Aashi
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A 35-year-old man with a past medical history of AIDS is admitted for fulminant herpes zoster and is started on intravenous Acyclovir. Two days later, the patient has multiple episodes of hematemesis and is transferred to the intensive care unit, where he is given four units of packed red blood cells. The following day, an upper endoscopy reveals esophagitis. He starts to improve, but two days later he develops jaundice. His labs show a rise in his creatinine from 1.2 to 2.5 mg/dL. His 24-hour urine output drops from 1,200 to 350 mL. Physical examination reveals jaundice. Laboratory studies reveal:
Potassium 5.6 mEq/L, bicarbonate 24 mEq/L, BUN 36 mg/dL, creatinine 2.5 mg/dL, hematocrit 32%. The urinalysis is dipstick-positive for blood, and there are pigmented tubular casts with no crystals or bilirubin. No red cells are seen on microscopic examination. The urine sodium is elevated, and the fractional excretion of sodium is >1%.
What is the next best management?
(A) Stop Acyclovir
(B) Repeat ABO testing of the patient's blood
(C) Coombs' test
(D) Hemodialysis
(E) Thiazide diuretic
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| new_n_lost
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(A) Stop Acyclovir
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| robin082006
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(A) Stop Acyclovir
Acyclovir induced Crystaluria
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| daych
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Stop acyclovir It definitely the cause of renal failure in this case.
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| Aashi
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C) Coombs' test
Explanation:
Transfusions with mismatched blood can result in pigment nephropathy. Hemoglobinuria as a result of hemolysis is directly toxic to kidney tubules. The patient seems to have a mismatch of the minor blood group antigens, such as Rh, Kell, Duffy, Louis, and Kidd. The clue to this is a delay in the development of jaundice until the following day. Coombs' test will tell us if there is an autoimmune hemolysis occurring. Repeating the crossmatch of minor antigens, not the ABO type, is appropriate.
Major blood-group antigen mismatch, such as an ABO incompatibility, would have given severe, immediate symptoms. Treatment involves volume repletion and the occasional use of mannitol and bicarbonate to alkalinize the urine and protect the kidney tubule. Thiazides would not be the right kind of diuretic to use. Bilirubin is absent from the urine because hemolysis elevates the level of indirect bilirubin. Indirect bilirubin is bound to albumin and does not filter at the glomerulus.
Acyclovir might be associated with crystals in the urine and usually gives a nonoliguric form of renal failure. Acyclovir is unlikely to give blood or hemoglobin in the urine. This patient's renal failure is not severe enough to need dialysis.
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