Dr.

Alis Uworld Notes For Step 2 CK

Urogenital

Urinary Tract Diseases

Dipsticks are commercially available kits that detect the presence of
leukocyte esterase and nitrites in the urine of patients with suspected UTI.
Leukocyte esterase in the urine indicates significant pyuria, whereas nitrites
signify the presence of Enterobacteriaceae, which converts urinary nitrates
to nitrites. (Remember that the most likely responsible organism of UTI is E
.coli.) The advent of dipstick testing has significantly reduced the cost
associated with urine culture; however, dipsticks are associated with a high
false positive rate and high false negative rate. For this reason, a negative
dipstick test in a patient with symptoms of UTI should still have urine
cultures done.
Chlamydia Urethritis - The diagnosis of chlamydial urethritis is usually
suggested by the presence of mucopurulent urethral discharge and
history of multiple sexual partners. Dysuria and urinary frequency can occur.
Urinalysis reveals absent Bacteriuria. Urine culture shows less than 100
colonies/ml.
Chlamydia Urethritis = Mucopurulent Discharge + Absent
Bacteriuria.
Gonococcal urethritis is less common than chlamydial urethritis. The
urethral discharge is purulent (rather than mucopurulent), and Gram stain
usually reveals the causative organisms.
Gonoccal Urethritis = Purulent Discharge + Bacteriuria.
Cystitis - Patients with acute bacterial cystitis present with dysuria, urinary
frequency, suprapubic discomfort and urinary findings of bacteriuria and

pyuria. Mucopurulent cervical discharge is not found. Urine culture shows

colonies in excess of 1000/ml.
The urinary tract is generally sterile, with the exception of the distal end of
the urethra and meatus. Normally, the enteric gram-negative bacilli that
commonly cause UTI do not colonize the vaginal introitus and distal urethra;
however, colonization may occur in the presence of predisposing factors
(e.g., alteration of the normal vaginal flora by antibiotics, genital infections,
contraceptives such as diaphragms and especially spermicide, poor genital
hygiene, etc.). It is currently a widely accepted theory that UTis most
commonly occur via the ascending route. In this patient, urethral massage
during intercourse most likely facilitated the entry of a small number of
periurethral bacteria into the bladder via the ascending route, which
consequently resulted in a UTI.
Uncomplicated cystitis refers to infections that occur in otherwise healthy,
young, nonpregnant women.
Complicated cystitis refers to infections in women who are pregnant,
very young, very old, diabetic, immunocompromised, or have
abnormal anatomy of the genitourinary tract.
Both can present with dysuria, increased urinary frequency, suprapubic
pain, and/or hematuria (usually indicates hemorrhagic cystitis).

Routine urine cultures are not indicated in UNcomplicated cystitis. Urine

culture is indicated only if the patient has complicated cystitis, urinary
symptoms not characteristic of cystitis, persistent symptoms of cystitis
despite treatment, or repeat symptoms of cystitis less than one month after
treatment for previous cystitis without a urine culture. Oral
trimethoprim/sulfamethoxazole and nitrofurantoin are the preferred
first-line agents for empiric treatment of uncomplicated cystitis, while a
fluoroquinolone (levofloxacin or ciprofloxacin) is the recommended firstline agent for complicated cystitis.
Interstitial cystitis (IC) is a chronic condition of the bladder of uncertain
etiology and pathophysiology. It is clinically characterized by the triad of
urinary urgency and frequency as well as chronic pelvic pain in the absence
of another disease that could cause the symptoms. Pelvic pain is occasionally
the presenting symptom or chief complaint. The pelvic pain in interstitial
cystitis is classically exacerbated by sexual intercourse, filling of the
bladder, exercise, spicy foods and certain beverages. The pain is

typically relieved by voiding. Cystoscopy classically demonstrates

submucosal petechiae or ulcerations.
Acute Pyelonephritis - Patients with acute pyelonephritis appear toxic and
present with fever, nausea, vomiting, flank pain, dysuria and
costovertebral tenderness. Urinalysis shows bacteriuria and pyuria. Urine
culture reveals greater than 10,000 colonies/ml.
Urine and blood cultures should be obtained routinely prior to administering
antibiotics.

Oral or parenteral antibiotics can be used to treat acute pyelonephritis,

depending upon the disease severity. Patients who can take the drugs orally,
who are compliant or who are not suffering from severe disease can be
started on oral ciprofloxacin as empiric therapy. When the disease is
severe or the patient cannot take the antibiotics orally, IV ampicillin plus
gentamicin is the appropriate empiric therapy. Failure to respond to
oral ciprofloxacin may indicate the presence of obstruction, abscess, or other
complications of acute pyelonephritis

When there is no adequate response to 72-hr treatment with the

appropriate antibiotics, urological imaging (e.g., CT scan or
ultrasound) is performed to search for any underlying pathologies (e.g.,
obstruction) or complications (e.g., renal, perirenal abscess).
Acute epididymitis is characterized by fever, painful enlargement of
the testes, and irritative voiding symptoms. It can be either sexually
transmitted or non-sexually transmitted.
Sexually transmitted acute epididymitis is more common in young
adults and is associated with urethritis, which causes pain at the tip of the
penis and urethral discharge. Chlamydia and gonococcus are the most
frequent causes of sexually transmitted acute epididymitis
Non-sexually transmitted acute epididymitis occurs in older persons
and is usually associated with a UTI. Both E. coli and Pseudomonas may
cause non-sexually transmitted acute epididymitis but E. coli is the most
frequent cause.
Acute Prostatitis - Acute prostatitis presents in a manner similar to other
urinary tract infections, but with the addition of perineal pain and a
tender, boggy prostate on exam. The diagnosis should be strongly
considered in male patients since acute cystitis is uncommon among men.
Overly vigorous prostatic massage should be avoided if acute prostatitis is a
possibility as it can result in bacteremia. Obtaining a mid-stream urine
sample would be the most appropriate next step in order to help direct
antibiotic therapy.
Patients with non-inflammatory chronic prostatitis are afebrile and have
irritative voiding symptoms. Physical examination is unremarkable and
urinalysis is normal. Expressed prostatic secretions show a normal
number of leukocytes and culture of these secretions is negative for
bacteria. There is usually no history of past UTI but voiding abnormalities
may be present in the past.
Postoperative UTI - Urinary tract infection (UTI) is a common complication
in postoperative patients. In addition, elderly patients and those with
diabetes are at increased risk of developing UTI. UTI typically presents
with complaints of dysuria, urgency, and frequency. However, elderly
patients with UTI may not describe these typical symptoms, and may instead
present with altered mental status. Therefore, there should be clinical

