QUESTION: 41

A 53-year-old White female, with a history of systemic lupus erythematosus (SLE), hypertension, and peripheral vascular disease, is admitted to the hospital for chest pain and dyspnea. Her cardiac enzymes were positive for acute MI. She subsequently undergoes a cardiac catheterization and stenting of the right coronary artery. Her postcardiac catheterization course is unremarkable, and she is discharged home 3 days later with adequate blood pressure control. Five days later, she is brought to the ER by her husband for abdominal pain and nausea. Her medications consist of aspirin, metoprolol, and prednisone. On physical examination, her blood pressure is 190/95 and her heart rate is 85 bpm. In general, she appears nauseated but is in no acute distress. Her cardiac examination reveals a regular rate and rhythm without murmur or rub.
Her lung fields are clear bilaterally. The abdominal examination is positive for diffuse discomfort, without guarding or rebound, and normoactive bowel sounds; her stool is positive for occult blood. Her lower extremities have trace edema bilaterally with 2+ distal pulses; moreover, she has a reddish-blue discoloration on both her lower extremities. You retrieve her records from prior hospitalization. The patient's laboratory results are as follows:

What is the most likely cause of this patient's acute renal failure?

contrast nephropathy from cardiac catheterization
acute interstitial nephritis
prerenal etiology from occult gastrointestinal (GI) bleeding
atheroembolic disease
lupus nephritis flare

Answer(s): D

Explanation:

This patient has atheroembolic disease, most likely from the dislodging of arterial plaque during or after the cardiac catheterization, with subsequent kidney embolization. The findings in her history and physical examination that would suggest this are the presence of significant hypertension, abdominal pain, the redblue rash on her extremities (livedo reticularis), and eosinophilia with urinary eosinophils. Furthermore, the time course of the development of acute renal failure is suggestive of atheroembolic disease. The typical time course for contrast nephropathy is of an immediate onset, usually with subsequent recovery. However, in patients with atheroembolic disease, the kidney failure can occur much later after the procedure. Contrast nephropathy is not associated with the laboratory abnormalities and physical examination findings seen in this case. Interstitial nephritis is unlikely, as is a lupus nephritis flare, given her classic presentation for emboli. Calculation of the fractional excretion of sodium (FeNa) is helpful in differentiating between "prerenal" causes (FeNa <1%) of acute renal failure versus intrinsic causes (FeNa >1%). A kidney ultrasound is helpful in determining the presence of urinary tract obstruction. Neither the anion gap nor calculation of glomerular filtration rate is helpful in determining if volume depletion is a possible etiology of acute renal failure. Examination of urine sediment would be helpful in determining the presence of a glomerular etiology of acute renal failure, not a prerenal etiology. Demerol and metabolites can accumulate in patients with depressed kidney function, leading to increased levels and, potentially, convulsions. NSAIDs should be avoided in patients with acute kidney failure, as these drugs are potential nephrotoxins and could prevent a recovery of kidney function. Ketorolac, indomethacin, and ibuprofen are all NSAIDs. Therefore, morphine is the best option of those given.WBC casts are suggestive of pyelonephritis. High levels of proteinuria are significant for the diagnosis of nephrotic syndrome, but not lupus nephritis specifically. Urine eosinophils are usually seen in patients with acute interstitial nephritis or atheroembolic disease. Lupus nephritis is usually associated with depressed serum complement levels. Of these tests, RBC casts are the most suggestive of glomerulonephritis.

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QUESTION: 42

A 53-year-old White female, with a history of systemic lupus erythematosus (SLE), hypertension, and peripheral vascular disease, is admitted to the hospital for chest pain and dyspnea. Her cardiac enzymes were positive for acute MI. She subsequently undergoes a cardiac catheterization and stenting of the right coronary artery. Her postcardiac catheterization course is unremarkable, and she is discharged home 3 days later with adequate blood pressure control. Five days later, she is brought to the ER by her husband for abdominal pain and nausea. Her medications consist of aspirin, metoprolol, and prednisone. On physical examination, her blood pressure is 190/95 and her heart rate is 85 bpm. In general, she appears nauseated but is in no acute distress. Her cardiac examination reveals a regular rate and rhythm without murmur or rub.
Her lung fields are clear bilaterally. The abdominal examination is positive for diffuse discomfort, without guarding or rebound, and normoactive bowel sounds; her stool is positive for occult blood. Her lower extremities have trace edema bilaterally with 2+ distal pulses; moreover, she has a reddish-blue discoloration on both her lower extremities. You retrieve her records from prior hospitalization. The patient's laboratory results are as follows:

