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GENITOURINARY SYSTEM

Chapter 1
KIDNEY FUNCTION TEST AND NEPHROTIC
SYNDROME
A K Tripathi,
KIDNEY FUNCTION TEST
a. Complete urine analysis: Urine is examined for
amount, specific gravity, pH, color, protein, glucose,
red blood cells, leukocytes, casts, and crystals.
b. Serum biochemistry: The estimation of blood urea,
serum creatinine, electrolytes are important. Raised
blood urea and serum creatinine suggests renal
dysfunction.
c. Estimation of glomerular filtration rate (GFR):
Creatinine clearance (ml/min) is the usual method of
estimation of GFR in clinical practice. GFR can be
estimated by using the Cockcroft-Gault formula for
creatinine clearance.
(in females, the value is multiplied by 0.85)
However, GFR can be measured more accurately by
radionuclide studies using 125
I-iothalamate,
diethylene triamine-penta-acetic acid labeled with
technetium (99mTc-DTPA), or dimercaptosuccinic
acid labeled with technetium (99mTc-DMSA).
d. Imaging studies include plain X-rays, ultrasound,
intravenous urography (IVU), CT scan, MRI, renal
arteriography and renal venography.
e. Renal biopsy: Light microscopy, electron microscopy
and immunofluorescence of the biopsy specimen are
helpful in the diagnosis, prognosis and treatment of
various renal disorders.
Proteinuria
Normal person excretes less than 150 mg protein and less
than 30 mg albumin daily.
Proteinuria is defined as excessive protein excretion in
the urine (>150 mg in 24 hours). The excretion of 30-300
mg albumin per 24 hour (20-200 µg/min) is known as
microalbuminuria. Microalbuminuria is an early marker
of glomerular disease in diabetes. Massive proteinuria
(>3.5 g/day) is the hallmark of nephrotic syndrome.
NEPHROTIC SYNDROME
It is characterized by
 Massive proteinuria (>3.5 g per 1.73 m 2 body surface
area per 24 hr)
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Kamal K Sawlani
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 Hypoalbuminemia
Edema
 Hyperlipidemia and
 Hypercoagulability
Massive proteinuria is the most important feature of
nephrotic syndrome.
Causes
Nephrotic syndrome can be due to primary glomerular
disease or secondary to systemic diseases. Important
causes of nephrotic syndrome are minimal change
disease (in children), membranous glomerulopathy,
diabetes mellitus, and amyloidosis.
Table 1: Causes of nephrotic syndrome
Primary renal disorders (idiopathic)
Minimal change disease
Mambranous glomerulopathy
Focal and segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
Systemic diseases and others
Diabetes mellitus
Amyloidosis
Infections (HIV, hepatitis, malaria)
Drugs (gold, penicillamine, NSAIDs,
captopril)
Autoimmune (systemic lupus erythematosis,
rheumatoid arthritis)
Pathophysiology
Proteinuria results in low serum albumin level
(hypoalbuminemia). Increased catabolism of protein in
the kidney and an inadequate synthesis by liver also
contribute to lower levels of serum albumin. The edema
is due to low plasma oncotic pressure resulting in
leakage of fluid in interstitium (underfilling hypothesis)
and/or primary salt and water retention by kidneys.
Escape of fluid into the interstitium causes low
intravascular volume which results into activation of
renin-angiotensin- aldosterone axis and the sympathetic
system, increased secretion of vasopressin (ADH), and
decreased secretion of atrial natriuretic peptide. The net
result is renal salt and water retention and increased
 160 Textbook of Family Medicine

intravascular volume and further leakage of fluid into 2. Protein loss: ACE inhibitors and ARBs are useful in
interstitial space. reducing proteinuria in patients who do not respond
to immunosuppressive therapy. The daily protein loss
Vitamin D deficiency that occurs due to enhanced
is compensated by the increased dietary protein
excretion of cholecalciferol binding protein may cause
1 hypocalcemia and secondary hyperparathyroidism. Loss
of transferrin in the urine may lead to iron-unresponsive
intake.
3. Hyperlipidemia: This is managed with the lipid
microcytic hypochromic anemia. lowering drugs such as statins (simvastatin,
atorvastatin, and rosuvastatin). Dietary modification
Increased synthesis of lipids by liver due to fall in
and exercise are also helpful.
oncotic pressure and altered metabolism of lipids leads to
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hyperlipidemia. Hypercoagulability is due to increased 4. Hypercoagulable states: Anticoagulation is needed in

