SEMINAR ON

EVIDENCE BASED PRACTICE

ON RENAL CALCULI(NEPHROLITHIASIS)

SUBMITTED TO: SUBMITTED BY:

Mrs. Bharti Sachdeva Sangeeta Yadav
Lecturer, ILBS M.Sc. Nursing I year
(CON)
SUBMITTED ON;
09/10/23

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A REVIEW OF RENAL SYSTEM ANATOMY AND PHYSIOLOGY OF RENAL SYSTEM
The renal system, which is also called the urinary system, is a group of organs in the body
that filters out excess fluid and other substances from the bloodstream.
The renal system organs include the:

• Kidneys
• Ureters
• Bladder, and
• Urethra.
ANATOMICAL POSITION
The kidneys are retroperitoneally (behind the peritoneum) in the abdomen, either side of the
vertebral column.
The typically extended from T1 to L3, although the right kidney is often situated slightly
lower due the presence of the liver. Each kidney is approximately three vertebrae in length.
The adrenal glands sit immediately superior to the kidneys within a separate envelope of
renal fascia.

KIDNEY STRUCTURE: The kidneys are encased in complex layers of fascia and
fat. They are arranged as follows (deep to superficial):
• Renal capsule – tough fibrous capsule.
• Perirenal fat – collection of extraperitoneal fat.
• Renal fascia (also known as Gerota’s fascia or perirenal fascia) – encloses the
kidneys and the suprarenal glands.
• Pararenal fat – mainly located on the posterolateral aspect of the kidney.

• Internally, the kidneys have an intricate and unique structure. The renal parenchyma
can be divided into two main areas – the outer cortex and inner medulla. The cortex

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 extends into the medulla, dividing it into triangular shapes – these are known as renal
pyramids.
• The apex of a renal pyramid is called a renal papilla. Each renal papilla is associated
with a structure known as the minor calyx, which collects urine from the pyramids.
Several minor calices merge to form a major calyx. Urine passes through the major
calices into the renal pelvis, a flattened and funnel-shaped structure. From the renal
pelvis, urine drains into the ureter, which transports it to the bladder for storage.
• The medial margin of each kidney is marked by a deep fissure, known as the renal
hilum. This acts as a gateway to the kidney – normally the renal vessels and ureter
enter/exit the kidney via this structure.

THERE IS THREE MAJOR REGIONS OF THE KIDNEY:

1. Renal cortex
2. Renal medulla
3. Renal pelvis
1.Renal cortex: The kidneys are surrounded by a renal cortex, a layer of tissue that is also
covered by renal fascia (connective tissue) and the renal capsule. The renal cortex is granular
tissue due to the presence of nephrons which are the functional unit of the kidney—that are
located deeper within the kidney, within the renal pyramids of the medulla. The cortex
provides a space for arterioles and venules from the renal artery and vein, as well as the
glomerular capillaries, to perfuse the nephrons of the kidney. Erythropoietin, a hormone
necessary for the synthesis of new red blood cells, is also produced in the renal cortex.

2.Renal Medulla

• The medulla is the inner region of the parenchyma of the kidney. It consists of
multiple pyramidal tissue masses, called the renal pyramids, which are triangle
structures that contain a dense network of nephrons.
• At one end of each nephron, in the cortex of the kidney, is a cup-shaped structure
called the Bowman’s capsule. It surrounds a tuft of capillaries called the glomerulus
that carries blood from the renal arteries into the nephron, where plasma is filtered
through the capsule.
1. After entering the capsule, the filtered fluid flows along the proximal convoluted tubule
to the loop of Henle and then to the distal convoluted tubule and the collecting ducts,
which flow into the ureter. Each of the different components of the nephrons are
selectively permeable to different molecules, and enable the complex regulation of
water and ion concentrations in the body.

3.Renal Pelvis

The renal pelvis contains the hilium. The hilum is the concave part of the bean-shape where
blood vessels and nerves enter and exit the kidney; it is also the point of exit for the ureters:
the urine-bearing tubes that exit the kidney and empty into the urinary bladder. The renal
pelvis connects the kidney to the rest of the body.

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ANATOMICAL RELATIONS

The kidneys sit in close proximity to many other abdominal structures which are important to
be aware of clinically:
ANTERIOR POSTERIOR
LEFT • Suprarenal gland • Diaphragm
• Spleen • 11th and 12th ribs
• Stomach • Psoas major,
• Pancreas quadratus lumborum
• Left colic flexure and transversus
• Jejunum abdominis
• Subcostal,
iliohypogastric and
ilioinguinal nerves

RIGHT • Suprarenal gland • Diaphragm

• Liver • 12th rib
• Duodenum • Psoas major,
• Right colic flexure quadratus lumborum
and transversus
abdominis
• Subcostal, Ilio
hypogastric and
ilioinguinal nerves

https://teachmeanatomy.info/abdomen/viscera/kidney/

ARTERIAL SUPPLY
1. The kidneys are supplied with blood via the renal arteries, which arise directly from
the abdominal aorta, immediately distal to the origin of the superior mesenteric artery.

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 2. Due to the anatomical position of the abdominal aorta (slightly to the left of the
midline), the right renal artery is longer, and crosses the vena cava posteriorly.
3. The renal artery enters the kidney via the renal hilum. At the hilum level, the renal
artery forms an anterior and a posterior division, which carry 75% and 25% of the
blood supply to the kidney, respectively. Five segmental arteries originate from these
two divisions.
4. The avascular plane of the kidney (line of Brodel) is an imaginary line along the
lateral and slightly posterior border of the kidney, which delineates the segments of
the kidney supplied by the anterior and posterior divisions.
1. It is an important access route for both open and endoscopic surgical access of the
kidney, as it minimises the risk of damage to major arterial branches.
Note: The renal artery branches are anatomical end arteries – there is no communication
between vessels. This is of crucial importance; as trauma or obstruction in one arterial branch
will eventually lead to ischaemia and necrosis of the renal parenchyma supplied by this
vessel.
5. The segmental branches of the renal undergo further divisions to supply the renal
parenchyma:
6. Each segmental artery divides to form interlobar arteries. They are situated either side
every renal pyramid.
7. These interlobar arteries undergo further division to form the arcuate arteries.
8. At 90 degrees to the arcuate arteries, the interlobular arteries arise.
9. The interlobular arteries pass through the cortex, dividing one last time to form
afferent arterioles.
10. The afferent arterioles form a capillary network, the glomerulus, where filtration takes
place. The capillaries come together to form the efferent arterioles.
11. In the outer two-thirds of the renal cortex, the efferent arterioles form what is a known
as a peritubular network, supplying the nephron tubules with oxygen and nutrients.
The inner third of the cortex and the medulla are supplied by long, straight arteries
called vasa recta.

VENOUS DRAINAGE
1. The kidneys are drained of venous blood by the left and right renal veins. They leave
the renal hilum anteriorly to the renal arteries, and empty directly into the inferior
vena cava.
As the vena cava lies slightly to the right, the left renal vein is longer, and travels anteriorly to
the abdominal aorta below the origin of the superior mesenteric artery. The right renal artery
lies posterior to the inferior vena cava.

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CLINICAL RELEVANCE: VARIATION IN ARTERIAL SUPPLY TO THE KIDNEY
The kidneys present a great variety in arterial supply; these variations may be explained by
the ascending course of the kidney in the retroperitoneal space, from the original
embryological site of formation (pelvis) to the final destination (lumbar area). During this
course, the kidneys are supplied by consecutive branches of the iliac vessels and the aorta.
Usually, the lower branches become atrophic and vanish while new, higher ones supply the
kidney during its ascent. Accessory arteries are common (in about 25% of patients). An
accessory artery is any supernumerary artery that reaches the kidney. If a supernumerary
artery does not enter the kidney through the hilum, it is called aberrant.

LYMPHATICS
Lymph from the kidney drains into the lateral aortic (or para-aortic) lymph nodes, which are
located at the origin of the renal arteries.

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 CLINICAL RELEVANCE - RENAL CELL CARCINOMA
1. The kidney is often the site of tumour development, most commonly renal cell
carcinoma.
2. Due to the segmental vascular supply of the kidney, it is often feasible to ligate the
relative arteries and veins and remove the tumour with a safe zone of healthy
surrounding parenchyma (partial nephrectomy) without removing the entire kidney or
compromising its total vascular supply by ischaemia.
FUNCTIONS OF RENAL SYSTEM

• The overall function of the system filters approximately 200 liters of fluid a day from
renal blood flow which allows for toxins, metabolic waste products, and excess ion to
be excreted while keeping essential substances in the blood.
• The kidney regulates plasma osmolarity by modulating the amount of water, solutes,
and electrolytes in the blood.
• It ensures long term acid-base balance and also produces erythropoietin which
stimulates the production of red blood cell.
• It also produces renin for blood pressure regulation and carries out the conversion of
vitamin D to its active form.
URINE PRODUCTION:
Urine is a waste byproduct formed from excess water and metabolic waste molecules during
the process of renal system filtration

i. Filtration: During filtration, blood enters the afferent arteriole and flows into the glomerulus
where filterable blood components, such as water and nitrogenous waste, will move towards
the inside of the glomerulus, and nonfilterable components, such as cells and serum
albumins, will exit via the efferent arteriole. These filterable components accumulate in the
glomerulus to form the glomerular filtrate.

ii. Reabsorption: The next step is reabsorption, during which molecules and ions will be
reabsorbed into the circulatory system. The fluid passes through the components of the
nephron (the proximal/distal convoluted tubules, loop of Henle, the collecting duct) as water
and ions are removed as the fluid osmolarity (ion concentration) changes. In the collecting
duct, secretion will occur before the fluid leaves the ureter in the form of urine.

iii. Secretion: During secretion some substance such as hydrogen ions, creatinine, and drugs—
will be removed from the blood through the peritubular capillary network into the collecting
duct. The end product of all these processes is urine, which is essentially a collection of
substances that has not been reabsorbed during glomerular filtration or tubular reabsorbtion.