suspicion for UTI in any case of postoperative fever and in elderly patients
with altered mental status. Urinalysis (UA) serves as a good screening test
for UTI. Abnormalities on UA that are suggestive of UTI include +nitrites,
+leukocyte esterase, >5 WBC/HPF, and the presence of bacteria. None of
these UA findings alone are 100% sensitive or specific for UTI, but taken
together and in the context of this patient's history and physical exam, it is
clear that UTI is the cause of his symptoms. Promptly initiating appropriate
antibiotic therapy (trimethoprim/sulfamethoxazole) in this patient is the
best next step in management.
Postop UTI Hx of Surgery + Altered Mental Status + Nitrates,
Esterases + Bacteria in Urine.
Postoperative AKI - Acute Kidney Injury (AKI) in a postop patient presents
with acute oliguria ( <250 ml urine in 12 hours), azotemia (rise in blood
urea nitrogen [BUN] level), and increased serum creatinine level.
Etiology of AKI can be prerenal, postrenal, or intrinsic renal.
AKI due to Postoperative urinary retention is common in men aged >50 years
due to the high incidence of underlying benign prostatic hyperplasia in this
population. A precipitating event, such as bladder distention during general
anesthesia or the use of epidural anesthesia, can lead to inefficient detrusor
muscle activity and acute urinary retention.
Foley catheterization is the next best step in management. It is
essential for distal obstructions to restore normal urine output and
resolve/prevent hydronephrosis, tubular atrophy, and renal injury. If
catheterization does not relieve the patient's oliguria, then alternative AKI
etiologies (i.e., intrinsic, prerenal) must be considered.
Intravenous fluids are critical in the treatment of prerenal AKI caused by
hypovolemia. In postrenal obstruction, administration of intravenous fluids
without first placing a catheter would increase the strain on the kidneys and
bladder.
Acute urinary retention in the elderly can be an emergency and is usually
caused by obstruction, Neurogenic bladder, or detrusor muscle underactivity.
The most common cause of urinary retention in older men is bladder outlet
obstruction due to benign prostate hyperplasia or carcinoma of the
prostate. Patients commonly present with postvoid dribbling, decreased
urinary stream, hesitancy, urgency, nocturia, and urinary retention.
Rectal examination shows an enlarged prostate and a high postvoid urinary
residual volume when a Foley catheter is inserted.

BPH = Urgency, Frequency, Hesitancy, Dribbling & Retentio & weak

stream.
The Achilles tendon reflex can be decreased or even be absent with
age. So this can be a normal finding in many elderly patients. Possible
etiologies include decreased sympathetic tone with age or, possibly, changes
in the muscles themselves.
The presence of lower extremity weakness, bowel/bladder
INCONTINENCE, or decreased rectal tone and brisk lower extremity
deep tendon reflexes would indicate a possible spinal cord lesion with
compression in the lumbar region.
BPH - Postvoid dribbling, decreased urinary stream, hesitancy,
urgency, nocturia, and urinary RETENTION.
Cord Compression - lower extremity weakness, bowel/bladder
INCONTINENCE, or decreased rectal tone and brisk lower extremity
deep tendon

Benign Prostatic Hyperplasia - These patients present with a history of

progressive urinary urgency, hesitancy, nocturia, and a weak urinary
stream & postvoid dribbling.. These are suggestive of prostatic
enlargement. Rectal exam is helpful in distinguishing benign prostatic
hyperplasia (BPH) from prostate cancer. Smooth, firm enlargement is
consistent with BPH. BPH starts in the center of the prostate. In
contrast, prostate cancer often presents with a palpable nodule at the
periphery of the prostate gland. Urinary obstruction should be considered in
any patient with suspected BPH who presents with an elevated creatinine.
Unilateral urinary obstruction, as occurs with an obstructing ureteral
calculus, will not usually cause an elevated creatinine.
Prolonged obstruction of more than two weeks duration can result in
permanent kidney damage. For these reasons, all elderly patients who
present with acute renal failure should have a Foley catheter placed as a
first step; if a large amount of urine is collected after inserting the catheter,
BPH is the most likely diagnosis.
In chronic, severe BPH, the hypertrophied prostate causes resistance to urine
flow. In such cases, it can be difficult to insert a Foley catheter through the
hypertrophied prostate. Sometimes, when the Foley catheter cannot be
placed, a suprapubic catheter is required, but remember that this is a
treatment of last resort.

Current guidelines recommend evaluating all patients with probable benign

prostatic hyperplasia based on history and rectal examination with a
urinalysis and serum creatinine measurement to assess for urinary
infection, obstruction, or hematuria. Patients with an elevated creatinine
level or abnormal urinalysis warrant further investigation.
Abdominal ultrasound is warranted here to assess for
hydronephrosis. If hydronephrosis is present, placement of a Foley
catheter will likely help to improve the patient's urinary obstruction. Surgical
intervention (e.g . transurethral resection of the prostate or TURP) is a good
option for improving the patient's urinary obstruction over the long term. The
drugs of choice are alpha-adrenergic blockers.
Severe pain in a patient with a mild urinary obstruction, such as
BPH, may cause urinary retention due to inability to Valsalva. The
pain may be due to Disk herniation or anything that prevents the patient
from increasing the intraabdominal pressure.

Urinary Fistula - Patients with a history of pelvic surgery or irradiation can

develop a urinary fistula, with continuous loss of urine through the
fistula. The diagnosis is made with intravenous pyelography, which shows
dye leaking from the fistula.
Diabetic autonomic neuropathy leads to a denervated bladder, which
results in urinary retention. The acontractile, hypotonic bladder gradually
overdistends, and when the bladder pressure rises above the urethral
pressure, urine is lost until the pressure equalizes. These events occur in a
cyclic manner, thus explaining why the incontinence occurs during both
day and night. Physical examination may reveal a distended bladder. Postvoid residual urine volumes are high. Aside from strict glycemic control,
treatment options include intermittent catheterization and cholinergic
medications such as bethanechol. Heavy alcohol intake may contribute to
the effects of autonomic neuropathy; therefore, advising this patient to stop
drinking alcoholic beverages may be helpful.

Drug Induced Urinary Retention - First-generation H1-antihistamines such

as diphenhydramine, chlorpheniramine, doxepin and hydroxyzine have
significant anticholinergic effects in addition to their antihistamine effects.
Amitriptyline also has anticholinergic activity. The anticholinergic effects of
these agents result from inhibition of the action of acetylcholine on
muscarinic receptors, which are found in the parasympathetic nervous
system. Common anticholinergic side-effects include dryness of the eyes,
oral mucosa and respiratory passages, urinary retention and dysuria.
Urinary retention caused by anticholinergic agents results from failure of
detrusor contraction. Detrusor activity is controlled by parasympathetic
input from the pelvic splanchnic nerves.
Urinary catheterization would serve two purposes in this case. First, it can
document a postvoid residual bladder volume of greater than 50 ml, which is
considered diagnostic of urinary retention. Plus, catheterization will provide
symptomatic relief as it drains urine from the bladder. The patient should
also discontinue the drug causing anticholinergic activity.

