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General Medicine · Cardiology: renovascular hypertension
Sample itemA 62-year-old chronic smoker with hypertension has an abdominal bruit and a history of recurrent episodes of sudden pulmonary oedema. One week after ramipril is started, serum creatinine rises from 1.1 to 2.0 mg/dL and potassium is 5.8 mmol/L. What best explains the deterioration?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Loss of efferent arteriolar constriction in bilateral renal artery stenosis
In significant bilateral renal artery stenosis (or stenosis in a single functioning kidney), glomerular filtration depends on angiotensin II constricting the efferent arteriole to maintain filtration pressure. An ACE inhibitor removes this, so GFR falls and creatinine and potassium rise. A rise greater than 30% after starting an ACE inhibitor should raise this suspicion, and the drug is stopped.
Option by option
A. Afferent arteriolar vasoconstriction caused by the drug
Afferent constriction is the mechanism of NSAIDs and calcineurin inhibitors, not ACE inhibitors.
B. Loss of efferent arteriolar constriction in bilateral renal artery stenosis (correct)
Efferent dilatation with low afferent perfusion pressure drops filtration pressure, which explains the abrupt rise in creatinine.
C. Direct tubular toxicity from ramipril
ACE inhibitors are not directly tubulotoxic; the injury is haemodynamic.
D. Allergic interstitial nephritis caused by the ACE inhibitor
Drug-induced interstitial nephritis is rare and typically shows rash, eosinophilia or sterile pyuria rather than a haemodynamic picture.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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