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https://www.ncbi.nlm.nih.gov/books/NBK538339/#article-28365.s6

3.Controlling acid-base balance

The acids and bases in the human body are always in a state of delicate equilibrium reflected
by a parameter known as pH. The normal pH of the blood is 7.35 to 7.45. To maintain this
healthy range, the kidneys excrete acids and bases when there’s an excess of them, or retain
these compounds when the body is lacking them.

4.Controlling water balance

The kidneys are one of the body’s main ways to maintain a stable water balance. By
regulating the volume of urine they produce, the kidneys adapt to one’s hydration level.
When you drink a lot, the kidneys produce more urine, and the opposite happens when you
are dehydrated.

The kidneys filter some electrolytes from the blood, return part of them back into circulation,
and excrete excess electrolytes into the urine. The levels of electrolytes like sodium and
phosphate are largely dependent on the health of one’s kidneys.

5.Controlling blood pressure

The kidneys produce an enzyme called renin. Renin converts the angiotensinogen produced
in the liver into angiotensin I, which is later converted in the lungs into angiotensin II.
Angiotensin II constricts the blood vessels and increases blood pressure as a result. On the

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other hand, when one’s blood pressure is too high, the kidneys produce more urine to reduce
the volume of liquid circulating in the body and somewhat compensate the high blood
pressure.

6. Producing the hormone erythropoietin

The kidneys produce a hormone called erythropoietin. The main function of this hormone is
to help the body create more red blood cells (erythrocytes), which are essential for the
transport of oxygen throughout all the tissues and organs.

7.Activating vitamin D
The kidneys transform calcifediol into calcitriol, the active form of vitamin D. Calcitriol
circulates in the blood and plays a vital role in regulating calcium and phosphate balance in
the body, which is essential for healthy bone growth.

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RENAL CALCULI/NEPHROLITHIASIS
DEFINITION
Kidney stones (also called renal calculi, nephrolithiasis or urolithiasis) are hard deposits
made of minerals and salts that form inside the kidneys.
Renal Calculi also called kidney stones, nephrolithiasis or urolithiasis are hard deposits made
of minerals and salts that form inside kidneys. They are hard, pebble-like pieces of material
that form in one or both of kidneys when high levels of certain minerals are present in urine.
These stones vary in size and shape. They may be as small as a grain of sand or as large as a
pea. Rarely, some kidney stones are as big as golf balls. Kidney stones may be smooth or
jagged and are usually yellow or brown.

Basic outline for nephrolithiasis

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Epidemiology
• Kidney stone is one of the oldest recorded disorder of human and one of the major
health burden. Globally, kidney stone disease prevalence and recurrence rates are
increasing, with limited options of effective drugs. Urolithiasis affects about 12% of
the world population at some stage in their lifetime.
• It affects all ages, sexes, and races but occurs more frequently in men than in women
within the age of 20–49 years. If patients do not apply meta phylaxis, the relapsing
rate of secondary stone formations is estimated to be 10–23% per year, 50% in 5–10
years, and 75% in 20 years of the patient. However, lifetime recurrence rate is higher
in males, although the incidence of nephrolithiasis is growing among females.

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• According to research conducted on The Demographic Diversity of Food Intake and
Prevalence of Kidney Stone Diseases in the Indian Continent in 2019 in journal
Foods by MDPI
 Kidney Stone Diseases is prevalent, with an expectancy of 12% in a total
population reported to be prone to urinary stones.
 Of this 12%, 50% of the population are severely affected by renal damage,
which even leads to a loss of kidneys.
 Unlike in South India, where a few reported percentages affected by
Urolithiasis, in North India, there is a steep 15% of the population within the
realm of Kidney stone diseases.
 Thus, considering the prospects of the kidney stone belt, which are affected
by Kidney stone diseases in India, a proper corollary needs to be established.
This stone belt occupies areas of Maharashtra, Gujarat, Rajasthan, Punjab,
Haryana, Delhi, Madhya Pradesh, Bihar, and West Bengal.

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 (C) Non-stone belt Indian states are also depicted with the rural and urban population and the
animal protein consumption per gram per day per capita. (D) Prevalence rates of kidney stones in a
global platform.

ETIOLOGY
Urolithiasis occurs when solutes crystallize out of urine to form stones. Urolithiasis may
occur due to following factors:
1. Anatomic features leading to urinary stasis: low urine flow rates favor crystal deposition on
the urothelium.
2. Low urine volume, dietary factors (e.g., high oxalate or high sodium)
3. Urinary tract infections:
Struvite stones are virtually always caused by a urinary tract infection (UTI) as a result of an
enzyme secreted by certain types of bacteria.
4. Systemic acidosis:
-Metabolic acidosis and hypokalemia lead to hypocitraturia, a risk factor for stones.
-Citrate in the urine complexes calcium and inhibits stone formation.
5. Medications include -Magnesium trisilicate;
ciprofloxacin; sulfa medications; triamterene; indinavir; and ephedrine, alone or in
combination with guaifenesin.
-These medications may lead to metabolic abnormalities that facilitate the formation of
stones.
6. Hyperparathyroidism:
When a person has high calcium all the time due to hyperparathyroidism the kidney will
always have extra calcium in it because it is filtering the calcium out. That extra calcium in
the kidney & the urine leads to kidney stone development.
7. Cancers:
-such as leukemia,
-multiple myeloma etc.
-Hypercalcemia is a frequent complication of multiple myeloma.
- A mild degree of nephrocalcinosis has been noted in occasional patients and renal calculi
are also sometimes present
8. Myeloproliferative diseases such as polycythemia vera:
-Abnormally high levels of uric acid can also cause kidney stones.
-Gout and kidney stone associated with polycythemia vera occur due to the high turnover of
red blood cells, which results in higher-than-normal uric acid production.
9. Genetic factors:
-such as cystinuria. The disorder causes a natural substance called “cystine” to leak into your
urine. When there is too much cystine in the urine, kidney stones can form. These stones can
get stuck in the kidneys, bladder, or anywhere in the urinary tract.

10. Inadequate hydration:

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 The most common cause of stone disease is inadequate hydration and subsequent low urine
volume. A low fluid intake results in the production of concentrated urine, causing
supersaturation and crystallization of stone–forming compounds.
11. Others:
The other four most common factors contributing to urinary stone formation are
hypercalciuria, hyperoxaluria, hyperuricosuria, and hypocitraturia.

RISK FACTORS

Factors that increase your risk of developing kidney stones include:

FAMILY AND
PERSONNEL
HISTORY

SURGERY CERTAIN DIETS

RISK
MEDICATIONS OBESITY

DIGESTIVE
DISEASE

1. Family or personal history: If someone in person’s family has had kidney stones, he
is more likely to develop stones, too. If he has already had one or more kidney stones,
he is at increased risk of developing another.
2. Certain diets. Eating a diet that's high in protein, sodium (salt) and sugar may
increase your risk of some types of kidney stones. This is especially true with a
highsodium diet. Too much salt in your diet increases the amount of calcium your
kidneys must filter and significantly increases your risk of kidney stones.
3. Obesity. High body mass index (BMI), large waist size and weight gain have been
linked to an increased risk of kidney stones.
4. Digestive diseases and surgery. Gastric bypass surgery, inflammatory bowel disease
or chronic diarrhea can cause changes in the digestive process that affect your

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 absorption of calcium and water, increasing the amounts of stone-forming substances
in your urine.
5. Certain supplements and medications, such as vitamin C, dietary supplements,
laxatives (when used excessively), calcium-based antacids, and certain medications
used to treat migraines or depression, can increase your risk of kidney stones

Research on Risk factors of kidney stone disease: a cross-sectional study in the

southeast of Iran. The aim of the present study was to investigate the prevalence of
risk factors of kidney stones in the adult population of Rafsanjani city based on the
data of the Rafsanjan Cohort Study (RCS).

In the baseline phase of this study, 10,000 people aged 35 to 70 years are enrolled
in the RCS, as one of the prospective epidemiological research studies in Iran.
From this population, 9932 participants completed related demographic
questionnaires as well as reported a history of diabetes mellitus, kidney stone, and
hypertension diseases. The obtained data were analyzed using univariable and
multivariable logistics regression.
According to the obtained results, 46.54% of the studied population were male and
53.46% were female. The mean age of the participants was 49.94 ± 9.56 years.
2392 people accounting for 24.08% of the population had kidney stones. After
adjustment of the variables, six variables of gender, WSI, no consumption of
purified water, BMI, and history of hypertension and diabetes were found to be
significant related factors of kidney stone disease. Gender, hypertension, obesity,
diabetes, and personal habits like alcohol consumption, opium use and, cigarette
smoking are effective in the development of kidney stones.