Detrusor-sphincter dyssynergia typically occurs in the setting of

neurologic disease. In this condition, the detrusor muscle contracts while the
urethral sphincter contracts causing difficulty in initiating urination and
inadvertent interruption of the urinary stream.

Nephrolitiasis Obstructive uropathy causes flank pain, low volume

voids with or without occasional high volume voids, and (if bilateral)
renal dysfunction.
Approximately 1-5% of the United States population is affected by renal
stones (nephrolithiasis). Men have twice the risk of women. The basic
pathophysiology involves the abnormal excretion of stone-forming salts
and/or a deficiency of urinary inhibitors of crystal formation due to metabolic
disorders or dietary factors. Renal stones are predominantly of four types:
1.
2.
3.
4.

Calcium oxalate/phosphate (75%)

Uric acid (1 0-15%)
Struvite/triple phosphate ( 1 0-15%)
Cysteine (<1%)

Calcium stones are the most common type of renal stones seen. These
are most commonly seen in the third or fourth decade of life. Most patients

present with hypercalciuria (24 hour urinary calcium excretion > 300 mg in
males and >250 mg in females;> 4 mg/kg in both males and females).
75% to 90% of kidney stones are composed of calcium oxalate. Calcium
oxalate crystals are envelope shaped and can be seen on microscopic
examination of urine. Small bowel disease, surgical resection or chronic
diarrhea can lead to malabsorption of fatty acids and bile salts; this
predisposes to the formation of calcium oxalate stones. (Fat malabsorption
leads to the increased absorption of oxalic acid because the unabsorbed
fatty acids chelate calcium, making oxalic acid free for absorption.)
Calcium phosphate stones are common in primary
hyperparathyroidism and renal tubular acidosis.
Uric acid stones are formed when the urine is acidic or when there is
increased cell turnover, thereby resulting in hyperuricemia and
hyperuricosuria. Dehydration is another important risk factor.
Cysteine stones are formed when there is increased excretion of cysteine,
which is an inborn error of metabolism. A positive family history may be
found in such cases.
Struvite stones are formed when urine is alkaline because of infection
with urease producing bacteria (e.g., Proteus). In such cases, a history of
recurrent UTI may be present.
The most common causes of calcium stones are:
1. Idiopathic hypercalciuria: This is characterized by hypercalciuria,
normal serum calcium levels, and absent metabolic disease. It is
the most common form of hypercalciuria.
2. Hypercalciuria due to systemic disorders (e.g. primary
hyperparathyroidism. sarcoidosis. etc.)
3. Hyperuricosuria
4. Hyperoxaluria: The cause may be hereditary, dietary (i.e., due to
ingestion of a large amount of vitamin C or green leafy vegetables), or
secondary to IBD or short bowel syndrome.
5. Decreased urinary citrate
6. Renal tubular acidosis: Typically, nephrocalcinosis is seen.

7. Chronic decrease in urine output This helps the precipitation of calcium

salts.
Idiopathic Hypercalciuria is best treated with increased fluid intake,
dietary sodium restriction, and thiazide/amiloride diuretics. Thiazide
diuretics decrease urinary calcium excretion (primarily by inducing mild
volume depletion. which leads to a compensatory rise in proximal
reabsorption of sodium and calcium) and prevent the precipitation of calcium
in the urine. Patients with recurrent calcium stones due to hyperuricosuria
can be treated with purine-restricted diet and allopurinol.
Recommendations for calcium oxalate urolithiasis (in order of
relative importance):
1. Increased fluid intake (>3 L per day)
2. Normal or increased calcium diet (recommended daily allowance is
1000 mg/dl)
3. Dietary sodium restriction ( < 100 mEq/dL)
4. Oxalate restriction (i.e .. dark roughage, chocolate and vitamin C)
5. Decreased dietary proteins (i.e .. beef. fish. eggs. and poultry)
Consider three possibilities when a flat film of the abdomen and pelvis does
not show a stone in a patient with typical renal colic:
1. radiolucent stone disease (uric acid stones)
2. calcium stones less than 1 to 3 mm in diameter
3. non-stone causes (e.g., obstruction by a blood clot or tumor)
Uric acid stones account for approximately 10-15% of cases of total
nephrolithiasis. These are most commonly seen in patients with unusually
low urine pH levels (which may be due to a defect in renal ammonia
secretion) and hyperuricosuria. These are radiolucent, but can be seen on
USG and CT scan. Urinanalysis may show needle shaped crystals.
Treatment includes hydration, alkalinization of urine, and a low-purine diet
with/without allopurinol, depending on the presence of hyperuricosuria. Since
uric acid stones are highly soluble in alkaline urine, alkalinization of urine to
pH > 6.5 with oral potassium bicarbonate or potassium citrate is
indicated.
Cysteine Stones Cystinuria is a group of disorders characterized by
impaired amino acid transport and several modes of inheritance. The
problem lies with the defective transport of dibasic amino acids (cystine,
ornithine, lysine & arginine COLA) by the brush borders of renal tubular and
intestinal epithelial cells. Cystine is poorly soluble in water; this leads to the

formation of hard, radio opaque renal stones. The clues to the correct
diagnosis are the patient's personal history of recurrent stones since
childhood, positive family history, typical hexagonal crystals on urinalysis
and positive urinary cyanide nitroprusside test. The urinary cyanide
nitroprusside test can detect elevated cystine levels, which can help confirm
the diagnosis; this test is widely used as a qualitative screening procedure,
and is particularly helpful for the detection of homozygotes
Patients with ureteral stones may have paralytic ileus. This gets treated
once the stones are passed.
Nephrolithiasis Management The following are important concepts in
the management of such patients.
1. Imaging study- CT scan of the abdomen without contrast is the
investigation of choice because of its high sensitivity and specificity. It
has the advantage over the plain abdominal x-ray (KUB) in detecting
the radiolucent stones.
2. Narcotics and NSAIDs - These are equally effective in relieving the
pain of acute renal colic; however, in patients with normal renal
function, NSAIDs are preferred over narcotics because the latter can
exacerbate nausea and vomiting.
3. Size of the stone - Stones measuring less than 5mm in diameter
typically pass spontaneously with conservative management. This
includes a fluid intake of greater than 2L daily. Increased
hydration increases the urinary flow rate and lowers the urinary solute
concentration, thus preventing stone formation.
4. Urology referral - Urgent urologic evaluation is warranted in patients
with anuria, urosepsis, or acute renal failure.
Renal stones in pregnancy require special consideration because many of the
investigative and treatment modalities will expose the fetus to radiation.
Since there is no risk of radiation with ultrasound, renal and pelvic
ultrasound is the investigative procedure of choice for pregnant
patients. In addition to avoiding radiation exposure, ultrasonography is also
useful for detecting secondary signs of obstruction, such as hydronephrosis
or hydroureter. Physiological hydronephrosis of pregnancy must be
distinguished from pathological hydronephrosis secondary to obstruction.
Renal Diseases