urinary loss of antithrombin III and altered levels of
protein C and S. Infections may occur more commonly
due to increased urinary loss of immunoglobulins.
Clinical Features
Edema is the main presenting feature of nephrotic
syndrome. Initially it is present in the dependant parts
(lower extremities) but later on it may become
generalized (anasarca). In the morning, the face and
upper limb may be more affected. Fluid collection can
present as pleural fluid, ascites, or pulmonary edema.
Fever may occur due to infection. Other uncommon
features are arterial and venous thrombosis, pulmonary
embolism, and renal vein thrombosis.
Investigations
Urine analysis:. Presence of >3.5 g protein /24 hours
urine is the hallmark of nephrotic syndrome.
Microscopic examination may reveal lipid casts.
Hematuria is rare.
Blood examination: The blood examination reveals low
serum albumin (<3 g/dL), low total serum protein and
hyperlipidemia. Blood urea level and serum creatinine
are generally normal.
Renal biopsy: It is required to know the type of primary
renal disease in adults.
Treatment
General Measures
1. Control of edema: The salt in diet is restricted to 1-2
gm per day. Diuretics (thiazide or loop diuretics or
both) are used carefully.
patients with the evidence of thrombosis.
5. Others: Vitamin D (1,25,dihydrocholecalciferol)
supplementation is required in patients with evidence
of vitamin D deficiency.
Specific Measures
Immunosuppressive therapy is required in primary renal
causes of nephrotic syndrome and in some secondary
diseases such as SLE. Initially oral prednisolone is given
in the dosage of 1-2 mg/kg/day. Once response is
obtained (monitored by urinary protein excretion) it is
tapered gradually. In patients who are steroid dependent,
steroid resistant, or patients who frequently undergo
relapse, treatment with cytotoxic or other
immunosuppressive drugs is indicated. Common agents
used are cyclophosphamide (2 mg/kg/day), chlorambucil
(0.1-0.2 mg/kg/day), cyclosporin (5 mg/kg/day) and
mycophenolate mofetil.
Prognosis
Remission occurs in 90 percent children and 50 percent
adults in minimal change disease. About 20-30 percent
patients with membranous nephropathy develop chronic
renal failure.

