesicovaginal and rectovesical fistula
DEFINITION
• Acute tubular necrosis (ATN) is a kidney disorder involving damage to
the tubule cells of the kidneys, which can lead to acute kidney
failure.

• The term ATN is actually a misnomer, as there is minimal cell necrosis

and the damage is not limited to tubules
PATHOPHYSIOLOGY OF ATN
Patchy necrosis in cases of ischemic type of acute tubular injury and
diffuse necrosis in toxic type of acute tubular injury
DIAGNOSIS
• History
• Urinalysis (UA)
In prerenal disease, the UA microscopy is normal or may contain
hyaline casts. On the other hand, the UA of acute tubular necrosis
shows muddy brown casts or renal tubular epithelial cells secondary to
the sloughing of tubular cells into the lumen due to ischemia or toxic
injury.
DIAGNOSIS
Fractional excretion of sodium (FENa)
• This is a good test to differentiate between acute tubular necrosis and
prerenal disease, with a value less than 1% favoring prerenal disease
and more than 2% acute tubular necrosis

Urine sodium concentration

• This test determines that the kidney is sodium avid in
hypovolemic states (prerenal) where kidneys try to conserve sodium
or lose sodium due to tubular injury with values more than 40 to 50
mEq/L indicating acute tubular necrosis and less than 20 mEq/L
suggestive of prerenal disease.
TREATMENT OF ATN
• Treatment is supportive and includes stopping nephrotoxins
whenever possible,
• Maintaining euvolemia, providing nutritional support
• Treating infections (preferably with drugs that are not nephrotoxic).
• Diuretics may be used to maintain urine output in oliguric acute
tubular necrosis but are of unproven benefit and do not alter the
course of kidney injury