Renal - Pathology Flashcards

1
Q

_____ (Red blood cells/White blood cells) are seen in the urine of patients with bladder cancer; also significant is the _____ (presence/absence) of casts.

A

Red blood cells; absence

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2
Q

Name three diseases in which red blood cell casts are seen on urinalysis.

A

Glomerulonephritis, renal ischemia, or malignant hypertension

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3
Q

Name three diseases in which white blood cell casts are seen on urinalysis.

A

Tubulointerstitial disease, acute pyelonephritis, or transplant rejection

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4
Q

What types of casts would be seen in the urine of a patient with advanced renal disease or chronic renal failure?

A

Waxy casts

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5
Q

In patients with acute cystitis, _____ (red blood cells/white blood cells) are found in the urine, as are the _____ (presence/absence) of casts.

A

White blood cells; absence

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6
Q

The presence of casts in the urine indicates disease of which organ?

A

The kidneys; as opposed to the bladder or lower urinary tract

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7
Q

What types of casts would be seen in the urine of a patient with acute tubular necrosis?

A

Granular (“muddy brown”) casts

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8
Q

Name five primary glomerular causes of nephrotic syndrome.

A

Minimal change disease, membranous glomerulonephritis, focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, mesangial proliferative glomerulonephritis

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9
Q

Name three secondary causes of nephrotic syndrome.

A

Diabetic nephropathy, amyloidosis, and systemic lupus erythematosus

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10
Q

Name seven causes of nephritic syndrome.

A

Immunoglobulin A nephropathy (Berger’s disease), poststreptococcal glomerulonephritis, systemic lupus erythematosus, thrombotic thrombocytopenic purpura - hemolytic uremic syndrome, Alport’s syndrome, membranoproliferative glomerulonephritis, and Henoch-Schönlein purpura

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11
Q

Name three categories of etiologies for rapidly progressive glomerulonephritis.

A

Antiglomerular basement membrane antibodies, immune-complex mediated glomerulonephritis, and pauci-immune glomerulonephritis

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12
Q

Which four diseases can cause immune-complex mediated rapidly progressive glomerulonephritis?

A

Henoch-Schönlein purpura, hypersensitivity vasculitis, cryoglobulinemia, and systemic lupus erythematosus

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13
Q

Which four diseases can cause pauci-immune rapidly progressive glomerulonephritis?

A

Wegener’s granulomatosis, microscopic polyarteritis, Churg-Strauss syndrome, and polyarteritis nodosa

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14
Q

What is the pattern of immunofluorescence in acute poststreptococcal glomerulonephritis?

A

Granular

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15
Q

Which cause of nephritic syndrome is characterized by mesangial deposits of immunoglobulin A seen on immunofluorescence and electron microscopy?

A

Immunoglobulin A nephropathy (Berger’s disease)

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16
Q

What cause of nephritic syndrome is characterized pathologically by a linear staining pattern with anti-glomerular basement membrane antibodies on immunofluorescence?

A

Goodpasture’s syndrome

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17
Q

What type of hypersensitivity reaction is Goodpasture’s syndrome?

A

Type II hypersensitivity

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18
Q

Which cause of nephritic syndrome is characterized pathologically by crescent-moon-shaped deposits in the urinary space seen by light microscopy and immunofluorescence?

A

Rapidly progressive (crescentic) glomerulonephritis

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19
Q

What are the major symptoms of Goodpasture’s syndrome?

A

Hemoptysis and hematuria

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20
Q

A genetic mutation in which protein results in Alport’s syndrome?

A

Collagen IV mutation

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21
Q

What glomerular pathology is associated with mild renal disease that often follows an upper respiratory infection or gastroenteritis in adults?

A

Immunoglobulin A glomerulopathy (Berger’s disease)

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22
Q

What cause of nephritic syndrome is characterized on histopathology by a basement membrane that appears to be split?

A

Alport’s syndrome

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23
Q

A 10-year-old boy presents with swollen ankles and periorbital edema, which were beginning to resolve without intervention. On electron microscopy, a kidney biopsy is found to have subepithelial immune complex humps. What form of nephritic syndrome does he have?

A

Acute poststreptococcal glomerulonephritis

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24
Q

Wegener’s granulomatosis is _____ (c-ANCA/p-ANCA) positive, while microscopic polyarteritis is _______ (c-ANCA/p-ANCA) positive.