CONCLUSION: Major risk factors for renal stones were:

 Gender,
 Hypertension,
 Obesity,
 Diabetes,
 personnel habbits like alcohol consumption,  smoking
TYPES
Types of kidney stones include:
A. CALCIUM STONES. Most kidney stones are calcium stones, usually in the form of calcium
oxalate. Oxalate is a substance made daily by your liver or absorbed from your diet. Certain
fruits and vegetables, as well as nuts and chocolate, have high oxalate content. Dietary
factors, high doses of vitamin D, intestinal bypass surgery and several metabolic disorders
can increase the concentration of calcium or oxalate in urine. Calcium stones may also occur
in the form of calcium phosphate. This type of stone is more common in metabolic
conditions, such as renal tubular acidosis. It may also be associated with certain medications
used to treat migraines or seizures, such as topiramate (Topamax, Trokendi XR, Qudexy XR).

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B. STRUVITE STONES. Struvite stones form in response to a urinary tract infection. These
stones can grow quickly and become quite large, sometimes with few symptoms or little
warning.
C. URIC ACID STONES. Uric acid stones can form in people who lose too much fluid because
of chronic diarrhea or malabsorption, those who eat a high-protein diet, and those with
diabetes or metabolic syndrome. Certain genetic factors also may increase your risk of uric
acid stones.
D. CYSTINE STONES. These stones form in people with a hereditary disorder called
cystinuria that causes the kidneys to excrete too much of a specific amino acid.

Fig: Kumar S. B. N., Kumar K. G., Srinivasa V., Bilal S. A review on urolithiasis. International
Journal of Universal Pharmacy and Life Sciences.

PATHOLOGY
• When the urine becomes supersaturated with one or more calculogenic (crystal-forming)
substances, a seed crystal may form through the process of nucleation.

• Heterogeneous nucleation (where there is a solid surface present on which a crystal can grow)
proceeds more rapidly than homogeneous nucleation (where a crystal must grow in a liquid
medium with no such surface), because it requires less energy.
• Adhering to cells on the surface of a renal papilla, a seed crystal can grow and aggregate into
an organized mass. Depending on the chemical composition of the crystal, the stone-forming
process may proceed more rapidly when the urine pH is unusually high or low.

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Reducing the pH to 5.0 decreases the solubility of uric acid to less than 8 mg/100 ml. The
formation of uric-acid stones requires a combination of hyperuricosuria (high urine uric-acid
levels)

 Inhibitors of stone formation: Normal urine contains chelating agents, such as citrate,
that inhibit the nucleation, growth, and aggregation of calcium-containing crystals.
The biochemical mechanisms of action of these vessels) and low urine pH.
substances have not yet been thoroughly elucidated. However, when these substances fall below
their normal proportions, stones can form from an aggregation of crystals.

 Hypocitraturia
Hypocitraturia or low urinary-citrate excretion (defined as less than 320 mg/day) can cause kidney
stones in up to 2/3 of cases. The protective role of citrate is linked to several mechanisms; citrate
reduces urinary supersaturation of calcium salts by forming soluble complexes with calcium ions
and by inhibiting crystal growth and aggregation.
ACCORDING TO RESEARCH ON DIETARY AND LIFESTYLE RISK FACTORS
ASSOCIATED WITH INCIDENT KIDNEY STONES IN MEN AND WOMEN J Urol. 2017

Oct;198(4):858-863, This study demonstrated how hypocitraturia affects stone disease

Hypocitraturia affects stone disease in several ways:

• Urinary citrate forms a soluble complex with calcium. This reduces ionic (free)
calcium's availability to form urinary crystals and stones. This effect is somewhat
pHdependent as it becomes more pronounced as the urinary pH increases.
• Urinary citrate directly inhibits calcium crystallization and crystal aggregation in the
urine.
• Urinary citrate increases pH, which drastically increases uric acid solubility as the pH
approaches 6.5 to 7. Uric acid stones will generally not form with a sustained urinary
pH of 6.5 or greater.
• Hypocitraturia reduces urinary osteopontin, an important constituent of the matrix
component of urinary calculi.
• Hypocitraturia decreases the inhibitory effect of urinary macromolecules (primarily
Tamm-Horsfall protein) on nephrolithiasis.
• Hypocitraturia increases urinary viscosity by reducing calcium binding in the urine,
increasing viscosity as free calcium interacts with urinary macromolecules such as
Tamm-Horsfall protein.

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 ACCORDING TO RESEARCH ON DIETARY AND LIFESTYLE RISK FACTORS
ASSOCIATED WITH INCIDENT KIDNEY STONES IN MEN AND WOMEN J Urol. 2017

Pathophysiology explained:
 In the kidney, urinary citrate levels are predominantly determined by acid/base status
and cellular metabolism in the proximal tubules of the renal cortex.
 The apical membrane cotransporter NaDC activity regulates the absorption of citrate,
while cellular metabolism is mediated by ATP citrate lyase and mitochondrial
enzymes in the proximal tubules.

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  In chronic acidosis, both citrate transport and cellular metabolism are increased,
causing hypocitraturia. Conversely, an alkaline load causes a reduction in these
cellular activities and results in higher urinary citrate excretion.
 Renal cells contain large amounts of adenosine triphosphate citrate lyase (ATP citrate
lyase). This enzyme will convert intracellular citrate into acetyl CoA The activity of
ATP citrate lyase is increased by metabolic acidosis, potassium deficiency, insulin,
glucose metabolites, and dietary factors such as high carbohydrate intake.
 The use of a competitive inhibitor that blocks the activity of ATP citrate lyase
(4Shydroxycitrate) has been shown to quadruple urinary citrate in chronic metabolic
acidosis.
Pathophysiology associated with dietary citrate
 Dietary citrate intake averages only about 4 grams daily, but it is readily absorbed from
the intestine in both healthy individuals and hypocitraturic stone formers. Serum
citrate is filtered in the renal glomerulus and reabsorbed in the proximal tubule, but
only about 25% (10% to 35%) of filtered citrate is ultimately excreted in the urine.
Hormones that affect bone health, such as estrogens, vitamin D, and parathyroid
hormone, all tend to increase urinary citrate excretion.

Clinical Manifestations

As a general rule, the larger the stone, the more noticeable are the symptoms.

The symptoms could be one or more of the following:

1. PAIN:
 Type pain: sharp pain, colic pain
 Location- side and back, below the ribs, originating in renal area radiated anteriorly
and downward the bladder in female and towards testes in male.

Kidney stone pain - also known as renal colic - is one of the most severe types of pain
imaginable. The pain is intense enough to account for more than 1 million visits to
emergency rooms each year. Usually, the pain starts when a stone moves into the narrow
ureter. This causes a blockage, which makes pressure build up in the kidney. The pressure
activates nerve fibers that transmit pain signals to the brain. Kidney stone pain often starts
suddenly. As the stone moves, the pain changes location and intensity.

OTHER TYPES OF PAIN:

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Pain that comes in waves and fluctuates in intensity
Pain or burning sensation while urinating

 Diarrhea and abdominal discomfort are due to renointestinal reflexes and the
anatomic proximity of kidneys to stomach pancreas and large intestines

 Blockage: Large kidney stones sometimes get stuck in a ureter. This blockage can
slow or stop the flow of urine.

 Cloudy or foul-smelling urine: The smell can come from the bacteria that cause
urinary tract infections. An odor may also come from urine that’s more concentrated
than normal.

 Hematuria or pyuria: Pink, red or brown urine: The minerals in concentrated urine
sometimes form crystals on the walls of kidneys or bladder damaging surrounding
capillaries. Bladder or kidney stones can also cause both gross and microscopic
bleeding.

 A persistent need to urinate, urinating more often than usual or urinating in small
amounts

 Nausea and vomiting: These symptoms happen because of shared nerve connections
between the kidneys and GI tract (9Trusted Source). Stones in the kidneys can trigger
nerves in the GI tract, setting off an upset stomach. The nausea and vomiting can also
be your body’s way of responding to intense pain

 Fever and chills if an infection is present. This can be a serious complication to a

kidney stone. It can also be a sign of other serious problems besides kidney stones.
Any fever with pain requires urgent medical attention. Fevers that occur with an
infection are usually high — 100.4˚F (38˚C) or more. Chills or shivering often occur
along with the fever.

RECENT STUDIES HAS SHOWN THE CAUSE OF NEPHROLITHIASIS

1. Microbiome of human body can cause kidney stones: Basically microbiome ids
defined as natural flora of our body, this flora include the colonies of various
bacteria’s like E. coli, veillonella parvula (bacteria of oral cavity), streptococcus,
klebsillia etc

According to Journal of the American Society of Nephrology (JASN) discusses how

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 Dr. Tasian and a team of CHOP researchers performed the first investigation of the
composition and function of gut microbial communities in early-onset calcium oxalate
kidney stone disease. They discovered that the gut microbiome is less diverse in children
and adolescents with calcium oxalate kidney stone disease than in individuals without
stones.

Background The relationship between the composition and function of gut microbial communities
and early-onset calcium oxalate kidney stone disease is unknown.

Methods We conducted a case-control study of 88 individuals aged 4–18 years, which included 44
individuals with kidney stones containing ≥50% calcium oxalate and 44 controls matched for age,
sex, and race. Shotgun metagenomic sequencing and untargeted metabolomics were performed on
stool samples.