Which of the following tests is helpful in distinguishing volume depletion as a possible cause of acute renal failure?

kidney ultrasound
calculation of the fractional excretion of sodium
estimation of the glomerular filtration rate
examination of the urine sediment under microscopy
calculation of the anion gap

Answer(s): B

Explanation:

This patient has atheroembolic disease, most likely from the dislodging of arterial plaque during or after the cardiac catheterization, with subsequent kidney embolization. The findings in her history and physical examination that would suggest this are the presence of significant hypertension, abdominal pain, the redblue rash on her extremities (livedo reticularis), and eosinophilia with urinary eosinophils. Furthermore, the time course of the development of acute renal failure is suggestive of atheroembolic disease. The typical time course for contrast nephropathy is of an immediate onset, usually with subsequent recovery. However, in patients with atheroembolic disease, the kidney failure can occur much later after the procedure. Contrast nephropathy is not associated with the laboratory abnormalities and physical examination findings seen in this case. Interstitial nephritis is unlikely, as is a lupus nephritis flare, given her classic presentation for emboli. Calculation of the fractional excretion of sodium (FeNa) is helpful in differentiating between "prerenal" causes (FeNa <1%) of acute renal failure versus intrinsic causes (FeNa >1%). A kidney ultrasound is helpful in determining the presence of urinary tract obstruction. Neither the anion gap nor calculation of glomerular filtration rate is helpful in determining if volume depletion is a possible etiology of acute renal failure. Examination of urine sediment would be helpful in determining the presence of a glomerular etiology of acute renal failure, not a prerenal etiology. Demerol and metabolites can accumulate in patients with depressed kidney function, leading to increased levels and, potentially, convulsions. NSAIDs should be avoided in patients with acute kidney failure, as these drugs are potential nephrotoxins and could prevent a recovery of kidney function. Ketorolac, indomethacin, and ibuprofen are all NSAIDs. Therefore, morphine is the best option of those given.WBC casts are suggestive of pyelonephritis. High levels of proteinuria are significant for the diagnosis of nephrotic syndrome, but not lupus nephritis specifically. Urine eosinophils are usually seen in patients with acute interstitial nephritis or atheroembolic disease. Lupus nephritis is usually associated with depressed serum complement levels. Of these tests, RBC casts are the most suggestive of glomerulonephritis.

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QUESTION: 43

A 53-year-old White female, with a history of systemic lupus erythematosus (SLE), hypertension, and peripheral vascular disease, is admitted to the hospital for chest pain and dyspnea. Her cardiac enzymes were positive for acute MI. She subsequently undergoes a cardiac catheterization and stenting of the right coronary artery. Her postcardiac catheterization course is unremarkable, and she is discharged home 3 days later with adequate blood pressure control. Five days later, she is brought to the ER by her husband for abdominal pain and nausea. Her medications consist of aspirin, metoprolol, and prednisone. On physical examination, her blood pressure is 190/95 and her heart rate is 85 bpm. In general, she appears nauseated but is in no acute distress. Her cardiac examination reveals a regular rate and rhythm without murmur or rub.
Her lung fields are clear bilaterally. The abdominal examination is positive for diffuse discomfort, without guarding or rebound, and normoactive bowel sounds; her stool is positive for occult blood. Her lower extremities have trace edema bilaterally with 2+ distal pulses; moreover, she has a reddish-blue discoloration on both her lower extremities. You retrieve her records from prior hospitalization. The patient's laboratory results are as follows:

Which of the following is the optimal therapeutic agent for this patient's pain management?

intravenous Demerol
intramuscular ketorolac
oral indomethacin
intravenous morphine sulfate
ibuprofen 400 mg orally three times daily as needed

Answer(s): D

Explanation:

This patient has atheroembolic disease, most likely from the dislodging of arterial plaque during or after the cardiac catheterization, with subsequent kidney embolization. The findings in her history and physical examination that would suggest this are the presence of significant hypertension, abdominal pain, the redblue rash on her extremities (livedo reticularis), and eosinophilia with urinary eosinophils. Furthermore, the time course of the development of acute renal failure is suggestive of atheroembolic disease. The typical time course for contrast nephropathy is of an immediate onset, usually with subsequent recovery. However, in patients with atheroembolic disease, the kidney failure can occur much later after the procedure. Contrast nephropathy is not associated with the laboratory abnormalities and physical examination findings seen in this case. Interstitial nephritis is unlikely, as is a lupus nephritis flare, given her classic presentation for emboli. Calculation of the fractional excretion of sodium (FeNa) is helpful in differentiating between "prerenal" causes (FeNa <1%) of acute renal failure versus intrinsic causes (FeNa >1%). A kidney ultrasound is helpful in determining the presence of urinary tract obstruction. Neither the anion gap nor calculation of glomerular filtration rate is helpful in determining if volume depletion is a possible etiology of acute renal failure. Examination of urine sediment would be helpful in determining the presence of a glomerular etiology of acute renal failure, not a prerenal etiology. Demerol and metabolites can accumulate in patients with depressed kidney function, leading to increased levels and, potentially, convulsions. NSAIDs should be avoided in patients with acute kidney failure, as these drugs are potential nephrotoxins and could prevent a recovery of kidney function. Ketorolac, indomethacin, and ibuprofen are all NSAIDs. Therefore, morphine is the best option of those given.WBC casts are suggestive of pyelonephritis. High levels of proteinuria are significant for the diagnosis of nephrotic syndrome, but not lupus nephritis specifically. Urine eosinophils are usually seen in patients with acute interstitial nephritis or atheroembolic disease. Lupus nephritis is usually associated with depressed serum complement levels. Of these tests, RBC casts are the most suggestive of glomerulonephritis.

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QUESTION: 44

A 63-year-old Native American male, with a 6-year history of DM, hypertension, and hyperlipidemia, comes to your office as a new patient for a routine examination. He has been experiencing frequent lower back pain and headaches for which he is taking ibuprofen daily for the past 5 weeks. Moreover, he is complaining of mild fatigue. In addition, he is taking aspirin, atorvastatin, verapamil, and glipizide. His physical examination shows a blood pressure of 165/80 and heart rate of 90 bpm. In general, he was not in any distress. His funduscopic examination reveals no signs of diabetic retinopathy. Cardiac examination reveals a regular rate and rhythm with an S4 gallop. His lungs are clear and abdominal examination is unremarkable without any bruit auscultated. He also has 2+ lower extremity pitting edema. Rectal examination reveals brown stool, negative for occult blood. His laboratory results are as follows:

Which of the following is a typical finding in this patient's condition?

hypocalcemia
macrocytic anemia
elevated thyroxine levels
hypocomplementemia
hematuria

Answer(s): A

Explanation:

This patient's presentation and laboratory data are consistent with nephrotic syndrome. Nephrotic syndrome is typically associated with proteinuria of greater than 3.5 g/day, hypoalbuminemia, edema, and hyperlipidemia. Abnormalities commonly seen in nephrotic syndrome include hypocalcemia (due to vitamin D deficiency), low thyroxine levels (due to loss of thyroxine-binding globulin [TBG]), and microcytic, hypochromic anemia (due to transferring loss). Hypocomplementemia may be found in some forms of nephrotic syndrome, but this is not a typical finding. Hematuria is one of the components found in nephritic syndrome.

This patient has history, physical, and laboratory findings that suggest possible multiple myeloma. For example, his history is pertinent for lower back pain and headaches. Moreover, Bence-Jones protein is not usually detected by urine dipstick but will be detected during a 24-hour urine collection. This would explain why there is relatively little urine protein detected on dipstick but over 5 g on the 24-hour urine. Lastly, multiple myeloma should be considered in an older patient with unexplained anemia. Given these findings, a serum and urine protein electrophoresis would be the best test to order next. A kidney biopsy would usually be diagnostic, but is unnecessary if the electrophoresis is positive. Complement levels and anti- GBM titer would not be of any use at the present time. Checking glycosylated Hgb will inform you of the adequacy of glucose control, but will be of little use with regard to the workup of the nephrotic syndrome. This patient has a low anion gap due to the presence of unmeasured cations in the blood. In this case, they arise from circulating immunoglobulins. The fractional excretion of sodium and urea can be helpful in differentiating prerenal causes from other etiologies of acute renal failure. A split 24-hour urine for protein is helpful in determining the presence of orthostatic proteinuria. Initiation of ACE inhibitors or angiotensin receptor blockers is the best option in patients with diabetic nephropathy, as these medications have been shown to slow the progression of kidney disease. The other medications listed may be used adjunctively, with an ACE inhibitor or angiotensin receptor blocker, if adequate blood pressure control could not be achieved with monotherapy. HIV-associated nephropathy is typically associated with a collapsing glomerulopathy, a variant of focal segmental glomerulosclerosis. Membranous nephropathy is associated with a number of other infections, including syphilis, hepatitis B, and hepatitis C virus. Membranoproliferative glomerulonephritis has also been associated with hepatitis C virus.

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