A

c-ANCA; p-ANCA

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25
Q

Name three disease processes that result in rapidly progressive glomerulonephritis.

A

Goodpasture’s syndrome, Wegener’s granulomatosis, and microscopic polyarteritis

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26
Q

Which two ANCA-positive vasculitides can result in rapidly progressive glomerulonephritis?

A

Wegener’s granulomatosis and microscopic polyarteritis

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27
Q

Which condition is associated with nerve disorders, ocular disorders, and deafness?

A

Alport’s syndrome; symptoms are due to a mutation in type IV collagen

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28
Q

What do the crescent deposits in “crescentic” glomerulonephritis consist of?

A

Fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages

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29
Q

Which cause of nephritic syndrome is characterized pathologically by enlarged hypercellular glomeruli, the presence of neutrophils, and a “lumpy-bumpy” appearance on light microscopy?

A

Acute poststreptococcal glomerulonephritis

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30
Q

What is the underlying mechanism resulting in diffuse proliferative glomerulonephritis due to systemic lupus erythematosus?

A

Subendothelial anti-DNA immune complex deposition

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31
Q

What are the findings on light microscopy and immunofluorescence in diffuse proliferative glomerulonephritis?

A

“Wire-looping” of capillaries on light microscopy and granular immunofluorescence due to subendothelial immune complex deposition

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32
Q

Diffuse proliferative glomerulonephritis is the most common cause of death in which systemic disease?

A

Systemic lupus erythematosus

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33
Q

What six features are the hallmarks of nephritic syndrome?

A

Hematuria, hypertension, oliguria, azotemia, with proteinuria and red blood cell casts in the urine

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34
Q

What is the most common cause of nephrotic syndrome in adults?

A

Membranous glomerulonephritis

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35
Q

What four features are the hallmarks of nephrotic syndrome?

A

Massive proteinuria, edema, fatty casts, and hyperlipidemia

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36
Q

In diabetic glomerulonephropathy, what causes the increased permeability and thickening of the glomerular basement membrane?

A

Nonenzymatic glycosylation of the glomerular basement membrane

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37
Q

Which types of nephrotic syndrome are characterized pathologically by a granular pattern seen on immunofluorescence?

A

Membranous and membranoproliferative glomerulonephritis

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38
Q

What are the characteristic findings in membranous glomerulonephritis on electron microscopy?

A

A “spike and dome” appearance with subepithelial deposits

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39
Q

When lupus presents as nephrotic syndrome, what renal pathology is likely to be found?

A

Membranous glomerulonephritis; diffuse capillary thickening with granular immunofluorescence

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40
Q

What are the characteristic findings of focal segmental glomerular sclerosis on light microscopy?

A

Sclerosis and hyalinosis of renal glomeruli

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41
Q

What cause of nephrotic syndrome is characterized pathologically by Kimmelstiel-Wilson lesions, mesangial expansion, and basement membrane thickening of renal glomeruli on light microscopy?

A

Diabetic glomerulonephropathy

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42
Q

In a patient with nephrotic syndrome due to amyloidosis, what are the characteristic findings on immunofluorescence?

A

Apple-green birefringence on a Congo red stain

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43
Q

Name three conditions that can predispose patients to nephrotic syndrome due to amyloidosis.

A

Multiple myeloma, tuberculosis, and rheumatoid arthritis; many chronic conditions are risk factors

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44
Q

Which type of renal pathology may present clinically as either nephritic or nephrotic syndrome?

A

Membranoproliferative glomerulonephritis

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45
Q

Membranoproliferative glomerulonephritis is associated with _____ (hepatitis B virus/HIV), while focal segmental glomerulosclerosis is associated with _____ (hepatitis C virus/HIV).

A

Hepatitis B virus; HIV

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46
Q

An 8-year-old girl who recently had viral gastroenteritis presents with edema and frothy urine. A renal biopsy shows foot process effacement on electron microscopy. What is her diagnosis and how would you treat her?

A

Minimal change disease, which should be treated with corticosteroids

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47
Q

Which type of nephrotic syndrome is characterized pathologically by diffuse capillary and basement membrane thickening seen on light microscopy?

A

Membranous glomerulonephritis

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48
Q

Name four etiologies of membranous glomerulonephritis.