Results Participants who were kidney stone formers had a significantly less diverse gut
microbiome compared with controls. Among bacterial taxa with a prevalence >0.1%, 31 taxa were
less abundant among individuals with nephrolithiasis. These included seven taxa that produce
butyrate and three taxa that degrade oxalate. The lower abundance of these bacteria was reflected
in decreased abundance of the gene encoding butyryl-coA dehydrogenase (P=0.02). The relative
abundance of these bacteria was correlated with the levels of 18 fecal metabolites, and levels of
these metabolites differed in individuals with kidney stones compared with controls. The oxalate-
degrading bacterial taxa identified as decreased in those who were kidney stone formers were
components of a larger abundance correlation network that included Eggerthella lenta and several
Lactobacillus species. The microbial (α) diversity was associated with age of stone onset, first
decreasing and then increasing with age. For the individuals who were stone formers, we found the
lowest α diversity among individuals who first formed stones at age 9–14 years, whereas controls
displayed no age-related differences in diversity.

Conclusions Loss of gut bacteria, particularly loss of those that produce butyrate and degrade
oxalate, associates with perturbations of the metabolome that may be upstream determinants of
early-onset calcium oxalate kidney stone disease.

CONCLUSION:
Whenever there is effect on the insitu flora of the body there is production of butyrate and
degrade oxalate, associated with the early onset calcium oxalate kidney stone disease.

APPROACH EVALUATION
1. Patients with established stone disease -All patients presenting with established
kidney stone disease

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 -A newly diagnosed or recurrent stones should undergo a
o focused history, o radiologic imaging, o stone
analysis (if available), o limited laboratory
evaluation.

2. The approach for patients with asymptomatic stones is discussed for patient are:
Focused history for stone risk factors — The purpose of the focused history is to
identify stone risk factors, such as a family history of stone disease and certain dietary
habits). These factors are described in detail elsewhere.

Summarized briefly, adverse dietary habits include, to be monitored

●Low fluid intake or a high fluid loss (eg, from sweating or gastrointestinal losses),
which leads to a lower urine volume and, therefore, a higher concentration of
lithogenic factors.
●A very high animal protein diet, which can lead to higher excretion of calcium and
uric acid and lower excretion of urine citrate.
●Higher sodium diet, which increases urinary calcium excretion.
●Increased intake of higher oxalate-containing foods, particularly spinach. The
magnitude of the contribution of dietary oxalate to urinary oxalate is controversial and
likely varies considerably from person to person.
●Lower calcium intake, which acts by increasing the absorption of dietary oxalate and
subsequent higher excretion of oxalate due to decreased calcium oxalate complex
formation within the intestinal lumen. The effect of lower calcium intake on oxalate
more than counterbalances the decrease in calcium absorption and excretion.
●Excessive vitamin C and D supplementation, which may increase urinary oxalate or
calcium, respectively.
●Excessive sugar (sucrose and fructose) intake, which may increase calcium and/or
oxalate excretion.
 In addition, certain medications can occasionally crystallize in the urine and lead to
stone formation. Examples include atazanavir, sulfadiazine, and triamterene.

DIAGNOSIS

1. Urinalysis: Colour may be yellow, dark brown, bloody. Commonly shows RBCs,
WBCs, crystals (cystine, uric acid, calcium oxalate), casts, minerals, bacteria, pus; pH
may be less than 5 (promotes cystine and uric acid stones) or higher than 7.5
(promotes magnesium, struvite, phosphate, or calcium phosphate stones).
2. Urine (24-hr): Creatinine, uric acid, calcium, phosphorus, oxalate, or cystine may be
elevated.
3. Urine culture: May reveal UTI (Staphylococcus aureus, Proteus, Klebsiella,
Pseudomonas).
4. Biochemical survey: Elevated levels of magnesium, calcium, uric acid, phosphates,
protein, electrolytes.

22
 5. Serum and urine BUN/Creatinine: Abnormal (high in serum/low in urine)
secondary to high obstructive stone in kidney causing ischemia/necrosis.
6. Serum chloride and bicarbonate levels: Elevation of chloride and decreased levels
of bicarbonate suggest developing renal tubular acidosis.
7. CBC:
a. Hb/Hct: Abnormal if patient is severely dehydrated or polycythaemia is
present (encourages precipitation of solids), or patient is anaemic
(haemorrhage, kidney dysfunction/failure).
b. RBCs: Usually normal.
c. WBCs: May be increased, indicating infection/septicaemia.
8. Parathyroid hormone (PTH): May be increased if kidney failure present. (PTH
stimulates reabsorption of calcium from bones, increasing circulating serum and urine
calcium levels.)
9. KUB x-ray: Shows presence of calculi and/or anatomical changes in the area of the
kidneys or along the course of the ureter.

10. Intravenous pyelogram (IVP): Provides rapid confirmation of urolithiasis as a

cause of abdominal or flank pain. Shows abnormalities in anatomical structures
(distended ureter) and outline of calculi.
11. Cystourethroscopy: Direct visualization of bladder and ureter may reveal stone
and/or obstructive effects.
12. CT scan: Identifies/delineates calculi and other masses; kidney, ureteral, and bladder
distension.
13. Ultrasound of kidney: To determine obstructive changes, location of stone; without
the risk of failure induced by contrast medium.

 Radiologic testing — If not yet performed during the initial evaluation, radiographic
examination, preferably with noncontrast, low-dose computed tomography (CT),
should be obtained to search for residual stones within the urinary tract.
 Stone analysis — Analysis of the stone is an essential part of the evaluation. Patients
should be encouraged to retrieve stones they pass spontaneously for analysis, although
novel CT imaging techniques may permit non-invasive discrimination among the
main subtypes of urinary calculi. Similarly, stones that are surgically removed should
also be submitted for analysis.

Number of stones to analyze: Individual crystalline components The most common

crystalline materials found in kidney stones are calcium oxalate, calcium phosphate, uric
acid, and struvite (magnesium ammonium phosphate). It is not uncommon for a stone to
contain more than one crystalline component.
●Calcium oxalate – Calcium oxalate is the most common component found in kidney
stones (approximately 70 to 80 percent). Calcium oxalate can be found in monohydrate
and dihydrate forms. Calcium oxalate can also be present in combination with uric acid
or calcium phosphate.

23
 ●Calcium phosphate – Calcium phosphate is found in approximately 15 percent of
kidney stones and can be present in combination with calcium oxalate or struvite.
Because of differences in solubility due to urine pH, calcium phosphate is not found
mixed with uric acid.
-The two forms of calcium phosphate include apatite (sometimes reported as carbonate
apatite), which is the crystal type found in bone, or calcium hydrogen phosphate
(brushite); the frequency of apatite is much greater than brushite.
- Calcium phosphate crystals in the urine sediment are typically dark and amorphous.

●Uric acid – Uric acid is the most common crystal form that contains urate. Rare
crystals that contain urate include sodium urate (which is present in the joint fluid of
patients with gouty arthritis) and ammonium urate.
-Uric acid is present in approximately 8 percent of analysed stones, sometimes in
combination with calcium oxalate.

●Struvite – Struvite is the crystal name for stones that form only in the presence of
urease-producing bacteria (eg, Proteus mirabilis, Klebsiella pneumoniae,
Corynebacterium species, Urea plasma urealyticum) in the upper urinary tract.
- Other names for this crystal type include "triple phosphate" (because the phosphate is
in the triple-negative form) and magnesium ammonium phosphate carbonate apatite.
-Struvite is found in approximately 1 percent of analyzed stones and is much more
common in females than in males (due to the higher risk of urinary tract infections in
females).

CLINICAL RELEVANCE
Knowing the composition of the stone assists with clinical decision-making for the treatment
of existing stones and prevention of new stone formation. Examples of how this knowledge
can impact clinical decision making include:
●Calcium oxalate monohydrate and brushite are hard stones and may not be
fragmented as easily with shock wave lithotripsy.
●Uric acid stones form in acid urine, and alkalinization of the urine can both dissolve
existing uric acid stones and prevent new stones from forming
●Calcium phosphate stones form in alkaline urine, and therefore, increasing the urine
pH may increase the likelihood of calcium phosphate precipitation. While reducing the
urine pH would be helpful, this is often not clinically possible for most patients who
form calcium phosphate stones.
●The presence of certain stone types may indicate the existence of an underlying
predisposing condition. As examples, calcium phosphate stones are more frequent in
individuals with primary hyperparathyroidism and distal renal tubular acidosis, and
struvite stones form in the presence of an upper urinary tract infection. Uric acid stones
may be more common in individuals with diabetes mellitus (due to impaired ammonia
genesis), metabolic syndrome, or gout.

When designing a preventive regimen for a patient, the individual components of the stone
need to be considered:
●For pure stones, the focus is on modifying the urine composition to prevent the
precipitation of that specific crystal type, even if the 24-hour urine composition
suggests a high risk for precipitation of another crystal type.

24
 ●For mixed stones, the treatment recommendations depend upon the specific
components and the relative amounts present.
Given the variability in reporting of mixed stones by commercial laboratories, it is important
to keep in mind the clinical setting and other available information and to question the
reliability of the stone composition report if it seems inconsistent with the patient's history. A
report indicating the presence of struvite, for example, is probably inaccurate in a patient
with no documented infection with a ureaseproducing bacterium. It is also important to
examine the urine sediment for crystals as this might help identify the crystal type.

