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USMLE Step 2 CK
l Internal Medicine
Rhabdomyolysis is associated with a very rapidly rising creatinine level. This is because of
both the renal failure and massive release of muscle products. Thus, the BUN:creatinine ratio
may be low, below 10:1.
Treatment. If there are EKG abnormalities from the hyperkalemia the best initial therapy is
calcium chloride or gluconate. In general, therapy consists of hydration and mannitol as a
diuretic to decrease the duration of contact between the nephrotoxic hemoglobin or myoglobin and the kidney tubule. Alkalinizing the urine with bicarbonate may help prevent the
precipitation of the pigment in the tubule.
Proteins
Bence-Jones proteins, such as in myeloma, also cause tubular damage. Myeloma is most
prominently a cause of nephritic syndrome, however, not tubular damage.
A man with myeloma is being evaluated for an elevated creatinine. His UA shows
trace positive for protein, but the 24-hour urine shows 5 grams of protein. What
is the etiology of this discrepancy?
Crystals
Oxalate. The most common cause of hyperoxaluria resulting in acute renal failure is from
ethylene glycol overdose in a suicidal person who ingests antifreeze. Look for an intoxicated
person with a metabolic acidosis with an elevated anion gap who is found to have renal insufficiency. The diagnosis is confirmed by finding oxalate crystals on a UA. Oxalate crystals are
shaped like envelopes.
Acute ethylene glycol overdose is treated with fomepizole infusion to prevent the formation of
the toxic metabolite of ethylene glycol, which is oxalic acid. Fomepizole is preferred. It is the
oxalic acid that causes the renal failure. Dialysis must also be used to then remove the ethylene
glycol. Sodium bicarbonate can be given to correct acidosis.
Chronic hyperoxaluria and kidney stones can be caused by Crohn’s disease because of fat and
calcium malabsorption.
Urate. Acute renal failure from uric acid toxicity occurs in the setting of tumor lysis syndrome. This is why patients with leukemia or lymphoma receive vigorous hydration and allopurinol prior to being given chemotherapy. Allopurinol reduces the production of uric acid
by inhibiting conversion of xanthine to hypoxanthine to uric acid. Uric acid stones precipitate
in an acidic urine, unlike oxalate crystals, which precipitate in alkaline urine. Allopurinol
treatment with alkalinization of urine markedly reduces the risk of uric acid nephropathy.
Chronically, gout causes renal impairment through a slower and milder version of the same
mechanism. The diagnosis is by finding uric acid crystals in the urine.
270
Hypercalcemia
Calcium precipitates in the kidney tubule, forming stones. In addition, hypercalcemia can lead
to distal RTA and nephrogenic diabetes insipidus. The most common cause of hypercalcemia is
primary hyperparathyroidism. If there is no renal damage or decrease in GFR and there are no
symptoms, then mild hyperparathyroidism is not treated surgically. If the hyperparathyroidism is
associated with evidence of renal impairment, then surgical resection of the glands is performed.
Toxins
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The most common toxins to be associated with renal insufficiency and ATN are NSAIDs, aminoglycosides, cephalosporins, contrast agents, amphotericin, chemotherapy such as cisplatin,
radiation effect, heavy metals such as lead, mercury, or gold, and cyclosporine. The difference
between the basis of allergic interstitial nephritis and direct toxins is that allergic nephritis
occurs with the first dose and is associated with fever, rash, joint pain, and eosinophils in both
blood and urine.
Direct acting toxins can take several days to weeks to result in enough cumulative toxicity to
lead to renal failure and are not associated with eosinophils, fever, joint pains, or rash. There
is no specific test to confirm a specific toxin as the etiology of the renal failure. You must
exclude the other causes of renal failure and find the toxin in the history. There is no specific
therapy to reverse the renal insufficiency of any of the direct acting toxins.
Aminoglycosides. Tobramycin is the least nephrotoxic compared with gentamicin and amikacin.