A

Drugs, infections, systemic lupus erythematosus, and solid tumors

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49
Q

What is the pathogenesis of minimal change disease?

A

The effacement of epithelial foot processes on the glomeruli leads to the selective loss of albumin from plasma (not globulins) due to glomerular basement membrane polyanion loss and failure of the charge barrier

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50
Q

What is the most common glomerular disease seen in patients with HIV?

A

Focal segmental glomerular sclerosis

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51
Q

What are the electron microscopy findings in type I and type II membranoproliferative glomerulonephritis?

A

Type I findings consist of a “tram-track” appearance due to glomerular basement splitting caused by mesangial ingrowth; type II findings consist of “dense deposits”

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52
Q

Type I membranoproliferative glomerulonephritis is associated with hepatitis _____ and type II membranoproliferative glomerulonephritis is associated with _____ nephritic factor.

A

B; C3

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53
Q

In diabetic glomerulonephropathy, what causes mesangial expansion?

A

Nonenzymatic glycosylation of the efferent arterioles, leading to an increased glomerular filtration rate and thus mesangial expansion

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54
Q

What type of glomerular disease is characterized on histopathology by large, irregular subepithelial deposits or “humps”?

A

Acute glomerulonephritis

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55
Q

What type of glomerular disease is characterized on histopathology by subendothelial deposits?

A

Lupus glomerulonephritis

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56
Q

What type of glomerular disease is characterized on histopathology by mesangial deposits?

A

Immunoglobulin A nephropathy

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57
Q

Of what element are kidney stones most commonly composed?

A

Calcium in the form of calcium oxalate, calcium phosphate, or both

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58
Q

Name two severe complications that result from the presence of kidney stones.

A

Hydronephrosis and pyelonephritis

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59
Q

What is the second most common type of kidney stone composed of?

A

Ammonium magnesium phosphate (struvite)

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60
Q

What types of conditions lead to increased risk for development of calcium kidney stones?

A

Conditions that cause hypercalcemia, such as cancer, increased parathyroid hormone, increased vitamin D, and milk-alkali syndrome

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61
Q

What types of kidney stones appear radiopaque on x-rays?

A

Struvite (which can be radiopaque or radiolucent), calcium, and cystine stones (which appear faintly radiopaque)

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62
Q

Infection by what class of microbe causes the development of kidney stones composed of ammonium magnesium phosphate (struvite)?

A

Urease-positive bugs (Proteus vulgaris, Staphylococcus, Klebsiella) make urine alkaline and favor formation of struvite stones

63
Q

What types of kidney stones appear radiolucent on x-rays?

A

Struvite (which can be either radiolucent or radiopaque) and uric acid

64
Q

What type of kidney stone is strongly associated with hyperuricemia (gout)?

A

Uric acid kidney stones

65
Q

Both antifreeze and vitamin C abuse can result in the formation of what type of crystals?

A

Oxalate crystals

66
Q

What type of kidney stone develops most often as a consequence of the genetic disease cystinuria?

A

Cystine kidney stone

67
Q

Are cystine stones treated with alkalinization or acidification of the urine?

A

Alkalinization of urine

68
Q

What is the term for a very large kidney stone? Which type of stone is most likely to present this way?

A

A hexagonal stone, which is most likely a cystine kidney stone

69
Q

An 80-year-old man with leukemia presents with hematuria and right-sided flank pain. With his medical history, what type of kidney stone is he at greatest for developing and how would you expect it to appear on x-ray?

A

Due to his leukemia (a disease with high cell turnover) he is at risk for developing uric acid stones due to hyperuricemia, which are radiolucent and do not appear on x-ray

70
Q

What lifestyle factors are associated with an increased incidence of renal cell carcinoma?

A

Smoking and obesity

71
Q

What is the most common renal malignancy in adulthood?

A

Renal cell carcinoma

72
Q

Deletions on which chromosome are associated with renal cell carcinoma?

A

Gene deletion on chromosome 3

73
Q

Renal cell carcinoma is most common in which demographic?

A

Men ages 50-70

74
Q

What genetic disease is associated with bilateral renal cell carcinoma?

A

von Hippel-Lindau disease

75
Q

What is the cellular origin of renal cell carcinoma?