LABORATORY TESTING
Approaches to laboratory testing — Three options have been proposed for laboratory
evaluation after a first stone:
1. a limited evaluation,
2. a complete metabolic evaluation, or
3. a targeted approach.

Although there is disagreement whether a complete metabolic evaluation should be

performed after the first kidney stone, there is general agreement that a complete metabolic
evaluation is indicated in all patients with multiple stones at first presentation. The decision
about which option to pursue should be shared by the clinician and patient.
●Limited evaluation – A limited laboratory evaluation includes a urinalysis and
routine blood chemistries. This approach is based upon the availability of nonoperative
therapy for most symptomatic stones and avoids unnecessary therapy in those who
would not have a recurrence.
●Complete metabolic evaluation – A complete metabolic evaluation consists of a
urinalysis, routine blood chemistries, and at least two 24-hour urine collections for
analysis of urine composition.
-Some clinicians recommend this approach after the first stone because of the
potentially high rate of recurrence and potential morbidity from recurrent stones. -
Limited data suggest that single-stone formers have similar metabolic abnormalities as
patients with recurrent nephrolithiasis.
-In addition, there are several studies suggesting that the likelihood of stone formation
can be predicted reasonably well from the 24-hour urine values. This approach should
be followed only in individuals willing to make changes to their diet or fluid intake or
to take medical therapy if warranted by the work-up.
●Targeted approach – A third approach is to base the extent of the laboratory
evaluation upon an estimation of the risk for new stone formation. A complete
metabolic evaluation would be performed in patients at moderate to high risk for
recurrent disease. Patients at high risk for recurrent disease include:
•Patients who have formed more than one kidney stone
•Patients with a family history of stones
•Patients with chronic diarrheal states and/or malabsorption, pathologic
skeletal fractures, osteoporosis, urinary tract infection, diabetes, and/or gout
•Patients taking medication that may put them at higher risk (eg, topiramate,
acetazolamide)
•Patients with stones composed of cystine, uric acid, or calcium phosphate

25
 •Patients with dietary habits associated with higher risk of stone formation
Complete metabolic evaluation — The complete metabolic evaluation for nephrolithiasis
consists of both blood and urine testing, including at least two 24-hour urine collections.
Urinalysis — A urinalysis should be performed on a voided urinary specimen. The urinalysis
should include pH determination since a pH greater than 7.5 raises the possibility of a stone
due to urease-producing bacteria, whereas a pH less than 5.5 favors uric acid lithiasis. The
urine sediment should also be examined for crystalluria since particular crystal types may
provide a clue as to the composition of stones .
●Uric acid crystals – Uric acid crystals are observed in acid urine (usually pH <5.5), a
milieu that favors the conversion of the relatively soluble urate salt into the insoluble
uric acid
●Calcium phosphate or calcium oxalate crystals – The formation of calcium oxalate
crystals is not dependent upon the urine pH, while calcium phosphate crystals only
form in a relatively alkaline urine (usually pH >6.8)
●Cystine crystals – Cystine crystals, with their characteristic hexagonal shape, are
diagnostic of cystinuria
●Magnesium ammonium phosphate crystals – Magnesium ammonium phosphate
(struvite) and calcium carbonate apatite are the constituents of struvite stones. Normal
urine is undersaturated with magnesium ammonium phosphate, and struvite stone
formation occurs only when ammonia production is increased and the urine pH is
elevated. Both of these requirements are only met when an upper urinary tract infection
occurs with a urease-producing bacterium, such as Proteus or Klebsiella.

BLOOD TESTS
A routine chemistry profile should be obtained, -
including measurement of serum electrolytes, -serum
creatinine, and serum calcium.
The results may help identify certain disorders, such as primary hyperparathyroidism,
hyperuricemia, and distal renal tubular acidosis, that are associated with nephrolithiasis.
 The serum calcium concentration should be measured looking for hypercalcemia; if
high-normal (which we define as above the midpoint of the normal range), the serum
calcium should be repeated. A measurement of intact parathyroid hormone is
warranted in patients with serum calcium values in the high-normal range or if the
urine calcium is high since primary hyperparathyroidism is often associated with only
intermittent and mild elevations in the serum calcium concentration.
 Although usually in the middle of the reference range, the presence of a lower serum
bicarbonate concentration raises the possibility of distal renal tubular acidosis or
chronic diarrhea.
24-hour urine collections: An important component of the evaluation of patients at moderate
to high risk for recurrent stone disease is the assessment of urine composition:
 Number of collections – At least two 24-hour urine collections should be obtained in
the outpatient setting, with the patient following their usual diet, fluid intake, and
physical activity. The differences among the collections are often substantial, so an
important contributor may be missed in many patients if only one sample is collected
the validity of this approach was illustrated in the following studies: o •A study of 75
recurrent idiopathic calcium kidney stone formers examined the relative diagnostic
utility of one, two, and three urine collections. When compared with one or any

26
 combination of two urine collections, three urine collections were significantly
associated with the highest yield of identifying a urinary abnormality.
•Similar findings were noted in another report of over 1000 stone formers in whom
three 24-hour urine collections were obtained.
 Differences in urinary biochemical risk factors among the three collections were
substantial enough that an important metabolic abnormality would have been missed
in many patients if only one sample had been collected.
Thus, we recommend that a minimum of two collections be performed as part of the
initial evaluation.
 Timing of collections – The urine collections should be obtained while the patient is
on his or her usual diet. Values should not be measured immediately after the acute
stone episode; it is common practice to wait at least one to two months after a stone
event to obtain the collections. One should also wait at least one to two months after
the patient has completely recovered from any interventions, such as shock wave
lithotripsy, ureteroscopy, or percutaneous stone removal. Ideally, the patient should be
free of pain, infection, and obstruction and following their "usual routine" when
performing their urine collections.
 Tests to include – The urine volume and excretion of calcium, uric acid, citrate,
oxalate, creatinine (to assess the completeness of the collection), pH, sodium, and
magnesium should all be measured. Ideally, the supersaturation of lithogenic
substances should be calculated. The results of the urine collections and stone analysis
(if available) dictate subsequent evaluation and management
A variety of definitions for "normal" are used by different laboratories for each of the
urinary parameters. Below are some more common definitions:
•Calcium − Less than 200 mg (5.0 mmol) per day in females or less than 250 mg
(6.25 mmol) per day in males
•Uric acid − Less than 750 mg (4.5 mmol) per day in females or less than 800 mg
(4.8 mmol) per day in males
•Oxalate − Less than 40 mg (0.44 mmol) per day in both females and males
•Citrate − Greater than or equal to 450 mg per day in both females and males

In a study conducted on Twenty-four-hour urine chemistries and the risk of kidney stones
among women and men, they obtained 24-hour urine collections from 807 men and
women with a history of kidney stone disease and 239 without a history who were
participants in three large ongoing cohort studies: the Nurses' Health Study I (NHS I;
mean age of 61 years), the Nurses' Health Study II (NHS II; mean age of 42 years), and
the Health Professionals Follow-up Study (HPFS; mean age of 59 years).

Mean 24-hour urine calcium excretion was higher and urine volume was lower in cases than
controls in NHS I (P < or = 0.01), NHS II (P < or = 0.13) and HPFS (P < or = 0.01), but urine
oxalate and citrate did not differ. Among women, urine uric acid was similar in cases and
controls but was lower in cases in men (P = 0.06). The frequency of hypercalciuria was
higher among the cases in NHS I (P = 0.26), NHS II (P = 0.03), and HPFS (P = 0.02), but 27,
17, and 14% of the controls, respectively, also met the definition of hypercalciuria. The
frequency of hyperoxaluria did not differ between cases and controls, but was three times
more common among men compared with women. After adjusting for the other urinary

27
 factors, the relative risk of stone formation increased with increasing urine calcium levels and
concentration in all three cohorts but not in a linear fashion. Compared with individuals with
a urine calcium concentration of <75 mg/L, the relative risk of stone formation among those
with a urine calcium concentration of > or =200 mg/L for NHS I was 4.34 (95% CI, 1.59 to
11.88), for NHS II was 51.09 (4.27 to 611.1), and for HPFS was 4.30 (1.71 to 10.84). There
was substantial variation in the relative risks for stone formation for the concentration of
other urine factors within the different cohorts.

The traditional definitions of normal 24-hour urine values need to be reassessed, as a

substantial proportion of controls would be defined as abnormal, and the association with risk
of stone formation may be continuous rather than dichotomous. The 24-hour urine
chemistries are important for predicting risk of stone formation, but the significance and the
magnitudes of the associations appear to differ by age and gender.

MANAGEMENT

Treatment for kidney stones varies, depending on the type of stone and the cause.

• SMALL STONES WITH MINIMAL SYMPTOMS

Most small kidney stones won't require invasive treatment. Patient may be able to pass a
small stone by:

• Drinking water. Drinking as much as 2 to 3 quarts (1.8 to 3.6 liters) a day will keep
urine dilute and may prevent stones from forming.

• Analgesics: Passing a small stone can cause some discomfort. To relieve mild pain,
pain relievers such as ibuprofen or naproxen sodium is prescribed. NSAIDs can also be
given because they provide specific pain relief and inhibit the synthesis of
Prostaglandin E.