Nephrotic Syndrome - Peripheral edema, hypoalbuminemia, and urinary

protein excretion of greater than 3g/day meets all major criteria for
nephrotic syndrome. While some patients with nephrotic syndrome may
develop acute renal failure, a normal creatinine does not exclude the
diagnosis. Abnormal lipid metabolism is found in many patients with
nephrotic syndrome, including an elevated LDL and/or a low HDL,
predisposing to accelerated atherosclerosis. Patients with nephrotic
syndrome are also hypercoagulable, although the mechanism of this
phenomenon is somewhat unclear. This hypercoagulability tends to affect the
venous more than the arterial system, particularly the renal veins.
Atherosclerosis and hypercoagulability together put affected
patients at increased risk for stroke or myocardial infarct. Aggressive
management, including statins or other medications to lower cholesterol
levels, are indicated.
The most common causes of nephrotic syndrome not secondary to a
systemic disease are minimal change disease, membranous
nephropathy, and focal segmental glomerulosclerosis (FSGS). Minimal
change disease is the most common etiology in children.

Glomerulonephritis
FSGN - The most common causes in adults are FSGS and membranous
nephropathy, with FSGS accounting for more than 1/2 of cases in African
American patients. FSGS also has an association with obesity, heroin
use and HIV.

Membranous Nephropathy - Active hepatitis B infection in children

often leads to development of membranous glomerulonephritis and
subsequent nephrotic syndrome. This phenomenon is particularly associated
with positivity for HBeAg.
PSGN - Post-streptococcal glomerulonephritis is seen 10-20 days after
streptococcal throat or skin infections. Presenting features may include
periorbital swelling, hematuria and oliguria. The patient may be
hypertensive and urinalysis shows hematuria with RBC casts and proteinuria.
Serum C3 complement levels are low.

IgA Nephropathy - Patients with lgA nephropathy typically present with

hematuria after an upper respiratory tract infection and a latent period
between infection and the actual onset of the disease. Development of
features of glomerular disease is less than 5 days. Serum complement
levels are normal in such cases.

Good Pasteurs Disease - Pulmonary-renal syndromes include a variety of

disorders with simultaneous involvement of the lung and kidney. Quick
differential diagnosis is important because the management differs per
disease. Emergency plasmapheresis is required in patients with
Goodpasture's syndrome. Granulomatosis with polyangiitis (Wegener's) is
treated with a combination of cyclophosphamide and steroids.
Membranoproliferative glomerulonephritis - Dense
intramembranous deposits that stain for C3 is a characteristic
microscopic finding for membranoproliferative glomerulonephritis, type 2
(also called dense deposit disease). This condition is unique among
glomerulopathies, because it is caused by lgG antibodies (termed C3
nephritic factor) directed against C3 convertase of the alternative
complement pathway. These antibodies reacting with C3 convertase lead to
persistent complement activation and kidney damage.
Renal vein thrombosis & Nephrotic Syndrome Renal Vein Thrombosis
is an important complication of nephrotic syndrome. Antithrombin III is lost in
the urine and puts patients at an increased risk of venous and arterial
thrombosis. Renal vein thrombosis presents with sudden onset of abdominal
pain, fever and hematuria. It can occur in any form of nephrotic syndrome,
but it is most common with membranous glomerulonephritis

Diabetic Nephropathy - In diabetic patients with moderate proteinuria and

progressive renal insufficiency, diabetic glomerulosclerosis is commonly
responsible. Approximately 50% of type 1 and type 2 diabetics develop
moderate or severe proteinuria over the course of the disease. In general,
the proteinuria becomes evident 12 to 22 years after the clinical onset of
diabetes and progresses to chronic renal failure and end-stage renal disease
within the subsequent 4 to 5 years. However, this sort of overt proteinuria is
preceded by mild or trace protein leakage into the urine, termed
"microalbuminuria," which may actually become detectable within a few
years of the onset of diabetes. The most common histologic lesion in diabetic
nephropathy is diffuse glomerulosclerosis. Nodular glomerulosclerosis
(with Kimmelstiei-Wilson nodules) is pathognomonic.
Glomerular hypefiltration is believed to be the earliest renal
abnormality present in patients with diabetes mellitus. It can be detected
as early as several days after the diagnosis of diabetes was made.
Thickening of the glomerular basement membrane is the first

change that can be quantitated. Moreover, glomerular hyperfiltration is

the major pathophysiologic mechanism of glomerular injury in these
patients. It creates intraglomerular hypertension leading to progressive
glomerular damage and renal function loss. You should remember that
effectiveness of ACE inhibitors in diabetic nephropathy is related to their
ability to reduce intraglomerular hypertension and, thereby, decrease
glomerular damage.

Hypertensive Nephropathy - These patients have has benign

nephrosclerosis secondary to hypertension. Hypertension is the second
leading cause of end stage renal disease in the United States. It is interrelated with kidney disease; hypertension causes nephropathy, and vice
versa. In particular, it is the renal vasculature that is exquisitely sensitive to
damages incurred by systemic hypertension. Arteriosclerotic lesions of
afferent and efferent renal arterioles and glomerular capillary tufts are the
most common renal vascular lesions seen. As the hypertension progresses,
there is a progressive decrease in renal blood flow and glomerular filtration
rate. The sequence of kidney damage evolves from nephrosclerosis to
glomerulosclerosis. Nephrosclerosis is characterized by hypertrophy and
intimal medial fibrosis leading to Intimal thickening & luminal
narrowing of renal arterioles; whereas, glomerulosclerosis is characterized
by progressive loss of the glomerular capillary surface area with glomerular
and peritubular fibrosis. Microscopic hematuria and proteinuria occur due to
these glomerular lesions. The kidneys generally decrease in size.
Amyloidosis - The clues to the correct diagnosis include history of chronic
inflammatory disease (rheumatoid arthritis) that predisposes to amyloidosis,
enlarged kidneys, and hepatomegaly. The typical findings on renal biopsy in
such a patient are amyloid deposits that show apple-green birefringence
under polarized light after staining with Congo red. Extracellular amyloid
fibrils demonstrated on electron microscopy are also typical.
Contrast-Induced nephropathy - The pathogenesis of contrast-induced
nephropathy involves renal vasoconstriction and tubular injury. Patients
with a history of diabetes and chronic renal insufficiency are at increased risk
of contrast nephropathy. The most common presentation is a spike in the
creatinine within 24 hours of contrast administration, followed by a
return to normal renal function within five days. Non-ionic contrast agents
are associated with lower incidence of nephropathy than the older ionic
hyperosmolar agents. In addition to using non-ionic contrast agents,
adequate IV hydration and acetylcysteine can decrease the incidence of
nephropathy.