Aminoglycoside toxicity generally takes 5–10 days of administration to result in toxicity. The
likelihood of toxicity is associated with trough levels. Renal failure due to aminoglycosides is
frequently non-oliguric (K+ levels not elevated). Hypokalemia and hypomagnesemia predispose
the patient to aminoglycoside toxicity. The ability of antibiotics to kill bacteria is associated with
the peak level, but the likelihood of toxicity is associated with the trough level. This is most likely
because a low trough allows time for the renal tubular cells and neural cells of the inner ear to
regenerate themselves. Aminoglycosides also exert a bactericidal effect after their level has become
low because they enter the bacteria and continue to kill. This ability to exert an effect despite low
or absent levels is called postantibiotic effect. Hence, aminoglycosides should be given once a day.
Once-a-day dosing allows high bactericidal levels with the same efficacy and very low trough levels. The low trough levels reduce toxicity. Aminoglycoside-related nephrotoxicity is estimated to
be between 10–20% of all drug-induced nephrotoxicity and is usually reversible.
Chapter 8
l Nephrology
Amphotericin B. This medication is associated with renal insufficiency as well as distal renal
will develop a high creatinine as well as a decreased magnesium, bicarbonate, and potassium
level. These often revert to normal after the medication is stopped. This form of toxicity is
from cumulative dosing.
Atheroembolic Disease. Look for a patient who undergoes a vascular catheter procedure such
as angioplasty who develops renal failure several days later. Atheroemboli are also associated
with eosinophilia, low complement levels, bluish discoloration of the fingers and toes, and
livedo reticularis. Although the most accurate test is a skin biopsy to see cholesterol crystals in
the skin, this is rarely done. There is no therapy for atheroemboli. High doses of statins have
been tried.
Contrast Agents. Radiocontrast material for CT scanning can result in renal failure in as
little as 12–24 hours after the use of the agent. This is one of the main ways to distinguish
this form of renal failure from aminoglycoside or amphotericin toxicity, which need several
days to weeks of cumulative exposure. The rise in creatinine peaks at 3–5 days after the injury.
The BUN and creatinine may be up in a 20:1 ratio, such as in prerenal azotemia, because the
hypertonicity of the agent provokes an intense vasospasm of the afferent arteriole. The worse
the underlying renal parenchyma, the more likely the patient is to have renal failure secondary
to contrast material. If you are elderly, diabetic, and hypertensive with myeloma, you are far
more likely to experience contrast-induced renal insufficiency.
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l Internal Medicine
Other Toxins. Pentamidine is associated with renal failure in addition to its toxicity on the
pancreas. Vancomycin, cyclosporine, and lithium can all cause renal failure in a dose-dependent fashion. Indinavir is a protease inhibitor that results in renal failure usually from the
drug precipitating out in the kidney tubules. Indinavir stones need contrast to be identified
on a spiral CT scan.
Analgesic nephropathy
NSAIDs are a frequent cause of renal failure. NSAIDS cause renal failure by several mechanisms:
• Interstitial nephritis
• Direct toxic effect on the tubules
• Papillary necrosis
• Inhibition of vasodilatory prostaglandins in the afferent arteriole
• Membranous glomerulonephritis
A person without underlying renal insufficiency should not experience a rise in creatinine
from the use of NSAIDs. This only occurs in those with significant impairment such as the
elderly or those with hypertension or diabetes. NSAIDs can also cause toxicity by a combination of these. More than half the patients have pyuria, which if persistently associated with
sterile urine can be an important clue to diagnosis. There is no specific test to confirm that
NSAIDs caused the renal failure. You see a rise in BUN and creatinine and a history of the use
of NSAIDs. There is no specific therapy.
Papillary necrosis
Acute papillary necrosis occurs in patients with a history of sickle cell disease, diabetes, urinary obstruction, or chronic pyelonephritis. It can be brought on acutely by the ingestion
of NSAIDs. The presentation is with the sudden onset of flank pain, hematuria, pyuria, and
fever. This can be very similar in presentation to acute pyelonephritis. In a patient with the
risks described above, symptoms for papillary necrosis will come on very suddenly. The findings of white and red cells on UA will not distinguish them. However, papillary necrosis will
not grow any organisms on culture. The most accurate diagnostic test for papillary necrosis
is a CT scan. The CT scan will show “bumpy” contours in the renal pelvis where the papillae
have sloughed off. There is no specific therapy for papillary necrosis.
