A 70-year-old man with hypertension and known bilateral renal artery stenosis greater than 70 percent is started on an angiotensin-converting enzyme inhibitor. Within one week, serum creatinine rises from 1.4 to 3.1 mg/dL. What is the mechanism of this acute kidney injury?
- A Direct nephrotoxic tubular injury
- B Loss of efferent arteriolar tone reducing glomerular filtration pressure ✓
- C Renin-mediated afferent arteriolar vasoconstriction
- D Cholesterol crystal embolization
Correct answer: B. Loss of efferent arteriolar tone reducing glomerular filtration pressure
Explanation
In bilateral renal artery stenosis or stenosis in a solitary kidney, glomerular filtration depends on angiotensin II-mediated efferent arteriolar constriction to maintain filtration pressure. ACE inhibitors block this efferent tone, causing a predictable drop in glomerular filtration rate and rise in creatinine. This hemodynamic effect is usually reversible on stopping the drug. Direct tubular injury is seen with aminoglycosides. Afferent vasoconstriction is not the mechanism. Cholesterol emboli cause subacute decline with eosinophilia and livedo reticularis.
Reference: Brenner and Rector's The Kidney, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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