Chapter 2
NEPHRITIC SYNDROME
A K Tripathi,
Nephritic syndrome arises due to acute glomerular
inflammation (glomerulonephritis, GN) and is
characterized by sudden onset (days to weeks) of
oliguria, edema, hypertension, hematuria, subnephrotic
proteinuria (<3 g/day) and worsening renal function.
Pathophysiology
The renal blood flow and glomerular filtration rate
(GFR) are reduced because of obstruction of glomerular
capillaries by inflammatory cells and glomerular cell
proliferation. Impaired GFR and increased reabsorption
of salt and water by tubules result in edema and
hypertension. Injury to the glomerular capillary wall
leads to the appearance of dysmorphic RBC, red blood
cell cast and protein in the urine. Hematuria is often
macroscopic.
Clinical Features
The onset is often sudden. The presenting features are
decreased urine output and edema. A urine output less
than 400 ml per day is defined as oliguria while less than
100 ml per day is called anuria. Hypertension and
hematuria are often present. Patients also have
generalized symptoms such as anorexia, nausea,
vomiting, headache and malaise.
Causes
The nephritic syndrome is classified on the basis of
pathological features into three broad categories.The
most common type is immune-complex glomerulo-
nephritis.
Tale 1: Causes of nephritic syndrome
1. Idiopathic
Proliferative glomerulonephritis (focal or
diffuse)
Rapidly progressive glomerulonephritis (RPGN)
2. Post-infectious
Streptococci
Bacterial endocarditis
Hepatitis B
Malaria
3. Multisystem disorders
SLE(lupus nephritis)
Henoch-Schönlein purpura
Goodpasture’s syndrome
Wegener’s granulomatosis
Investigations
Serum chemistry: Blood urea and creatinine are raised.
Other tests which help in diagnosing different types of
GN are serum complement levels (C3), anti-GBM
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Kamal K Sawlani
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antibody, ANCA (anti-neutrophil cytoplasmic antibody),
antinuclear antibody (ANA), and ASO titers. Tests like
serum electrolytes, arterial blood gases, and complete
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blood count may be needed.
Urine examination: The urine examination reveals
dysmorphic red blood cells, red blood cell cast, and
proteinuria. A 24 hours urine output is measured which is
low.
Renal biopsy: The biopsy of kidney is the gold standard
for the diagnosis, treatment plan and the prognosis of the
disease. Light microscopy, immunofluorescence, and
electron microscopy of biopsy specimen are helpful in
distinguishing the major types of acute nephritis.
Treatment
General Measures
1. Control of edema and volume overload: The salt in
diet is restricted to 1-2 g per day. Water intake is
restricted to the urine output plus 500 ml/day.
Diuretics (thiazide or loop diuretics or both) are used
carefully.
2. To minimize protein loss: ACE inhibitors and ARBs
are useful in reducing proteinuria. However, serum
potassium and serum creatinine should be monitored
carefully.
3. Dialysis: Dialysis may be needed to control
hypervolemia and uremia.
4. Control of hypertension: The blood pressure is
controlled with antihypertensive agents. This helps in
decreasing proteinuria and slowing the progression of
the disease. The target BP should be 130/80 mm Hg.
Specific Measures
Corticosteroids (prednisolone, methylprednisolone) and
other immunosuppressive drugs (cyclophosphamide,
azathioprine, cyclosporine and mycophenolate mofetil)
are generally used for the control of glomerular
inflammation. Antibiotic is given in post-streptococcal
glomerulonephritis. Patients who do not respond to
immunosuppressive therapy and progress to end stage
renal disease (ESRD) require dialysis or renal
transplantation.
Prognosis
The course of the disease varies according to the cause
and histopathological types. Majority of patients with
post-streptococcal nephritic syndrome remits sponta-
neously and few patients (<5%) may develop RPGN or
ESRD.
 162 Textbook of Family Medicine

Chapter 3
ACUTE RENAL FAILURE (ARF)
1 A K Tripathi, D Mukherjee

Acute renal failure is defined as sudden decline in renal

Management
ability to maintain fluid and electrolyte homeostasis and
to excrete nitrogenous wastes. Clinically ARF manifests 1. Fluid management: Intravenous fluid replacement is
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as rising blood urea and serum creatinine levels or
decreased urine output over hours or days.
The most common type of ARF is prerenal failure. This
is a response to renal hypoperfusion. The prolonged and
severe hypoperfusion may lead to acute tubular necrosis,
a type of intrinsic renal failure.
Acute renal failure may be oliguric or nonoliguric. In
non-oliguric form, the urine output is not reduced
although blood urea and serum creatinine are raised.
Table 1: Causes of acute renal failure
1. Prerenal failure
Hypotension or volume contraction ( blood
or fluid loss)
Heart failure
2. Intrinsic renal failure
Acute tubular necrosis
Glomerulonephritis
Interstitial nephritis
Reno-vascular diseases
3. Postrenal failure (Obstructive)
Ureteric obstruction ( stone, clot, tumor,
external
compression)
Bladder outlet obstruction ( prostate
hypertrophy/ carcinoma, stone, clot)
Clinical Manifestations
Usual symptoms are nausea, vomiting, malaise, and
anorexia. Cardiac manifestations include pulmonary
edema due to fluid retention, pericardial effusion and
arrhythmias. Encephalopathic features such as
drowsiness, confusion, asterixis, seizures and coma may
occur. There may be a bleeding tendency due to platelet
dysfunction and altered coagulation. Features of
hyperkalemia and metabolic acidosis are common.
Anemia occurs due to blood loss or decreased RBC
production. Infection is a serious complication and the
most common cause of death in ARF patients.
done in patients with hypovolemia with prerenal
ARF. In other types of ARF, fluid intake is restricted
according to the urine output (500 ml plus urine
output in last 24 hours). Diuretics are used in cases
with volume overload.
2. Dialysis: Majority of patients improve on conser-
vative management. However, the dialysis is
indicated in refractory hyperkalemia, acidosis or
volume overload and uremic complications
(encephalopathy, pericarditis and seizures).
3. Management of metabolic complications: Hyper-
kalemia is managed with the use of calcium, insulin,
bicarbonate and glucose. Sodium bicarbonate is
given to control acidosis. Hypocalcemia and
hyperphosphatemia require prompt management.
4. Adjustment of drug dosage: The dosage of the drugs
is adjusted according the severity of renal failure.
Nephrotoxic drugs should be avoided.
5. Bleeding complications: Bleeding can be controlled
by the use of desmopressin or estrogen. Regular use
of antacids reduces the incidence of gastrointestinal
hemorrhage.
6. Management of anemia: Severe anemia is managed
by blood transfusion. Erythropoietin, though useful
in CRF is not helpful in ARF.
7. Control of infections: Aseptic precautions should be
practiced to avoid infections. Prompt use of
antimicrobial agent is necessary to manage infection.
8. Diet management: Adequate caloric intake should be
maintained to avoid excessive catabolism. Protein
intake is restricted upto 0.6 gm/kg/day. Salt,
potassium and phosphorus intake should also be
restricted.