Prevention of contrast-induced renal failure
In those patients with significant underlying renal disease who have an unavoidable radiologic procedure requiring contrast, you must hydrate with 1–2 liters of normal saline over 12
hours before the procedure. Hydration has been shown to decrease the likelihood of contrastinduced renal failure. Bicarbonate and N-acetyl cysteine have also been shown to decrease the
risk of renal failure. Ineffective preventive measures are diuretics such as furosemide or mannitol. If the question asks, “Which of the following is most likely to prevent the development
of renal failure with contrast?” you should answer hydration.
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GLOMERULONEPHRITIS
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Glomerulonephritis (GN) is an inflammation of the glomerulus, often on the basis of an autoimmune event, circulating antibodies, or vasculitis. Diabetes and hypertension cause glomerular disease and are certainly the most common causes of nephrotic syndrome and end stage
renal disease. Diabetes and hypertension, however, do not have the acute inflammatory stage of
glomerulonephritis characterized by hematuria.
All forms of GN can be characterized by edema, hematuria, red cell casts, and hypertension.
The red cells develop an abnormal shape as they squeeze through the abnormal glomerulus
and are termed “dysmorphic.” The edema of GN is found first in areas of low tissue tension,
such as the periorbital area or the scrotum. When more severe, edema can be found anywhere.
With the salt and water retention leading to edema, you also develop hypertension. GN is also
characterized by modest amounts of protein in the urine with the daily total being <2 grams
per 24 hours, although by definition nephrotic syndrome does not begin until there are >3.5
grams per 24 hours. The most important distinction between GN and nephrotic syndrome is
the degree of proteinuria.
Glomerulonephritis is also characterized by low urine sodium with a fractional excretion of
sodium of <1%.
Many, but not all, forms of GN have a characteristic blood test such as ANCA, basement
membrane antibodies, ANA, or antistreptolysin. However, the single most important test
to diagnose GN is the renal biopsy. Unlike in tubular diseases, the renal biopsy is extremely
important in GN because it guides therapy. There are few treatments to reverse a form of
ATN based on the specific etiology. In GN, however, there are cytotoxic medications such as
cyclophosphamide to use, or other treatments such as mycophenolate for SLE nephritis or
plasmapheresis for Goodpasture syndrome. Hence, before we commit a patient to long-term
therapy with potentially harmful medications (cyclophosphamide causes hemorrhagic cystitis), we should obtain a precise diagnosis.
Chapter 8
l Nephrology
Table 8-2. Causes of Glomerulonephritis Disease Spectrum
Vascular Disease Glomerular Disease
Wegener granulomatosis Goodpasture syndrome
Churg-Strauss syndrome Postinfectious glomerulonephritis
Henoch-Schönlein purpura IgA nephropathy (Berger disease)
Polyarteritis nodosa SLE
Thrombotic thrombocytopenic
purpura (TTP)
Hemolytic uremic syndrome (HUS) Alport syndrome
Cryoglobulinemia Diabetes and hypertension (most common
Idiopathic rapidly progressive
glomerulonephritis
causes)
Amyloid
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Wegener Granulomatosis
Wegener granulomatosis (WG) is characterized by systemic vasculitis that most often involves
the kidney, lung, and upper respiratory tract such as the sinuses or middle ear. In a patient with
chronic upper and lower respiratory illness, not responding to antibiotics should evoke WG as a
possibility. If there is renal disease as well, then WG is the most likely diagnosis. In addition, WG
can have involvement of the skin (50%), joints, eyes (50%), and GI tract, as well as neuropathy.
Laboratory abnormalities are elevated ESR, anemia, and leukocytosis. Rheumatoid factor is
positive in 50%. These findings are rather nonspecific and could be found in almost any vasculitis or chronic infectious or inflammatory condition. The best initial test that is specific
for WG is the anti-proteinase-3 antibody, which is also known as cytoplasmic antineutrophil
cytoplasmic antibody, or C-ANCA. The perinuclear pattern, or P-ANCA, is found in a much
smaller number. The other name for P-ANCA is antimyeloperoxidase antibody. Complement
levels are normal in WG.
The most accurate test for WG is a biopsy of the kidney, nasal septum, or lung looking for
granulomas. Sinus biopsy, specifically the nasal septum, is less sensitive and has more false
negative results. Treatment is with cyclophosphamide and steroids.