Adequate pre-CT intravenous hydration is the single most important

intervention for preventing contrast nephropathy. Intravenous isotonic
bicarbonate or normal saline is typically used, and administration should
begin prior to the procedure and continue for several hours afterwards.
Acetylcysteine has also been shown to prevent nephropathy, likely due to its
vasodilatory and antioxidant properties

Hodgkins Lymphoma Induced Nephrotic Syndrome - Glomerular

disease may be seen in patients with a wide variety of malignancies.
Nephrotic syndrome presents as high-range proteinuria, hypoalbuminemia,
and edema (as seen in this patient), and is a well-known complication of
Hodgkin's lymphoma. The most common cause of nephrotic syndrome in
patients with Hodgkin's lymphoma is minimal change disease but focal
glomerulosclerosis can also occur. The pathophysiology of this condition is
poorly understood, but lymphocyte dysregulation and cytokine production
(IL-13) may play a role. Nephrotic syndrome usually resolves with successful
treatment of the lymphoma.
Rhabdomyolysis - One should suspect myoglobinuria whenever test results
demonstrate a large amount of blood on urinalysis with a relative absence of
RBCs on urine microscopy. Myoglobinuria is usually caused by
rhabdomyolysis, which frequently leads to acute renal failure.
Cocaine & Rhabdomyolysis - The two strong risk factors for
rhabdomyolysis are: immobilization and cocaine abuse. Prolonged
immobilization causes direct muscle damage and the release of creatine
phosphokinase (CPK). Similarly, cocaine is a potent vasoconstrictor that
causes diffuse ischemia, seizures, agitation, incidental trauma, hyperpyrexia
and a direct toxic effect on myocytes. All of these may contribute to
increased muscle breakdown. Second, the elevated potassium and CPK
concentrations are strongly suggestive of rhabdomyolysis. As muscle cells
break down, potassium, CPK, and myoglobin are released into the blood
stream. In fact, 20% of cocaine overdoses are complicated by these
laboratory abnormalities.
Renal failure in rhabdomyolysis is caused by acute tubular necrosis from
excessive filtered myoglobin. The risk of myoglobin-induced renal failure is
significant when the CPK concentration is greater than 20,000 units/L. Aside
from an elevated creatinine, potassium, and CPK, rhabdomyolysis is
suggested when a urine dipstick tests positive for blood, but no red
blood cells are seen on microscopy. This finding is caused by myoglobin in
the urine. The risk of rhabdomyolysis-induced renal failure may be decreased

with aggressive hydration. Mannitol and urine alkalinization may also be

beneficial.
Drug Induced/Interstitial Nephritis - Drug induced interstitial nephritis is
usually caused by cephalosporins, penicillins, sulfonamides, NSAIDs,
rifampin, phenytoin and allopurinol. Patients present with arthralgias,
rash, renal failure and the urinalysis will show eosinophiluria.
Discontinuing the offending agent is the treatment of drug-induced
interstitial nephritis.
Analgesic nephropathy is the most common form of drug-induced chronic
renal failure. It accounts for 3-5% of end stage renal disease in the USA, and
is most commonly seen in females (peak at age 50-55 years) who
habitually use combined analgesics (e.g., aspirin and naproxen). It is
generally seen after cumulative ingestion of 2-3 kg (4.4-6.6 lbs) of the index
drug. Papillary necrosis and chronic tubulointerstitial nephritis are
the most common pathologies seen. Polyuria and STERILE PYURIA (WBC
casts may also be seen) are early manifestations. Microscopic hematuria and
renal colic may occur following sloughing of renal papilla. Hypertension,
mild proteinuria, and impaired urinary concentration commonly occur as the
disease advances. In severe cases, nephrotic range proteinuria can be seen.
Patients with chronic analgesic abuse are also more likely to develop
premature aging, atherosclerotic vascular disease, and urinary tract cancer.

Analgesic Nephropathy Long term analgesics Hx + Gradual Renal

Failure + Sterile Pyuria.

Papillary necrosis refers to ischemic necrosis in the renal papillae.

Analgesic overuse is the most common cause, but diabetes mellitus,
infections, urinary tract obstruction, hemoglobinopathies like Sickle
Cell Trait, cirrhosis, congestive heart failure, shock and hemophilia can also
be associated. There would not be a palpable mass on physical examination.

Crystalline Nephropathy - Acyclovir is excreted principally in the urine via

glomerular filtration and tubular secretion. When the acyclovir concentration
in the collecting duct exceeds its solubility, crystallization, crystalluria and
renal tubular damage may result. In most cases, this toxic complication is
transient and can be prevented (as well as treated) with adequate
hydration and dosage adjustment, which includes slowing the rate of
intravenous infusion.
Cyclosporine Induced Nephrotoxicity - Cyclosporine is a commonly used
immunosuppressant. It acts by inhibiting the transcription of inferleukin-2
and several other cytokines, mainly the T-helper lymphocytes.
Some of the most common side effects of cyclosporine are:
1. Nephrotoxicity: This is the most common and serious side effect. It
may manifest as reversible acute azotemia or irreversible progressive
renal disease. Hyperuricemia with accelerated gout, hyperkalemia,
hypophosphatemia, and hypomagnesemia can be seen as
manifestations of renal-induced dysfunction. Rarely, hemolytic uremic
syndrome (HUS) may be seen.
2. Hypertension: This is due to renal vasoconstriction and sodium
retention. It is generally seen in the first few weeks of therapy. Calcium
channel blockers are the drugs of choice for treatment.
3. Neurotoxicity: This is often reversible. It manifests as headache.
visual disturbances, seizure, mild tremors & akinetic mutism.
4. Glucose intolerance: This is fairly common. Patients who are
concurrently taking prednisone (steroids) might develop significant
hyperglycemia.
5. Infection: Chronic therapy with cyclosporine is associated with
infection in 40% of patients.