Chapter 4
CHRONIC RENAL FAILURE (CRF)
D Mukherjee,
Chronic renal failure is defined as irreversible loss of
renal function which develops over a period of months to
years. Eventually clinical symptoms and signs ensue due
to severe loss of metabolic, excretory and endocrinal
functions of the kidneys (uremia). Blood urea and serum
creatinine are raised.
End stage renal disease (ESRD) is a severe stage of
CRF (GFR 10-15 ml/min), in which the patient is
permanently dependant on renal replacement therapy to
avoid life-threatening uremia.
Causes of CRF
Diabetes mellitus and hypertension are most common
causes of CRF. Other important causes are glome-
rulonephritis, polycystic renal disease, tubulointerstitial
diseases, and obstructive nephropathies.
Table 1: Important features of CRF
Chronic features (>3 months) of uremia
Hypertension
Anemia
Renal osteodystrophy
Isosthenuria (fix low specific gravity of urine)
Broad cast in the urine
Small contracted kidneys (on ultrasonography)
Management
1. Diet management: Adequate caloric intake should
be maintained to avoid excessive catabolism.
Protein intake is restricted up to 0.6 g/kg/day to
reduce accumulation of nitrogenous waste products
and to slow down the progression of renal failure.
Fluid, salt, potassium and phosphorus intake should
also be restricted.
2. Management of renal osteodystrophy: Hyper-
phosphatemia is management by restriction of
phosphate (milk, cheese, eggs) in the diet and use of
phosphate binding drugs such as calcium carbonate
and aluminium hydroxide gel. Supplementation of
vitamin D (1-alpha hydroxyl vitamin D3 or 1,25
dihydroxy vitamin D3) and calcium is needed to
correct hypocalcemia.
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3. Management of metabolic complications: Hyper-
kalemia is managed with the use of calcium,
insulin, bicarbonate and glucose. Sodium bicarbo-
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nate is given to control acidosis.
4. Management of proteinuria: ACE inhibitors and
ARBs are helpful in reducing proteinuria and
slowing the progression of renal damage.
5. Control of blood pressure: Hypertension must be
controlled rigorously with a target of blood pressure
less than 130/80 mmHg.
6. Adjustment of drug dosage: The dosage of the
drugs is adjusted according the severity of renal
failure. Nephrotoxic drugs should be avoided.
7. Management of anemia: Erythropoietin (subcuta-
neous or intravenous) is useful in the management
of anemia. Iron stores must be adequate to ensure
response to erythropoietin. Intravenous iron (Ferric
gluconate or iron sucrose) may be needed to
replenish iron stores. Supplementation of vitamin
B12 and folic acid is also required. Anemia not
responding to erythropoietin is corrected by blood
transfusion.
8. Bleeding complications: Bleeding can be controlled
by the use of desmopressin or estrogen. Regular
uses of antacids reduce the incidence of gastro-
intestinal hemorrhage.
9. Dialysis: Dialysis is indicated in refractory
hyperkalemia, acidosis or volume overload and
uremic complications (encephalopathy, pericarditis
and seizures).
10. Renal replacement therapy: This is indicated in
ESRD patients. Different forms of replacement
therapy are (a) peritoneal dialysis, (b) hemodialysis
and (c) renal transplantation.
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