Churg-Strauss Syndrome
Churg-Strauss syndrome (CS) is a vasculitis similar to Wegener granulomatosis and is also
characterized by chronic lung involvement, neuropathy, skin lesions, GI, cardiac, and renal
involvement. All forms of vasculitis are characterized by fever, weight loss, and a generalized
malaise. CS is characterized by a history of asthma, eosinophilia, and other atopic diseases.
The characteristic diagnostic tests are the elevated eosinophil count and positive P-ANCA or
antimyeloperoxidase. The most accurate test is a lung biopsy showing the granulomas and
eosinophils. Treatment is with glucocorticoids and cyclophosphamide.
Goodpasture Syndrome
Goodpasture syndrome (GP) is an idiopathic disorder of renal and lung disease characterized by a unique antibasement membrane antibody. Unlike Wegener or Churg-Strauss, GP
does not affect multiple organs or sites in the body besides the lung and the kidney. Hence,
the absence of skin or eye findings is a clue to the diagnosis. One-third of patients have no
lung involvement and they only present with hematuria and proteinuria. Lung involvement is
characterized by hemoptysis, cough, and shortness of breath. There will be hemosiderin-laden
macrophages. The macrophages are cells that phagocytose free hemoglobin in the lung where
it is metabolized to hemosiderin. The best initial test to confirm the diagnosis is the level of
antibasement membrane antibodies to type IV collagen. The single most accurate test is a
lung or kidney biopsy. The biopsy shows linear deposits on immunofluorescence. Therapy is
with plasmapheresis and steroids. Cyclophosphamide may also help.
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Polyarteritis Nodosa
Polyarteritis nodosa (PAN) is a systemic vasculitis of small- and medium-sized arteries that
affects virtually every organ in the body with the exception of the lung. In PAN, renal involvement is common and manifests as hypertension, renal insufficiency, and hemorrhage due to
microaneurysms. The most accurate diagnostic test is a biopsy, and treatment is with cyclophosphamide and steroids.
Like all vasculitides, PAN is associated with fever, weight loss, and malaise. Like WG and
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Churg-Strauss, there is involvement of the skin, eyes, muscles, GI tract, heart, kidneys, and
neurologic system. Although the liver is involved, there is usually no clinically evident hepatic
effect. Hepatitis B is associated with 10–30% of patients. This is especially true in injection
drug users. Abdominal pain and joint pain may be prominent. The abdominal pain may mimic
mesenteric ischemia, and the pain will occur with eating. In this case, an angiogram of the
involved vessels in the GI tract may eliminate the need for a biopsy. The sural nerve is a frequent location for the biopsy. Anemia and an elevated sedimentation rate are present but are
too nonspecific to be useful diagnostically. P-ANCA is only present in a minority of patients.
Treatment of PAN is with steroids and cyclophosphamide.
Chapter 8
l Nephrology
IgA Nephropathy (Berger Disease)
IgA nephropathy presents with mild hematuria that resolves spontaneously in 30% of patients.
About 40–50% of patients progress to end stage renal disease. Like HSP, this is a disorder of the
deposition of IgA, however, symptoms arise only from the kidney. Hypertension is frequent.
This is most likely secondary to abnormally increased salt and water retention by the kidney.
Look for an Asian patient under 35 years of age who has had a recent viral illness or pharyngitis
who develops hematuria 1–2 days later. This is to distinguish it from poststreptococcal
glomerulonephritis, in which the renal involvement occurs 1–2 weeks later or longer. Although
this is an IgA deposition disease, blood IgA levels are elevated in only 50% of patients.
Complement levels are normal. The diagnosis is based on finding IgA deposited in the kidney
on biopsy.
The treatment of IgA nephropathy is difficult. There is no proven effective therapy. Anyone
with proteinuria should receive ACE inhibitors or angiotensin receptor blockers (ARB).
When the proteinuria is massive, steroids should be tried. The value of fish oil is marginal.
You trade fishy breath for a minimal possibility of improvement that is not proven. The
presence of proteinuria and hypertension imply a worse course.