6. Malignancy: There is an increased risk of squamous cell carcinoma of

the skin and lymphoproliferative diseases.
7. Gingival hypertrophy and hirsutism.
8. Gl manifestations such as anorexia, nausea, vomiting, and diarrhea:
These are fairly common but mild.
Tacrolimus is a macrolide antibiotic produced by fungi. It has the same
mechanism of action as
cyclosporine and has a similar toxicity profile (including nephrotoxicity and
hyperkalemia); however, in contrast to cyclosporine, tacrolimus does not
cause hirsutism or gum hypertrophy, and has a higher incidence of
neurotoxicity, diarrhea, and glucose intolerance.
The major toxicity of azathioprine is dose-related diarrhea, leukopenia,
and hepatotoxicity.
The major toxicity of Mycophenolate is bone Marrow suppression.
Aminoglycosides are antibiotics used to treat serious gram-negative
infections. They are potentially nephrotoxic and drugs levels and renal
function must be monitored closely during therapy.
Mixed Cryoglobulinemia - Suspect mixed cryoglobulinemia in a patient
who presents with palpable purpura, proteinuria and hematuria. Other
suggestive clinical manifestations include nonspecific systemic symptoms,
arthralgias, hepatosplenomegaly and hypocomplementemia. The
demonstration of circulating cryoglobulins is confirmatory. Majority of
patients have an underlying HCV infection. For this reason, all such patients
should be tested for HCV antibodies.
AKI is divided into prerenal (structurally intact nephrons), intrinsic renal
(structural and functional nephron damage) and postrenal causes (urinary
obstruction). Prerenal AKI is a functional response to decreased effective
arterial volume to the kidney, which activates the renin-angiotensinaldosterone axis and the sympathetic nervous system. Initially, angiotensin
constricts the glomerular efferent arterioles and prostaglandins dilate the
glomerular afferent arteriole to try and maintain glomerular filtration rate
(GFR). However, further volume depletion overwhelms this adaptive
response and leads to renal vasoconstriction & a further decrease in the
GFR and worsening renal function. Prerenal azotemia due to intravascular
volume depletion is rapidly reversible with intravenous volume resuscitation

but persistent untreated renal hypoperfusion will lead ultimately to intrinsic

renal failure due to ischemia.
The elderly, who have a diminished thirst response and a reduced
ability to self-administer fluids, are at the greatest risk of prerenal
azotemia. She also takes lisinopril (which prevents the action of
angiotensin) and aspirin (which inhibits the effects of prostaglandins), which
further worsens the above response and the prerenal azotemia.
Elderly patients with poor oral intake living in nursing homes and
taking medications such as NSAIDs, ACE inhibitors and diuretics
should be suspected of having prerenal azotemia due to
intravascular volume depletion and poor renal perfusion.
Hematuria Location of Origin - Blood at the beginning of urination (initial
hematuria) typically indicates a lesion in the urethra such as urethritis.
Hematuria at the end of voiding, called terminal hematuria, often suggests a
prostatic or bladder cause. Hematuria during the entire urinary cycle (total
hematuria) may indicate disease within the ureters or kidneys. A renal cause
of hematuria will not show clots. This patient has painless terminal hematuria
with clots and should be evaluated for bladder cancer by cystoscopy.
Renal Casts
Muddy brown granular cast- Acute tubular necrosis
RBC casts - Glomerulonephritis
WBC casts - Interstitial nephritis and pyelonephritis
Fatty casts - Nephrotic syndrome
Broad and waxy casts - Chronic renal failure

Renal Cysts
Simlpe Renal Cysts - Such cysts are most commonly seen in patients over
the age of 50. These are benign and often discovered incidentally by
radiological examination. Most of the time, these do not cause hypertension,
flank pain, hematuria, or proteinuria. Rarely, infection may occur. On a CT
scan, they appear as unilocular mass with regular borders & septae
within the cavity. Simple observation is all that is needed. No follow-up
evaluation is required.

Before giving the diagnosis of simple renal cyst, it is important to make sure
that the mass does not have the following findings of a Complex cyst.
1.
2.
3.
4.

A multilocular mass
Thickened, irregular walls
Thickened septae within the mass
Contrast enhancement

Autosomal Dominant Polycystic Kidney Disease (ADPKD)- The clues to

the correct diagnosis are hypertension, palpable bilateral abdominal
masses and microhematuria. Intracranial berry aneurysm is a
common complication, and is seen in 5 to 1 0% of the cases. Although
such aneurysms are common and dangerous when coupled with
hypertension, routine screening for intracranial aneurysms is not
recommended. The other major extra-renal complications of ADPKD are:
1. Hepatic cysts - most common extrarenal manifestations of ADPKD
2. Valvular heart disease - most often mitral valve prolapse and aortic
regurgitation
3. Colonic diverticula
4. Abdominal wall and inguinal hernia
Please note: the enlarged right kidney is easier to palpate because
it lies lower than the left kidney! The liver might be enlarged due to
cystic involvement.
Dehydration - The classic signs of dehydration are altered mental status,
dry oral mucosa, marginally high values of serum electrolytes and

hematocrit, and a BUN/creatinine ratio more than 20. Elderly patients

are especially prone to dehydration after various or even minor insults (a
minor febrile illness). The predisposing factors of elderly patients to
dehydration include: decreased thirst response to dehydration, impaired
renal sodium conservation, and impaired renal concentration ability. The
mainstay of treatment is administration of intravenous sodiumcontaining crystalloid solutions. Rehydration therapy in elderly patients
should be undertaken with caution because sodium loading can unmask
subclinical heart failure.

End stage renal disease is a progressive condition that is fatal if left

untreated. Once end stage renal disease develops. There are only two
treatment options available: dialysis or renal transplantation. The choice
depends on the patient and co-morbid conditions; however, if both options
are available, renal transplantation is preferred. as it is associated with
better survival and quality of life. The advantages of renal transplantation
over dialysis are:
1. Better survival and quality of life.
2. Anemia, bone disease and hypertension persist in spite of dialysis;
these are better controlled with transplantation.
3. Transplant patients have a return of normal endocrine, sexual, and
reproductive functions and enhanced energy levels; thus, returning to
fulltime employment and more strenuous physical activity is possible.
4. In diabetics, autonomic neuropathy persists or worsens after dialysis;
whereas. it stabilizes or improves with transplantation.
5. Expected survival rate after transplantation is 95% at one year and
88% at five years.
The major disadvantages of renal transplantation are difficulty in finding a
donor, surgical risk and cost, and side effects of immunosuppression.
Transplantation from a living related donor has the least graft rejection
and best graft survival, followed by a living non-related donor, and
cadaver graft.
Dialysis options include hemodialysis (home or in-center) or peritoneal
dialysis (chronic ambulatory or cyclic peritoneal dialysis). In the US, 85% of
patients have in-center hemodialysis. 15% have peritoneal dialysis, and
approximately 1% have home hemodialysis. The choice depends on the
patient. Peritoneal hemodialysis provides the patient with more control and
mobility, but the risk of peritonitis is high. The five-year survival rate in