• Alpha blockers: The alpha blocker is advised, relaxes the muscles in ureter, helping
pass the kidney stone more quickly and with less pain. Examples of alpha blockers
include tamsulosin (Flomax) and the drug combination dutasteride and tamsulosin
(Jalyn).
LARGE STONES AND THOSE THAT CAUSE SYMPTOMS

Kidney stones that are too large to pass on their own or cause bleeding, kidney damage or
ongoing urinary tract infections may require more-extensive treatment. Procedures may
include:

1. Extracorporeal shock wave lithotripsy: For certain kidney stones depending on size and
location procedure called extracorporeal shock wave lithotripsy (ESWL) is done.

28
 • ESWL uses sound waves to create strong vibrations (shock waves) that break the
stones into tiny pieces that can be passed in urine. The procedure lasts about 45 to 60
minutes and can cause moderate pain, so patient may be under sedation or light
anesthesia to make him comfortable.
• ESWL can cause blood in the urine, bruising on the back or abdomen, bleeding
around the kidney and other adjacent organs, and discomfort as the stone fragments
pass through the urinary tract.

2. Percutaneous nephrolithotomy: A procedure called percutaneous nephrolithotomy

involves surgically removing a kidney stone using small telescopes and instruments
inserted through a small incision in back.

29
3. Parathyroid gland surgery. Some calcium phosphate stones are caused by overactive
parathyroid glands, which are located on the four corners of thyroid gland, just below
your Adam's apple. When these glands produce too much parathyroid hormone
(hyperparathyroidism), calcium levels can become too high and kidney stones may
form as a result. Hyperparathyroidism sometimes occurs when a small, benign tumor
forms in one of parathyroid glands or you develop another condition that leads these
glands to produce more parathyroid hormone. Removing the growth from the gland
stops the formation of kidney stones.

4. Ureteroscopy. To remove a smaller stone in ureter or kidney, a thin lighted tube

(ureteroscope) equipped with a camera is passed through urethra and bladder to ureter.

Once the stone is located, special tools can snare the stone or break it into pieces that
will pass in urine. A small tube (stent) in the ureter can also placed to relieve swelling
and promote healing. This is also performed under sedation.

30
5. Electrohydraulic lithotripsy: Electrohydraulic lithotripsy is one of many methods to
treat kidney stones . It uses an electrohydraulic device with a flexible probe to deliver
to break kidney stones.

6.Chemolysis: stone dissolution using infusions of chemical solutions e.g. alkylating

agents for the purpose of dissolving stone.

The research is done on efficacies of various surgical regimens on treatment of renal

calculi patients in 2018 in China. Controlled clinical trials (CCTs) related to different
surgical treatment approaches for renal calculi were included in this study by retrieving
them from electronic English databases. The odds ratios (OR), the weighted mean
difference (WMD), 95% confidence intervals (95% CI) and surface under the cumulative
ranking curves (SUCRA) were evaluated, followed by a cluster analysis. Compared with
the extracorporeal shockwave lithotripsy (SWL), minimally invasive percutaneous
nephrolithotomy (mini-PCNL), retrograde intrarenal surgery (RIRS), standard
percutaneous nephrolithotomy (standard PCNL), ureterorenoscopy (URS) and
micropercutaneous nephrolithotomy (microperc) regimens, the open anatrophic
nephrolithotomy (Open AN), URS + RIRS and laparoscopic pyelolithotomy (LP) surgical
procedures all presented with a higher stone-free rate in renal calculi. Lower auxiliary
procedures were found in the URS + RIRS treatment approach compared with SWL, RIRS,
URS and microperc regimens. In addition, the SWL regimen indicated a lower stone-free
rate than the mini-PCNL, standard PCNL, Open AN, URS + RIRS and LP regimens.
Finally, the RIRS regimen presented with the shortest in-patient stay compared to the mini-
PCNL, standard PCNL, Open AN, URS, URS + RIRS and LP regimens. This meta-
analysis demonstrated that the URS + RIRS surgical procedure has the best stone-free rate
and the lowest number of auxiliary procedures. The RIRS and Microperc both have the
shortest hospital stay and operative time.

31
 PERIOPERATIVE CONSIDERATIONS
1. Antibiotic prophylaxis — For patients undergoing elective ureteroscopy (URS) or
percutaneous nephrolithotomy (PNL), we suggest prophylactic antibiotics to reduce
the incidence of post procedure urinary tract infection (UTI).

• Administer a single dose of oral or intravenous antibiotics within one hour of

the procedure that covers gram-positive and gram-negative microorganisms
Choice of antibiotic prophylaxis should also be based upon local antibiotic
resistance patterns. This practice is consistent with guidelines from the
American Urological Association, European Association of Urology, and
others]. Antibiotic prophylaxis is not typically administered before shock
wave lithotripsy (SWL).

In a systematic review and meta-analysis of four trials (500 patients) evaluating the use of
prophylactic antibiotic therapy in patients undergoing URS, a single dose of prophylactic
antibiotics reduced post procedure pyuria (risk ratio [RR] 0.65, 95% CI 0.51-0.82) and
bacteriuria (RR 0.26, 95% CI 0.12-0.60) but did not significantly reduce rates of UTI
compared with no prophylaxis. An observational study of patients undergoing PNL found
that in those with a negative baseline urine culture, antibiotic prophylaxis, compared with no
prophylaxis, was associated with a lower rate of postoperative fever (2.5 versus 7.4 percent)
and other complications (2 versus 22 percent.

2. Removal of secondary stones — There is no consensus regarding the management of

secondary, asymptomatic kidney stones that are detected on preoperative CT imaging.
Removing secondary stones, especially on the ipsilateral side of the symptomatic
stone removal, to render a patient stone free may help to reduce the risk of stone
relapse requiring additional surgery.
3. Ureteral stent placement — Ureteral stents are sometimes placed after URS, in part
to help prevent ureteric obstruction and pain resulting from ureteral edema or passage
of a stone fragment. Stent placement is frequently uncomfortable for patients.
• In three meta-analyses of trials evaluating patients who underwent
ureteroscopic lithotripsy, compared with those who did not receive a stent,
patients receiving stents had lower urinary tract symptoms (dysuria,
frequency or urgency, and haematuria) The 2016 American Urological
Association guidelines state that ureteral stent placement can be omitted in
patients who meet all of the following criteria:
●No suspected ureteric injury during URS
●No evidence of ureteral stricture or other anatomical impediments to stone fragment
clearance
●Normal contralateral kidney
●No kidney function impairment
●No secondary URS procedure planned
4. Stone analysis — Stone material that is retrieved from surgery should be sent for
analysis of stone composition. This is discussed in greater detail elsewhere.

32
POST-OPERATIVE CONSIDERATION

1.Postoperative imaging — The presence of residual stone fragments after stone removal
increases the risk for future clinical stone disease, and therefore, all attempts to render a
patient completely stone free should be made.
2.Medical therapy — The effectiveness of surgical therapies must not overshadow the
importance of medical therapy to prevent new stone formation. A treatable metabolic etiology
of stone formation can be detected in more than 95 percent of patients evaluated for stone
disease
Examples for which controlled trials have demonstrated benefit include a high fluid intake
for all forms of stone disease, a thiazide diuretic for hypercalciuria, allopurinol or potassium
citrate for hyperuricosuria, potassium citrate for hypocitraturia, and potassium citrate for uric
acid stone formation due to persistently acid urine. These therapies are discussed in more
detail elsewhere.
Several randomized trials and observational studies of medical therapy after an initial surgical
intervention have demonstrated efficacy in preventing the recurrence of clinical stone disease
as examples:
●In a study of 100 patients with calcium stones who had residual stone fragments after
shock wave lithotripsy (SWL), patients who were randomly allocated to receive
hydrochlorothiazide were significantly less likely than those given placebo to have
growth of residual stone fragments (18 versus 58 percent) or to require repeat SWL
(18 versus 42 percent) .
●In a second trial, 90 patients with calcium oxalate stones who underwent SWL
(approximately one-third of whom had residual stone fragments) were randomly
assigned to potassium citrate or no therapy; potassium citrate significantly reduced
future clinical stone episodes . The incidence of recurrent clinical stones was also
significantly lower among the subset of patients with residual stone fragments (65
versus 78 percent).

COMMON COMPLICATIONS

1.Stent discomfort — Stent discomfort is common following ureteral stent placement

For patients who receive a ureteral stent, we suggest treatment with an alpha blocker (eg,
tamsulosin 0.4 mg daily, until the stent is removed) to reduce stent discomfort.

2.Ureteral obstruction — The accumulation of stone fragments or stone gravel in the ureter,
known as stein Strasse, occurs in approximately 4 to 7 percent of cases of SWL and may
cause ureteral obstruction. Larger stone size appears to be the major predictive factor in stein
Strasse formation.

3.Urinary tract infection — Urinary tract infection (UTI) may occur following SWL, URS,
or percutaneous nephrolithotomy (PNL).

33
 -A follow-up urinalysis should be performed in all patients following stone removal. We
typically obtain a urinalysis at two to three weeks after stone surgery when the patient returns
for a postoperative follow-up visit or at any time if the patient is symptomatic.
-In postoperative patients who are symptomatic, a urine culture should also be obtained, and
culture-specific antibiotic therapy should be administered as appropriate.
4.Residual stone fragments and additional surgery — One of the primary goals of stone
surgery is to render patients stone free following SWL, URS, or PNL. Several studies suggest
that even small residual stones, particularly those larger than 4 mm, may grow and ultimately
result in return visits to the emergency department or require additional surgical intervention.