Postinfectious Glomerulonephritis
In addition to group A beta hemolytic streptococci (Streptococcus pyogenes), numerous other
infections can be associated with postinfectious glomerulonephritis. Virtually any infectious
agent can cause it, including hepatitis B and C, CMV, and chronic staphylococcal infections
such as endocarditis. In the pre-antibiotic era, glomerulonephritis was the most common
cause of death in endocarditis. Poststreptococcal glomerulonephritis (PSGN) can occur with
either throat or skin infection with Streptococcus pyogenes, although rheumatic fever only
occurs with the strains that cause pharyngitis. PSGN occurs in about 10–15% of patients with
pharyngitis infected with a nephritogenic strain.
Note
Most common glomerulopathy
worldwide.
The presentation is characterized by smoky, cola, or tea-colored urine. This abnormal urine
color is from hematuria, red cell casts, and proteinuria. Periorbital edema and hypertension
are common. The best initial test is the antistreptolysin (ASO) test and the antihyaluronic acid
(AHT) test. Complement levels, particularly C3, are low. The most accurate test is the renal
biopsy showing “humps” on electron microscopy. IgG and C3 will be deposited in the mesangium as subepithelial humps.
Treatment is largely supportive, with management of the fluid overload and hypertension
with diuretics. The vast majority of cases resolve spontaneously. This is why a biopsy is rarely
needed. Antibiotics should be given to eradicate the organism from the pharynx.
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Cryoglobulinemia
Renal disease from cryoglobulinemia is associated with chronic hepatitis C or less commonly
B. Besides the renal disease, cryoglobulinemia is associated with joint pain, neuropathy, and
purpuric skin lesions. This is similar to other types of vasculitis. There is no GI involvement
as there is with Henoch-Schönlein purpura. Cryoglobulinemia is associated with an elevated
ESR and low levels of complement and is confirmed with a test for the cryoglobulins. A positive rheumatoid factor is a marker for the disease as well. The main treatment is to manage
the underlying chronic hepatitis with interferon and ribavirin. For severe disease, pulse doses
of steroids and occasionally plasmapheresis are also used.
Diabetes
The incidence of glomerular involvement in diabetes is directly proportional to the duration
of the diabetes. The standard dipstick becomes positive for albumin at a level 150–300 mg per
24 hours of excretion. Microalbuminuria is a level of protein excretion that is abnormal but is
<300 mg. If albumin is not present on dipstick all patients with diabetes should be screened
for microalbuminuria annually. Annual screening with a serum creatinine level should also be
performed. Treatment for albuminuria is with an ACE inhibitor or ARB. The blood pressure
goal is also lower in diabetes, and <130/80 is optimal. Although a renal biopsy is the most
accurate test for renal involvement in diabetes, it is not routinely performed unless there is the
possibility of another disease causing the renal failure.
SLE
SLE is associated with an enormously wide variation in the degree of renal involvement.
There may be asymptomatic proteinuria or hematuria, or there may be severe renal disease
requiring dialysis. Double-stranded DNA levels go up and complement levels go down as
a marker of severity in flare-ups of the disease. The most accurate test is a biopsy. Biopsy is
essential with lupus nephritis in order to guide therapy.
Sclerosis: No therapy needed. This is simply scarring of the kidney.
Proliferative disease: Use steroids combined with mycophenolate. Mycophenolate is superior
to cyclophosphamide.
Alport Syndrome
Alport syndrome is the combination of glomerular disease with congenital eye and ear abnormalities. There is sensorineural hearing loss.
Idiopathic Rapidly Progressive Glomerulonephritis
RPGN may occur with any of the glomerular diseases described above, in which case it simply
refers to a time course of the disease. In addition, there is an idiopathic form associated with
crescent formation in the kidney and the presence of ANCA negative. Diagnosis is with renal
biopsy, and the treatment is with steroids and cyclophosphamide.
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Amyloidosis
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There are 2 common types of amyloidosis:
• AL: Plasma cell dyscrasia causing deposition of protein derived from immunoglobulin
light chains. This may be associated with multiple myeloma.