non-diabetic patients who are on dialysis is 30-40%; whereas, in diabetics, it

is 20%.
Uremic Pericarditis these patients present with chest pain (i.e .. nonradiating. retrosternal, relieved by leaning forward). The typical EKG findings
are also given (i.e .. diffuse ST elevation that is typically concave up, and
elevation of the PR segment in lead aVR), PR segment depression in the
other limb leads is also characteristic. Pericardial friction rub may be
found on examination.
The most common cause of acute pericarditis is a viral infection. Other
causes include bacterial infections, connective tissue diseases (e.g .. SLE)
and uremia. In Uremic Pericarditis, the patient's oliguria, hypertension,
urinalysis findings (e.g .. red cell casts. proteinuria) and azotemia suggest
the diagnosis of nephritic syndrome, which led to the development of uremic
pericarditis.
The development of pericarditis in a patient with renal failure is an indication
for dialysis. Hemodialysis is the procedure of choice in such cases.
The indications for hemodialysis are:
1. Refractory hyperkalemia
2. Volume overload or pulmonary edema not responding to diuretics
3. Refractory metabolic acidosis (pH <7.2)
4. Uremic pericarditis
5. Uremic encephalopathy or neuropathy
6. Coagulopathy due to renal failure.
Cardiovascular disease is the most common cause of death in the general
population, but the rates are declining. Interestingly, this recent trend has
not been observed in the dialysis population. Cardiovascular disease
remains as the most common cause of death in dialysis patients. It
accounts for approximately 50% of deaths in this group of patients. Of these
deaths, 20% are attributed to acute myocardial infarction and approximately
60% to sudden cardiac deaths.
The following risk factors are associated with cardiovascular disease in
dialysis patients:
Risk factors not related to dialysis: A large number of patients on dialysis
already have multiple risk factors for cardiovascular disease. These are:
Hypertension (96%)
Diabetes (54%)
Low serum HDL cholesterol (33%)
Left ventricular hypertrophy by ECG criteria (22%)

 Coronary artery disease: Approximately 75% of patients with total endstage renal disease have at least a 50% narrowing of at least one coronary
artery.
Increased age: The average age of patients at the start of dialysis is about
60 years.
Additional risk factors due to end stage renal disease and dialysis are:
End stage renal disease: This, by itself, is an independent risk factor for
cardiovascular disease.
Anemia.
Metabolic abnormality, particularly hyperphosphatemia, and increased
PTH levels.
Increased homocysteine levels: These are due to impaired metabolism and
decreased removal.
Accelerated atherogenesis in dialysis patients: This is due to
enhanced oxidant stress due to uremia and bio-incompatible renal
replacementtherapies.
Increased calcium intake (calcium is given to correct hyperphosphatemia in
dialysis patients):
This enhances coronary artery calcification.
Inhibition of NO: This is a common finding in dialysis patients, and can
cause vasoconstriction and hypertension.
Hyperkalemia It is when K + > 5.2 mmol/L. Hyperkalemia can be caused
by decreased renal K + excretion, transcellular shift, increased K + intake,
medications (e.g ..potassium-sparing diuretics, ACE inhibitors, NSAIDS) and
pseudohyperkalemia. Pseudohyperkalemia should always be considered in
asymptomatic patients, as occasionally the lab sample can become
hemolysed during venipuncture. Always look for drugs that might cause
hyperkalemia.
Treatment of hyperkalemia depends on the cause and rapidity of rise of
serum potassium levels. The available options are calcium gluconate, sodium
bicarbonate, insulin drip with dextrose, diuretics, cation exchange resins,
beta agonist inhalations, and dialysis.
Of all the available options, removal of K+ from the body can be achieved
using diuretics, cation-exchange resin, or dialysis. Kayexalate, or
sodium polystyrene sulfonate is a cation-exchange resin which acts in the Gl
tract by promoting the exchange of Na+ for K +, and thereby increasing the
excretion of K +.
The most serious effect of hyperkalemia is cardiac toxicity; therefore, all
patients with hyperkalemia should have an EKG performed. The earliest EKG
changes include increased T-wave amplitude (peaked T waves), followed by

prolonged PR interval and QRS duration and eventual loss of P waves.

Progressive widening of the QRS complex and merging with the T wave
produces a sine-wave pattern. This can progress towards the terminal event,
which is usually ventricular fibrillation or asystole.
The approach to treatment depends on the EKG changes and degree of
hyperkalemia. Immediate treatment is indicated if there is cardiac
toxicity (as evidenced by EKG changes), muscular paralysis or K + > 6.5.
For these patients, 10 ml of 10% calcium gluconate should be
administered to stabilize the myocardial membrane. To lower the K + level,
insulin and/or B2-agonists may be used since either of these drugs can shift
K + into cells. Sodium bicarbonate can also be used to shift K + into cells.
Slower acting treatments to increase K + excretion include loop and thiazide
diuretics if renal function is adequate, and cation exchange resins. Dialysis
should be reserved for patients with renal failure and those with severe lifethreatening hyperkalemia that is unresponsive to the more conservative
measures.
In case the patient is asymptomatic and with normal EKG findings (i.e ..
without indications for immediate drug therapy); He may be treated less
aggressively by simply stopping usage of the causative drug (i.e ..
amiloride) and rechecking his blood levels after one week.

Anemia of Renal Failure - Normochromic normocytic anemia due to

erythropoietin deficiency is very common in patients with end stage renal
disease. Recombinant erythropoietin is the treatment of choice; however,
iron supplements should be given before erythropoietin in patients with
evidence of iron deficiency. All patients with chronic renal failure and
hematocrit < 30% (or hemoglobin < 1 Og/dl) are candidates for recombinant
erythropoietin therapy
after iron deficiency has been ruled out. Erythropoietin is also indicated in
hemodialysis patients who have symptoms attributed in part to anemia.
Some of the most common side effects of erythropoietin therapy are:
1. Worsening of hypertension: This is seen in approximately 30% of
patients. 20-50% of patients receiving IV erythropoietin. Patients will
have more than a 10 mmHg rise in diastolic BP. This rise in BP is less
common after the S.C. route of erythropoietin, as compared to the IV
route. Even hypertensive encephalopathy can occur when there is a
rapid rise in BP. Exactly how erythropoietin causes hypertension is not
well understood. Treatment includes fluid removal (by dialysis) and use
of anti-hypertensive drugs (beta blockers and vasodilators are
preferred). Prevention involves slowly raising the hematocrit, with a
goal hematocrit of 30-35%.

2. Headaches: These are seen in 15% of patients.

3. Flu-like syndrome: This is seen in 5% of patients. It is responsive to
anti-inflammatory drugs, and is less commonly seen with
subcutaneous erythropoietin administration.
4. Red cell aplasia: This is a rare, but potential side effect.

Uremic Platelet Dysfunction - Abnormal hemostasis is a common

manifestation seen in patients with chronic renal failure. Abnormal bleeding
and bruising are characteristic of uremic coagulopathy. Nowadays,
ecchymoses and epistaxis are the only major bleeding manifestations seen
due to the advent of dialysis; however, Gl bleeding, hemopericardium,
subdural hematoma, and bleeding from surgical or invasive sites can
still occur due to uremic coagulopathy.
The pathogenesis is multifactorial, but the major defect involves plateletvessel wall and platelet-platelet interaction. Several uremic toxins have been
implicated in the pathogenesis of platelet dysfunction seen in chronic renal
failure (CRF), the chief among which is guanidinosuccinic acid. Activated
partial thromboplastin ( aPTT), prothrombin (PT), and thrombin times (TT) are
generally normal. Bleeding time (BT) is reflective of platelet function, and
is usually prolonged. The platelet count is normal, but there is platelet
dysfunction that causes bleeding.
A number of agents such as desmopressin (DDAVP), cryoprecipitate, and
conjugated estrogens have been used to correct the coagulopathy in uremic
patients. DDAVP increases the release of factor Vlll:von Willebrand factor
multimers from endothelial storage sites.

