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.