• AA: Amyloid is produced as a proteinaceous material in association with multiple
chronic infectious or inflammatory conditions, such as rheumatoid arthritis, inflammatory bowel disease, or myeloma. The amyloid protein builds up in the kidney, causing glomerulonephritis, and in the GI tract, nerves, and muscles. In the heart, amyloid
is associated with restrictive cardiomyopathy, rhythm disorders, and heart block. A
large tongue (macroglossia) is also characteristic. Neural involvement produces carpal
tunnel syndrome. Malabsorption may occur from GI involvement.
The diagnosis of amyloidosis is established by biopsy of an involved organ such as the kidney.
Other unique methods of diagnosis are aspirating the abdominal fat pad or taking a sample of
the rectum. Congo red testing shows green birefringence. Amyloidosis treatment is very difficult
and consists of controlling the underlying disease. Melphalan and prednisone can control protein
production.
Chapter 8
l Nephrology
Nephrotic Syndrome
Nephrotic syndrome is defined as the presence of renal disease sufficient to produce a level of
proteinuria >3.5 grams per 24 hours, hyperlipidemia, edema, and a low serum albumin level.
Nephrotic syndrome refers to the severity of glomerular disease and does not, by itself, imply
one specific etiology. The edema is from increased salt and water retention by the kidney, as
well as low oncotic pressure in the serum. Hyperlipidemia is of unclear etiology but is most
likely from the loss of the lipoprotein markers or signals on the surface of chylomicrons and
LDL that lead to the clearance of these lipids from the bloodstream.
One-third of nephrotic syndrome is associated with systemic diseases such as diabetes, hypertension, or amyloidosis. In addition, patients with any of the diseases associated with glomerulonephritis described above may develop nephrotic syndrome if the severity of disease is bad
enough to cause massive proteinuria and low serum albumin levels. Nephrotic syndrome is a
descriptor of severity, not a specific etiology. When the glomerular basement membrane loses
its negative charges, protein is spilled into the urine.
Nephrotic syndrome is associated with hyperlipiduria, which gives a droplet found on urinalysis that may form the shape of Maltese crosses.
Hypercoagulable states or thrombophilia develops from the urinary loss of natural anticoagulant proteins such as antithrombin, protein C, and protein S. Patients can develop spontaneous arterial or venous thrombosis. There is also iron, copper, and zinc deficiency from the
urinary loss of their transport proteins such as transferrin and ceruloplasmin.
Diagnosis. The diagnosis of nephrotic syndrome is based on the presence of a high protein level
in the urine, a low protein level in the blood, edema, and hyperlipidemia. The 24-hour urine
shows >3.5 grams of protein; however, this test is cumbersome to perform. An easier test with
equal accuracy is a single spot urine for albumin and creatinine. When you correct the albumin
level in a single spot urine, the ratio that is found is equivalent to the 24-hour urine. In other
words, if you find a protein:creatinine ratio of >3.5 on a single urine, this is equal to 3.5 grams
of protein on a 24-hour urine. Remember that Bence-Jones protein is not found on the routine
urine dipstick, which only detects albumin. You must do a urine immune electrophoresis to detect
Bence-Jones protein.
Figure 8-1. Maltese cross
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The most accurate test to determine the specific etiology of nephrotic syndrome is a renal
biopsy.
Treatment. Treatment of nephrotic syndrome is to control the underlying disease. In addition, steroids are used to treat all forms of idiopathic primary renal causes of nephrotic
syndrome, such as membranous, nil lesion, membranoproliferative, mesangial, and focal-segmental disease. If steroids do not work, the next best step in therapy is to add cyclophosphamide or mycophenolate. Azathiaprine is sometimes useful. ACE inhibitors or ARBs are used
for all patients with proteinuria, but they do not reverse the underlying disease.
All of the following syndromes are diagnosed as described above and treated with steroids
and sometimes cyclophosphamide or mycophenolate.
Focal-Segmental Glomerulosclerosis (FSGS). Associated with the use of heroin as well as
HIV. Limited response (only 20–40%) to steroids. May progress to end stage renal disease
(ESRD) over 5–10 years. FSGS is the most common cause of nephrotic syndrome in adults.
Membranous. Associated with cancer such as lymphoma or breast cancer, and infections such
as endocarditis or chronic hepatitis B or C. Other etiologies are lupus, penicillamine, gold
salts, and NSAIDs.