Hepatorenal syndrome (HRS) is one of the most dangerous complications

of end-stage liver disease, occurring in up to 10% of patients with cirrhosis.
HRS is characterized by decreased glomerular filtration in the absence of
shock, proteinuria, or other clear cause of renal dysfunction, and a failure
to respond to a 1 .5 L normal saline bolus. It is thought to result from
renal vasoconstriction in response to decreased total renal blood flow and
vasodilatory substance synthesis. There are 2 subtypes of HRS. Type 1 is
rapidly progressive; most patients die within 10 weeks without treatment.
Type 2 progresses more slowly, with an average survival of 3-6 months. The
most common causes of death are infection and hemorrhage.

Unfortunately, no medication has consistently proven beneficial in HRS and

the mortality for these patients placed on dialysis is very high. Liver
transplantation is the only intervention with established benefit.

Renal transplant dysfunction in the early post-operative period can be

explained by a variety of causes, including ureteral obstruction, acute
rejection, cyclosporine toxicity, vascular obstruction, and acute tubular
necrosis. Radioisotope scanning, renal ultrasound, MRI, and renal biopsy can
be employed in conducting a differential diagnosis. Acute rejection is best
treated with intravenous steroids

Metformin should not be given to patients with acute renal failure, hepatic
failure, or sepsis. These conditions all increase the chance of developing
lactic acidosis.

Fibromuscular Dysplasia - These patients present with headache,

elevated blood pressure & a renal bruit. It is highly suggestive of
renovascular hypertension secondary to renal artery stenosis.
The usual cause of renal artery stenosis in young adults is fibromuscular
dysplasia.
In older patients, the cause is usually an atheromatous plaque.
The goals of treatment are to decrease blood pressure and restore perfusion
to the ischemic kidney. lnterventional therapy is more effective than medical
management alone; hence. angioplasty with stent placement is the best
treatment option for this patient.
For patients with fibromuscular dysplasia, surgery is recommended only if
angioplasty fails.
Angioplasty with stent placement remains the treatment of choice in this
patient.
Renal Cell Carcinoma - Most RCC patients are asymptomatic until the
disease is advanced. The classic triad of RCC (flank pain, hematuria, and
a palpable abdominal renal mass) is found in only 10% of patients; when
present, it strongly suggests advanced/metastatic disease. Hematuria is
seen in about 40% of patients and signifies tumor invasion of the collecting
system. Scrotal varicoceles (most are left-sided) are observed in about

10% of patients. Varicoceles typically fail to empty when the patient is

recumbent due to tumor obstruction of the gonadal vein where it enters the
renal vein. Presence of this finding should always raise suspicion for mass
obstruction to venous flow, as is seen in RCC.

Twenty percent of patients may also have constitutional symptoms such as

fever, night sweats, anorexia, weight loss, or easy fatigability. Ectopic
production of erythropoietin by the tumor can produce polycythemia &
thrombocytosis, although most advanced tumors are associated with
anemia. CT scan of the abdomen is the most sensitive and specific
test for diagnosing RCC and should be obtained when the index of
suspicion is high.
Bladder Cancer - These patients experience gross painless hematuria.
In adults, gross hematuria should be considered to be due to a kidney, ureter
or bladder malignancy until proven otherwise as it is the initial presenting
sign in up to 80% of such tumors. The appropriate initial investigations in a
patient with painless gross hematuria are assessment of the upper urinary
tract with a contrast CT scan or intravenous pyelogram as well as
endoscopic assessment of the bladder and urethra. The most common
causes of hematuria in the United States are neoplasms, infections, trauma,
nephrolithiasis, glomerulonephritis and prostatic disease. The presence of
erythrocytes in the urine should always be confirmed microscopically
because grossly red urine may also occur in myoglobinuria, hemoglobinuria
or porphyria, following the consumption of a large amount of beets or as an
adverse effect of certain medications such as rifampin.

External Genital Diseases

Priapism - Trazodone is an antidepressant which is mainly used for sleep
disturbances. Its disturbing side effect is priapism, which is a persistent,
painful erection that develops without sexual stimulation and has a long
duration. Remember the common causes of priapism:
1. Sickle cell disease and leukemia - usually in children or adolescents
2. Perineal or genital trauma - results in laceration of the cavernous
artery
3. Neurogenic lesions- such as spinal cord injury, cauda equina
compression, etc.
4. Medications - such as trazodone and prazosin.

Cholesterol Embolization - This characteristic syndrome occurs when

portions of an atherosclerotic plaque break off and travel distally into the
circulation. While cholesterol embolization may occur spontaneously, the
majority of cases are preceded by angiography where the plaque is
presumably disrupted by a catheter or guidewire. Skin manifestations in the
feet are common, with this disorder sometimes referred to as "blue toe"
syndrome. Livedo reticularis, or reddish to cyanotic reticular
discoloration of the skin, may be seen as well. Acute renal failure, as
manifested by this patient's elevated creatinine, is commonly present in the
disorder secondary to emboli traveling to the renal arteries. Gastrointestinal
symptoms such as abdominal pain and nausea are often present. Patients
may develop pancreatitis as well. Increased eosinophils in the blood
and/or urine as well as decreased complement levels are suggestive of the
diagnosis.
Anabolic Steroids Abuse - Anabolic steroids are commonly used by many
bodybuilders and athletes to enhance performance and muscle mass.
Anabolic steroids contain exogenous androgens that inhibit GnRH release
by the hypothalamus (due to feedback inhibition), which causes decreased
LH and FSH release by the pituitary gland and leads to decreased sperm
and testosterone production by the testes. The exogenous androgen
suppresses native testosterone production but is detected as testosterone by
current assays, so patients can have normal serum testosterone levels. Other
adverse effects include acne, gynecomastia (due to conversion of the
androgens to estrone), decreased testicular size, aggressiveness, and
psychotic symptoms. Laboratory findings can show erythrocytosis (due
to increased erythropoiesis) with elevated hemoglobin, cholestasis, hepatic

failure, dyslipidemia, and slightly elevated creatinine (due to increased

muscle mass).
Multiple Myeloma - Any elderly patient with bone pain, renal failure,
and hypercalcemia has multiple myeloma until proven otherwise.
Approximately 50% of multiple myeloma patients develop some degree of
renal insufficiency; this is most likely due to obstruction of the distal and
collecting tubules by large laminated casts containing paraproteins
(mainly Bence Jones protein).