NUTRITIONAL THERAPY:

1. Plenty of fluid: 2-3 quarts/day: This includes any type of fluid such as water, coffee and
lemonade which have been shown to have a beneficial effect with the exception of grapefruit
juice and soda. This will help produce less concentrated urine and ensure a good urine
volume of at least 2.5L/day.
2. Limit foods with high oxalate content: Spinach, many berries, chocolate, wheat bran, nuts,
beets, tea and rhubarb should be eliminated from your diet intake
3. Eat enough dietary calcium: Three servings of dairy per day will help lower the risk of
calcium stone formation. Eat with meals.
4. Avoid extra calcium supplements: Calcium supplements should be individualized by your
physician and registered kidney dietitian
5. Eat a moderate amount of protein: High protein intakes will cause the kidneys to excrete
more calcium therefore this may cause more stones to form in the kidney
6. Avoid high salt intake: High sodium intake increases calcium in the urine which increases
the chances of developing stones. Low salt diet is also important to control blood pressure.
7. Avoid high doses of vitamin C supplements: It is recommended to take 60mg/day of
vitamin C based on the US Dietary Reference Intake Excess amounts of 1000mg/day or more
may produce more oxalate in the body.

Calcium Oxalate Stones: Eat and drink calcium foods such as milk, yogurt, and some
cheese and oxalate-rich foods together during a meal. The oxalate and calcium from the foods
are more likely to bind to one another in the stomach and intestines before entering the
kidneys. This will make it less likely that kidney stones will form. Don't reduce the calcium
in your diet. Work to cut back on the sodium in your diet and to pair calcium-rich foods with
oxalate-rich foods. The recommended calcium intake to prevent calcium stones is 1000-1200
mg per day. Extra sodium causes you to lose more calcium in your urine. Sodium and
calcium share the same transport in the kidney so if you eat high sodium foods it will
increase calcium leakage in the urine. Therefore, a high sodium diet can increase your
chances for developing another stone. There are many sources of "hidden" sodium such as
canned or commercially processed foods as well as restaurant-prepared and fast foods.

34
  You can lower your sodium intake by choosing fresh low sodium foods which can help
to lower calcium leakage in the urine and will also help with blood pressure control if
you have high blood pressure.
Uric acid stones: red meat, organ meats, and shellfish have high amounts of a natural
chemical compound known as purines. High purine intake leads to a higher production of
uric acid and a larger acid load for the kidneys to excrete. Higher uric acid excretion leads
to more acidic urine. The high acid concentration of the urine makes it easier for uric acid
stones to form.

NURSING CONSIDERATIONS NURSING

ASSESSMENT

• Assess for pain and discomfort, including severity, location, and radiation of pain.
• Assess for associated symptoms, including nausea, vomiting, diarrhea, and abdominal
distention.
• Observe for signs of urinary tract infection (chills, fever, frequency, and hesitancy) and
obstruction (frequent urination of small amounts, oliguria, or anuria).
• Observe urine for blood; strain for stones or gravel.
• Focus history on factors that predispose patient to urinary tract stones or that may have
precipitated current episode of renal or ureteral colic.
• Assess patient’s knowledge about renal stones and measures to prevent recurrence.

NURSING DIAGNOSIS
• Acute pain related to inflammation, obstruction, and abrasion of the urinary tract.
• Deficient knowledge regarding prevention of recurrence of renal stones.

PLANNING AND GOALS

• Major goals may include relief of pain and discomfort, prevention of recurrence of renal
stones, and absence of complications.

NURSING INTERVENTIONS RELIEVING

PAIN

• Administer opioid analgesics (IV or intramuscular) with IV NSAID as prescribed.

• Encourage and assist patient to assume a position of comfort.
• Assist patient to ambulate to obtain some pain relief.
• Monitor pain closely and report promptly increases in severity.

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 MONITORING AND MANAGING COMPLICATIONS

• Encourage increased fluid intake and ambulation.

• Begin IV fluids if patient cannot take adequate oral fluids.
• Monitor total urine output and patterns of voiding.
• Encourage ambulation as a means of moving the stone through the urinary tract.
• Strain urine through gauze.
• Crush any blood clots passed in urine, and inspect sides of urinal and bedpan for clinging
stones.
• Instruct patient to report decreased urine volume, bloody or cloudy urine, fever, and pain.
• Instruct patient to report any increase in pain.
• Monitor vital signs for early indications of infection; infections should be treated with the
appropriate antibiotic agent before efforts are made to dissolve the stone
• Explain causes of kidney stones and ways to prevent recurrence.
• Encourage patient to follow a regimen to avoid further stone formation, including
maintaining a high fluid intake.
• Encourage patient to drink enough to excrete 3,000 to 4,000 mL of urine every 24 hours.
• Recommend that patient have urine cultures every 1 to 2 months the first year and
periodically thereafter.
• Recommend that recurrent urinary infection be treated vigorously.
• Encourage increased mobility whenever possible; discourage excessive ingestion of vitamins
(especially vitamin D) and minerals.
• If patient had surgery, instruct about the signs and symptoms of complications that need to be
reported to the physician; emphasize the importance of followup to assess kidney function
and to ensure the eradication or removal of all kidney stones to the patient and family.
• If patient had ESWL, encourage patient to increase fluid intake to assist in the passage of
stone fragments; inform the patient to expect hematuria and possibly a bruise on the treated
side of the back; instruct patient to check his or her temperature daily and notify the physician
if the temperature is greater than 38C (about 101F), or the pain is unrelieved by the
prescribed medication.

CONTINUING CARE

• Closely monitor the patient to ensure that treatment has been effective and that no
complications have developed.
• Assess the patient’s understanding of ESWL and possible complications; assess the
patient’s understanding of factors that increase the risk of recurrence of renal calculi and
strategies to reduce those risks.
• Assess the patient’s ability to monitor urinary pH and interpret the results during
followup visits.
• Ensure that the patient understands the signs and symptoms of stone formation,
obstruction, and infection and the importance of reporting these signs promptly.
• If medications are prescribed for the prevention of stone formation, explain their actions,
importance, and side effects to the patient.

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EVALUATION
Patient is evaluated for:

• Reports relief of pain

• States increased knowledge of healthseeking behaviors to prevent recurrence
• Experiences no complications

PREVENTION
1. Stay hydrated

Drinking more water is the best way to prevent kidney stones. If person don’t drink enough,
his urine output will be low. Low urine output means urine is more concentrated and less
likely to dissolve urine salts that cause stones. Lemonade and orange juice are also good
options. They both contain citrate, which may prevent stones from forming.

Drink around eight glasses of fluids daily, or enough to pass two liters of urine. If exercise or
sweat a lot, or if person have a history of cystine stones, he’ll need additional fluids.

A Study conducted on Urinary volume, water and recurrences in idiopathic calcium

nephrolithiasis: a 5-year randomized prospective study, in which 101 controls and 199
patients from the first idiopathic calcium stone episode are studied. After a baseline study
period the stone formers were divided by randomization into 2 groups (1 and 2) and they
were followed prospectively for 5 years. Followup in group 1 only involved a high intake of
water without any dietetic change, while followup in group 2 did not involve any treatment.
Each year clinical, laboratory and radiological evaluation was obtained to determine urinary
stone risk profile (including relative supersaturations of calcium oxalate, brushite and uric
acid by Equil 2), recurrence rate and mean time to relapse.

The original urine volume was lower in male and female stone formers compared to controls
(men with calcium oxalate stones 1,057 +/- 238 ml./24 hours versus normal men 1,401 +/-
562 ml./24 hours, p < 0.0001 and women calcium oxalate stones 990 +/- 230 ml./24 hours
versus normal women 1,239 +/- 440 ml./24 hours, p < 0.001). During followup recurrences
were noted within 5 years in 12 of 99 group 1 patients and in 27 of 100 group 2 patients (p =
0.008). The average interval for recurrences was 38.7 +/- 13.2 months in group 1 and 25.1 +/-
16.4 months in group 2 (p = 0.016). The relative supersaturations for calcium oxalate,
brushite and uric acid were much greater in baseline urine of the stone patients in both groups
compared to controls. During followup, baseline values decreased sharply only in group 1.
Finally the baseline urine in patients with recurrences was characterized by a higher calcium
excretion compared to urine of the patients without recurrences in both groups.

37
 They concluded that urine volume is a real stone risk factor in nephrolithiasis and that a large
intake of water is the initial therapy for prevention of stone recurrences. In cases of
hypercalciuria it is suitable to prescribe adjuvant specific diets or drug therapy.
2. EAT MORE CALCIUM-RICH FOODS

The most common type of kidney stone is the calcium oxalate stone, leading many people to
believe they should avoid eating calcium. The opposite is true. Low-calcium diets may
increase your kidney stone risk and your risk of osteoporosis. Calcium supplements,
however, may increase risk of stones. Taking calcium supplements with a meal may help
reduce that risk. Low-fat milk, low-fat cheese, and low-fat yogurt are all good calcium-rich
food options.

3. EAT LESS SODIUM

A high-salt diet increases risk of calcium kidney stones. According to the Urology Care
Foundation, too much salt in the urine prevents calcium from being reabsorbed from the
urine to the blood. This causes high urine calcium, which may lead to kidney stones. Eating
less salt helps keep urine calcium levels lower. The lower the urine calcium, the lower the
risk of developing kidney stones. To reduce your sodium intake, read food labels carefully.
Foods notorious for being high in sodium include:

• processed foods, such as chips and crackers

• canned soups
• canned vegetables
• lunch meat
• condiments
• foods that contain monosodium glutamate
• foods that contain sodium nitrate
• foods that contain sodium bicarbonate (baking soda)

To flavor foods without using salt, try fresh herbs or a salt-free, herbal seasoning blend.