Nil Lesion (Minimal Change Disease). Most common form in children, although it may
account for 15% of adult disease. NSAIDs have also been associated with nil lesion disease.
Light microscopy is normal and electron microscopy is needed to see fusion of foot processes.
Nil lesion disease is treated with steroids. Hodgkin’s lymphoma has an association with nil
lesion disease.
Mesangial. Mostly idiopathic, steroid-resistant type of nephrotic syndrome. Immunofluorescent staining shows IgM deposits in an expanded mesangium.
Membranoproliferative. Associated with chronic hepatitis and low serum complement levels.
Dipyridamole and aspirin are also useful therapeutically. Cryoglobulins are treated with interferon and ribavirin, which address the hepatitis.
DIAGNOSTIC TESTING IN RENAL DISEASE
Urinalysis
There is no recommendation for routine testing of the general population by urinalysis.
Diabetics or those with systemic diseases such as hypertension are not the general population.
Proteinuria. The urine dipstick detects albumin but no other proteins, such as immunoglobulin light chains. This can be from either glomerular or tubular diseases, although glomerular diseases can give greater amounts. Microalbuminuria is defined as levels 30–300 mg
per 24 hours. Mild amounts of proteinuria under 1 gram per day can be seen in up to 10% of
the population and most often resolve spontaneously. Proteinuria can also occur from stressors such as fever, CHF, and severe exercise. Proteinuria is also caused by prolonged standing,
which is known as orthostatic proteinuria. It is diagnosed by splitting the 24-hour urine
sample. If you find no protein in the first 8 hours and then find it in the second part, it is
orthostatic proteinuria, which is considered benign.
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Hematuria. Red cells can be found in the urine from any cause of disease in the bladder or
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kidney. Etiologies are stones, cancer, bleeding disorders, trauma to urinary system, and treatment such as cyclophosphamide (which causes hemorrhagic cystitis or glomerular disease).
Hematuria is also from infections such as cystitis or prostatitis. The red cells change shape in
glomerular disease and can be dysmorphic.
Nitrites. Gram-negative bacteria reduce nitrate to nitrite, which is a marker of infection.
Bacteriuria. By itself, the isolated finding of bacteria in the urine is of very limited significance.
The most important exception is in pregnant women, whom you should screen for bacteria
and treat. About 30% of pregnant women with bacteriuria progress to pyelonephritis.
Table 8-3. Casts
Casts Significance
Hyaline Dehydration. These casts develop as an accumulation of the normal
amount of tubular protein. They do not necessarily mean disease.
Red cell Glomerulonephritis
Broad, waxy Chronic renal failure
Chapter 8
l Nephrology
Granular Also called “dirty” or “muddy.” They are associated with acute
tubular necrosis and represent accumulated epithelial cells.
White cell Pyelonephritis, interstitial nephritis
END-STAGE RENAL DISEASE/DIALYSIS
The most common causes of end stage renal disease (ESRD) that require dialysis are diabetes
and hypertension. Glomerulonephritis is the etiology of about 15%, with cystic disease and
interstitial nephritis causing 4–5% each.
The indications for dialysis are life-threatening abnormalities that cannot be corrected another
way, such as fluid overload refractory to diuretics, acidosis, pericarditis, encephalopathy, and
other severe neuropathies including myoclonus, wrist or foot drop, and hyperkalemia. Another
indication is persistent nausea, vomiting, and bleeding diathesis attributable to uremia.
Hemodialysis is used in 85% of patients and peritoneal dialysis in 15%. The most common
complication of peritoneal dialysis is peritonitis.
Other complications of ESRD are as follows.
Anemia. This is from the loss of production of erythropoietin from the kidney. It is treated
with replacement of erythropoietin. The anemia of ESRD is normochromic and normocytic.
Hypocalcemia/Hyperphosphatemia. This is from the loss of 1,25-dihydroxyvitamin D production. The hypocalcemia is treated with vitamin D replacement. Hyperphosphatemia is
from the inability of the kidney to excrete phosphate. High phosphate levels contribute to low
calcium levels by precipitating out in tissues in combination with the calcium. High phosphate levels are treated with phosphate binders, such as calcium carbonate or calcium acetate.
Sevelamer and lanthanum are two phosphate binders that do not contain either aluminum
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