A 63-year-old man is in stable condition after an acute myocardial infarction when he became hypotensive for 3 hours before paramedical personnel arrived. Over the next week, the serum urea nitrogen level increases to 48 mg/dL, the serum creatinine level increases to 5 mg/dL, and the urine output decrease. He undergoes hemodialysis for the next 2 weeks and then develops marked polyuria, with urine output of 2 to 3 L/day. His renal function gradually returns to normal. Release of which of the following substances most likely participated in the elevation of BUN, creatinine, and reduced urinary output?
Correct Answer: Endothelin
Description: The most common cause of acute tubular necrosis is ischemic injury. The hypotension that develops after myocardial infarction causes decreased renal blood flow, with intrarenal vasoconstriction. Sublethal endothelial injury from reduced renal blood flow leads to the increased release of the vasoconstrictor endothelin and diminished amounts of the vasodilators nitric oxide and prostaglandin. The ischemic form of acute tubular injury is often accompanied by the rupture of the basement membrane (tubulorrhexis). An initiating phase that lasts approximately 1 day is followed by a maintenance phase during which progressive oliguria and increasing blood urea nitrogen levels occur, with salt and water overload. This is followed by a recovery phase, during which there is a steady increase in urinary output and hypokalemia. Eventually, the tubular function is restored. Treatment of this acute renal failure results in the recovery of nearly all patients. Aldosterone plays a role in sodium absorption. Erythropoietin drives RBC production. Natriuretic peptide increases when there is congestive heart failure, but does not lead to renal ischemia. Vasopressin (antidiuretic hormone) controls free water clearance.
Category:
Pathology
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