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4. EAT FEWER OXALATE-RICH FOODS

Some kidney stones are made of oxalate, a natural compound found in foods that binds with
calcium in the urine to form kidney stones. Limiting oxalate-rich foods may help prevent the
stones from forming.

Foods high in oxalates are: Spinach, chocolate, sweet potatoes, coffee, beets, peanuts, soy
products, wheat bran etc. Oxalate and calcium bind together in the digestive tract before
reaching the kidneys, so it’s harder for stones to form if a person eats high-oxalate foods and
calcium-rich foods at the same time.

5. EAT LESS ANIMAL PROTEIN

Foods high in animal protein are acidic and may increase urine acid. High urine acid may
cause both uric acid and calcium oxalate kidney stones. Limit or avoid foods like beef,
poultry, fish, pork etc.

6. AVOID VITAMIN C SUPPLEMENTS

Vitamin C (ascorbic acid) supplementation may cause kidney stones, especially in men.

According to Ascorbic Acid Supplements and Kidney Stone Incidence Among Men: A
Prospective Study in Sweden. In which, 48 850 men, aged 45 to 79 years at baseline, were
recruited in 1997 (response rate, 49%). Detailed diet and lifestyle data were collected at
baseline using a self-administered questionnaire. Based on validated questions, men reported
their use of ascorbic acid (sensitivity=67% and specificity=93%)4 and of 20 other supplement
types. They excluded users of supplements other than ascorbic acid as this may be a
significant source of confounding (n=12 873).

For comparison, They repeated the analysis for multivitamin (only) users. First incident cases
of kidney stones (International Statistical Classification of Diseases, 10th Revision code N20)
were ascertained from January 1, 1998, to December 31, 2009, using registry data. They
estimated hazard ratios (hereafter, relative risks [RRs]) with Cox proportional hazards
regression models using attained age as the timescale. Follow-up was censored at date of
kidney stone diagnosis, death, or end of follow-up, whichever occurred first. The Schoenfeld
residual test indicated no violation of the proportional hazard assumption.

Dose-response was assessed using the frequency-ofuse data, which were available for 91.5%
of ascorbic acid users. During 11 years of follow-up they ascertained 436 first incident cases
of kidney stones. Ascorbic acid use was associated with a statistically significant 2-fold
increased risk. In contrast, multivitamin use was not associated with kidney stone risk (RR,

39
 0.86 [95% CI, 0.62-1.19]). Users of only ascorbic acid taking fewer than 7 (median) and 7 or
more tablets per week showed increased risks of RR, 1.66 (95% CI, 0.99-2.79) and RR, 2.23
(95% CI, 1.28-3.88), respectively, compared with supplement nonusers in the full multivariate-
adjusted model (P value for trend = .001).

7. Explore herbal remedies

Chanca Piedra, also known as the “stone breaker” is a popular herbal folk remedy for kidney
stones. The herb is thought to help prevent calcium-oxalate stones from forming. It’s also
believed to reduce the size of existing stones. Use herbal remedies with caution. They’re not
well-regulated or well-researched for the prevention or treatment of kidney stones.

COMPLICATIONS
Complications of kidney stones include:

• Recurring kidney stones, since people who have had kidney stones at least once, have 80 %
chance of getting them again.

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• Obstruction or blockage in the urinary tract: When urine cannot leave the body and starts to
build up in the kidneys, it is called obstructive uropathy. Obstructive uropathy can lead to
hydronephrosis (swelling of the kidneys).
• Kidney failure: If left untreated, obstruction of the ureter can cause serious problems like
kidney failure, sepsis and death.
• Sepsis: which can occur after the treatment of a large kidney stone
• Injury to the ureter while undergoing a surgery for the removal of the kidney stone
• Urinary tract infection: several findings do indicate a possible association between urinary
stones and bacteria, including the high rate of urinary tract infections (UTI) in urinary stone
patients and multiple case series of culture-positive urinary stones, including stones
composed of CaOx or CaPhos.
• Severe pain: Severe renal bleeding caused by a ruptured renal sheath: case report of a rare
complication of percutaneous nephrolithotomy.

Clinical Vignette
A 65-year-old woman with a 2-day of fever and lumbodynia to emergency department. the
patient had been suffering from lumbodynia and discomfort for more than 20 years without
any examination and treatment. Day 6 after completing thoracic spine surgery at the local
hospital, the patient had chills and fever, with a maximum temperature of 40 °C and blood
pressure of 85/58mmHg. Later transferred to hospital. The patient had previous hypertension
and no history of diabetes.

Physical examination on admission: body temperature: 37.3 °C, pulse: 99 times/min,

respiration: 24 times/min, blood pressure: 78/49mmHg.With a face of pain and bilateral renal
area knock pain. Routine laboratory studies revealed the following: white cell count,22.94
(10 9/L); hemoglobin, 68.00 (g/L); platelets, 81.00 (10 9/L); albumin,27.00 (g/L); sodium,
127.6 (mmol/L); creatinine, 217.00 (pg/L); C-reactive protein,181.52 (mg/L);
procalcitonin,162.14 (ng/ml); lactic acid, 2.11 (mmol/L).CT showed effusion and
accumulation of gas in both kidneys, and multiple stones in both kidneys (Fig. 1, Fig. 2).

41
Fig. 1. Gas accumulation and stones in both kidneys.
Fig. 2. The size of both kidneys increased significantly, and the parenchyma of both kidneys
became thinner. Multiple stones were seen in the double pelvis, calyces, and the upper part
of the right ureter, and gas accumulation in the collective system.

After admission, 1g meropenem every 8 h for anti-infection, fluid resuscitation and dopamine
was pumped to correct the shock. After the condition was slightly stabilized, bilateral ureteral
stenting was performed under intravenous anesthesia in the emergency department on the
same day, and purulent fluid was seen flowing out of bilateral ureteral orifice under
ureteroscopy.Postoperative blood pressure was still low, and fluid resuscitation (including
crystals, colloid and plasma), meropenes and norepinephrine combined with dopamine was
performed to correct shock (according to the regulation BP and CVP).Multidisciplinary
consultations are invited to assist in diagnosis and treatment, including cardiology, infectious
diseases, orthopedics, etc., Symptomatic treatments such as concentrated red blood cell and
platelets input, supplementation of intravenous nutritional fluids, and maintenance of water
and electrolyte balance.

No bacterial growth was found in the patient's multiple blood and urine cultures. After the
body temperature is stable, the antibiotics are downgraded and the broad-spectrum
ceftazidime is used. Under a comprehensive treatment plan, the patient's back pain symptoms
gradually eased, and various biochemical indicators improved. Re-examination CT showed
that the kidney gas accumulation was significantly reduced, and kidney stones were still
present (Fig. 3). The patient recovered clinically and was discharged 10 days after admission.
However, huge kidney stones still exist, and further staged treatment of kidney stones is
needed.

Fig. 3. Reexamination of CT renal effusion and gas accumulation were significantly

reduced compared to the previous, the renal parenchyma became thinner, and the
kidney stones showed typical Staghorn calculus.

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DISCUSSION:

Stones in the urinary system may cause urinary tract obstruction, provide favorable
conditions for bacterial growth and reproduction, thereby causing urinary tract infections and
triggering urinary sepsis. In addition, with age, systemic degeneration, decreased
autoimmunity, and surgical stress increase the incidence of bacterial infections. In this case, a
female patient experienced surgical trauma 1 week ago and her resistance decreased. She had
a history of repeated low back pain and developed a double kidney cast stone without
attention. This type of stone is mostly infectious stone. It can cause patients with difficulty in
excreting urine, induce intrarenal infection, damage the patient's renal function, and cause
severe septic shock, which is life-threatening.

REFERENCES

• Alelign, T., & Petros, B. (2018). Kidney Stone Disease: An Update on Current
Concepts. Advances in Urology, 2018, 1–12. https://doi.org/10.1155/2018/3068365
• Belleza, R. M. N. (2021a, February 11). Urinary System Anatomy and Physiology.
Nurseslabs. Retrieved December 7, 2021, from https://nurseslabs.com/urinary-system/
• Borghi, L., Meschi, T., Amato, F., Briganti, A., Novarini, A., & Giannini, A. (1996).
Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year
randomized prospective study. The Journal of urology, 155(3), 839–843
• Guha, M., Banerjee, H., Mitra, P., & Das, M. (2019). The Demographic Diversity of
Food Intake and Prevalence of Kidney Stone Diseases in the Indian Continent. Foods
(Basel, Switzerland), 8(1), 37. https://doi.org/10.3390/foods801003
• Khalili, P. (2021, October 8). Risk factors of kidney stone disease: a cross-sectional
study in the southeast of Iran - BMC Urology. BioMed Central. Retrieved December
8, 2021, from https://bmcurol.biomedcentral.com/articles/10.1186/s12894-021-
009055
• McDermott, A. (2019, March 8). 9 Ways to Prevent Kidney Stones. Healthline.
Retrieved December 12, 2021, from
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stones#_noHeaderPrefixedContent
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