A

Polygonal clear cells of the renal tubule

76
Q

Name four paraneoplastic syndromes associated with renal cell carcinoma.

A

Ectopic erythropoietin, ACTH, parathyroid hormone-related protein, and prolactin secretion

77
Q

Name six clinical manifestations of renal cell carcinoma.

A

Hematuria, palpable mass, secondary polycythemia, flank pain, fever, and weight loss

78
Q

Via what route does renal cell carcinoma metastasize? To which organs?

A

Renal cell carcinoma spreads hematogenously via invasion of the inferior vena cava; it most commonly metastasizes to lung and bone

79
Q

What is the most common renal malignancy of early childhood (ie, 2-4 years old)?

A

Wilms’ tumor

80
Q

Wilms’ tumor is a component of the WAGR disease complex. What are the other components?

A

WAGR complex: Wilms’ tumor, Aniridia, Genitourinary malformation, and mental-motor Retardation

81
Q

How does Wilms’ tumor most commonly present?

A

As a large palpable abdominal mass and/or hematuria in young children; it may be associated with genetic hemihypertrophy syndromes

82
Q

What gene deletion is associated with Wilms’ tumor?

A

The deletion of WT1 on chromosome 11 (tumor suppressor gene)

83
Q

In which four anatomic structures of the urinary tract can transitional cell carcinoma occur?

A

Renal calyces, renal pelvis, ureters, and bladder

84
Q

What is the most common tumor of the urinary tract system?

A

Transitional cell carcinoma

85
Q

What is the most common clinical presentation of bladder cancer?

A

Painless hematuria

86
Q

What exposures are associated with transitional cell carcinoma?

A

Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide (remember: “problems in the Pee SAC”)

87
Q

In acute pyelonephritis, the renal cortex is _____ (affected/spared), the glomeruli are _____ (affected/spared), and the vessels are _____ (affected/spared).

A

Affected; spared; spared

88
Q

What finding on urinalysis would suggest pyelonephritis in a febrile patient with flank tenderness?

A

White blood cell casts

89
Q

A patient who presents with fever, nausea, vomiting, and costovertebral angle tenderness likely has what condition?

A

Acute pyelonephritis

90
Q

In chronic pyelonephritis, what substance can fill the tubules of the renal nephrons?

A

Eosinophilic casts, a histopathologic biopsy finding known as thyroidization of the kidney

91
Q

What gross anatomic changes of the kidneys occur with chronic pyelonephritis?

A

Coarse, asymmetric corticomedullary scarring and blunted calices

92
Q

What are the presenting symptoms of drug-induced interstitial nephritis?

A

Fever, rash, hematuria, and costovertebral angle tenderness 1-2 weeks after drug exposure

93
Q

How long after the ingestion of a substance does drug-induced interstitial nephritis occur? What lab findings are suggestive of the diagnosis?

A

After approximately 1-2 weeks a patient may present with pyuria (eosinophils) and azotemia

94
Q

Name five types of drugs that are associated with interstitial nephritis.

A

Nonsteroidal antiinflammatory drugs, rifampin, diuretics, penicillin derivatives, and sulfonamides

95
Q

What is the pathologic consequence on the kidneys of severe vasospasm and disseminated intravascular coagulation, often secondary to obstetric complications?

A

Diffuse cortical necrosis

96
Q

Name two disease processes that are associated with diffuse cortical necrosis.

A

Obstetric catastrophes, such as placental abruption, and septic shock

97
Q

Define diffuse cortical necrosis of the kidneys.

A

Acute generalized infarction of cortices of both kidneys

98
Q

What is the treatment for acute tubular necrosis?

A

Dialysis until recovery of kidney function occurs

99
Q

What is the most common cause of renal failure in hospitalized patients?

A

Acute tubular necrosis

100
Q

What are three causes of acute tubular necrosis?

A

Renal ischemia (shock), crush injury to muscles (myoglobulinuria), and toxins

101
Q

During which phase of acute tubular necrosis do most deaths occur?

A

During the initial oliguric phase if dialysis is not initiated

102
Q

What is the pathophysiology of acute tubular necrosis?

A

Loss of renal tubule cell polarity, epithelial cell detachment, necrosis, and granular (“muddy brown”) casts; the findings are due to acute toxic or ischemic injury

103
Q

How long does it take to recover from acute tubular necrosis?

A

2-3 weeks

104
Q

What is the clinical presentation of renal papillary necrosis?

A

Gross hematuria and proteinuria as the result of sloughing of the renal papillae

105
Q

What are three general categories of renal dysfunction that can lead to acute renal failure?

A

Prerenal (eg, hypotension and reduced renal blood flow), intrinsic renal (eg, tubular necrosis), and postrenal (outflow obstruction)

106
Q

What is acute renal failure?

A

A renal condition characterized by an abrupt decline in renal function with elevated blood urea nitrogen and creatinine levels over several days

107
Q

Is urine osmolality highest in patients with prerenal, intrarenal, or postrenal causes of acute renal failure?

A

Prerenal

108
Q

Reduced glomerular filtration rate as a result of hypotension and reduced renal blood flow results in the retention of what three substances by the kidney?

A

Sodium, water, and urea are retained in an attempt to maintain blood volume

109
Q

Why does the blood urea nitrogen to creatinine ratio increase in patients who have low renal blood flow?

A

When renal blood flow and glomerular filtration rate are reduced, urea is retained to attempt to preserve blood volume; the resulting increase in blood urea nitrogen is also known as prerenal azotemia

110
Q

Name two main causes of acute intrinsic renal failure.

A

Acute tubular necrosis and toxic injury

111
Q

What finding is seen on urinalysis of patients with acute renal failure as a result of intrinsic renal disease?

A

Epithelial/granular casts

112
Q

Name four possible causes of postrenal outflow obstruction that can lead to acute renal failure.

A

Kidney stones, benign prostatic hyperplasia, congenital anomalies, and neoplasia

113
Q

True or False? Unilateral postrenal outflow obstruction can lead to acute renal failure.

A

False; bilateral, not unilateral, postrenal outflow obstruction leads to acute renal failure

114
Q

Is the urine sodium level highest in patients with prerenal, renal, or postrenal causes of acute renal failure?

A

Postrenal

115
Q

Is the fractional excretion of sodium lowest in patients with prerenal, renal, or postrenal causes of acute renal failure?

A

Prerenal; a low fractional excretion of sodium shows the kidneys are functional and working to maintain blood volume

116
Q

Is the blood urea nitrogen/creatinine ratio lowest in patients with prerenal, renal, or postrenal causes of acute renal failure (acute kidney injury)?

A

Renal; the injured kidneys are unable to absorb urea to maintain blood volume

117
Q

A patient’s urine osmolarity is >500 mOsm/L, urine sodium level is <10 mEq/L, fractional excretion of sodium is <1%, and the blood urea nitrogen/creatinine ratio is >20:1. Does the patient most likely have a prerenal, renal, or postrenal etiology of his acute renal failure?

A

Prerenal

118
Q

A patient’s urine osmolarity is <350 mOsm/L, urine sodium level is >20 mEq/L, fractional excretion of sodium is >2%, and the blood urea nitrogen/creatinine ratio is <15:1. Does the patient most likely have a prerenal, renal, or postrenal etiology of his acute renal failure?

A

Renal

119
Q

A patient’s urine osmolarity is <350 mOsm/L, urine sodium level is >40 mEq/L, fractional excretion of sodium is >4%, and the blood urea nitrogen/creatinine ratio is >15:1. Does the patient most likely have a prerenal, renal, or postrenal etiology of his acute renal failure?

A

Postrenal

120
Q

In renal failure, is the potassium level abnormally high or low?

A

High

121
Q

What are the two main forms of renal failure?

A

Acute (acute tubular necrosis or rapidly progressive glomerulonephritis) and chronic (diabetes and hypertension)

122
Q

By what mechanism does renal failure lead to anemia?

A

Impaired erythropoietin production

123
Q

Renal osteodystrophy as a part of the clinical abnormalities in patients with uremia is a result of the failure of what kidney function?

A

Production of active vitamin D, resulting in hypocalcemia and leading to a secondary increase in parathyroid hormone, resulting bone loss

124
Q

In renal failure, is the total body sodium level (as opposed to serum concentration) abnormally high or low?

A

High

125
Q

What acid-base disorder is a consequence of renal failure?

A

Metabolic acidosis

126
Q

What electrolyte abnormality resulting from renal failure can lead to cardiac arrhythmia?

A

Hyperkalemia

127
Q

Name three cardiovascular consequences of excess sodium and water retention in patients with renal failure.

A

Congestive heart failure, hypertension, and pulmonary edema

128
Q

Name six signs and symptoms of uremia.

A

Nausea, anorexia, pericarditis, asterixis, encephalopathy, and platelet dysfunction

129
Q

What metabolic diseases can cause Fanconi’s syndrome?

A

Wilson’s disease and glycogen storage diseases

130
Q

What is Fanconi’s syndrome?

A

A disease caused by defects in the proximal tubule transport of amino acids, glucose, phosphate, uric acid, and electrolytes

131
Q

Which drugs can cause Fanconi’s syndrome?

A

Expired tetracycline, cisplatin

132
Q

What is the complication of the decreased phosphate reabsorption associated with Fanconi’s syndrome?

A

Rickets

133
Q

What is the result of the decreased bicarbonate reabsorption associated with Fanconi’s syndrome?

A

Metabolic acidosis (type 2 renal tubular acidosis)

134
Q

What is the result of the decreased proximal tubular sodium reabsorption of Fanconi’s syndrome?

A

Hypokalemia; if the proximal tubule does not reabsorb sodium, the distal tubule must excrete more potassium to reabsorb sodium

135
Q

Name the autosomal recessive disease that presents with multiple bilateral kidney cysts and renal failure in infancy.

A

Autosomal recessive polycystic kidney disease (infantile polycystic kidney disease)

136
Q

What is autosomal dominant polycystic kidney disease?

A

An autosomal-dominant disease characterized by multiple bilateral cysts that destroy the kidney parenchyma during adulthood

137
Q

Name five clinical manifestations of autosomal dominant polycystic kidney disease.

A

Flank pain, hematuria, hypertension, urinary tract infection, and progressive renal failure in adulthood

138
Q

What mutation causes autosomal dominant polycystic kidney disease (formerly adult polycystic kidney disease)?

A

An autosomal dominant mutation in the APKD1 or APKD2gene

139
Q

What are the characteristics of renal medullary cystic disease?

A

Small kidneys on ultrasound, cysts in the medullary area that can sometimes lead to fibrosis and progressive renal insufficiency with urinary concentrating defects, and a very poor prognosis

140
Q

Name three nonrenal pathologies associated with autosomal dominant polycystic kidney disease.

A

Polycystic liver disease, berry aneurysms, and mitral valve prolapse

141
Q

What is the cause of death associated with autosomal dominant polycystic kidney disease?

A

Death is most commonly due to complications of chronic kidney disease or hypertension (due to increased renin production)

142
Q

What liver disease is associated with autosomal recessive polycystic kidney disease?

A

Congenital hepatic fibrosis

143
Q

What are the complications of autosomal recessive polycystic kidney disease in utero and after the neonatal period?

A

Renal failure in utero from autosomal recessive polycystic kidney disease can lead to the Potter sequence; after the neonatal period, potential complications include hypertension, portal hypertension, and progressive renal insufficiency

144
Q

High serum levels of chloride are usually a result of what primary acid-base disturbance?

A

Non-anion gap acidosis

145
Q

What are the consequences of low sodium levels?

A

Disorientation, stupor, and coma

146
Q

What are four causes of low serum levels of chloride?

A

Metabolic alkalosis, hypokalemia, hypovolemia, and elevated aldosterone

147
Q

U waves on electrocardiogram, flattened T waves, arrhythmias, and paralysis are consequences of a low serum level of what electrolyte?

A

Potassium

148
Q

What are the symptoms of hypocalcemia?

A

Tetany and neuromuscular irritability

149
Q

What are the symptoms of hypercalcemia?

A

Delirium, renal stones, and abdominal pain

150
Q

What are two consequences of low serum levels of magnesium?

A

Neuromuscular irritability and arrhythmias

151
Q

What are three consequences of high serum levels of magnesium?

A

Delirium, decreased deep tendon reflexes, and cardiopulmonary arrest

152
Q

What are the consequences of low phosphate levels?

A

Bone loss and osteomalacia

153
Q

What are the electrocardiogram findings associated with hyperkalemia?

A

Peaked T waves and widened QRS complexes

154
Q

What are the consequences of high phosphate levels?

A

Metastatic calcification and renal stones