In an elderly patient with hypertension and atherosclerosis who develops AKI after starting an ACE inhibitor, what is the most likely cause?

Study for the NBME Form 13 Test with our comprehensive quiz collection, featuring flashcards and multiple-choice questions to ensure your readiness. Enhance your knowledge with detailed explanations for each question.

Multiple Choice

In an elderly patient with hypertension and atherosclerosis who develops AKI after starting an ACE inhibitor, what is the most likely cause?

Explanation:
ACE inhibitors can precipitate kidney injury when renal perfusion relies on angiotensin II to maintain GFR. In renal artery stenosis, especially when disease is present in both kidneys, the efferent arteriole remains constricted to sustain glomerular pressure. Blocking angiotensin II with an ACE inhibitor removes this compensatory mechanism, causing dilation of the efferent arteriole, a drop in intraglomerular pressure, and an acute fall in GFR leading to AKI. In an elderly patient with atherosclerosis, bilateral atherosclerotic renal artery stenosis is a common scenario, making ACE inhibitors particularly risky. By contrast, acute tubular necrosis would arise from ischemia or toxins and is not the direct consequence of ACE inhibition in this setting; nephrotic syndrome wouldn’t explain a sudden AKI after starting the medication. If only one kidney were diseased, the other intact kidney often maintains GFR, so AKI would be less likely.

ACE inhibitors can precipitate kidney injury when renal perfusion relies on angiotensin II to maintain GFR. In renal artery stenosis, especially when disease is present in both kidneys, the efferent arteriole remains constricted to sustain glomerular pressure. Blocking angiotensin II with an ACE inhibitor removes this compensatory mechanism, causing dilation of the efferent arteriole, a drop in intraglomerular pressure, and an acute fall in GFR leading to AKI. In an elderly patient with atherosclerosis, bilateral atherosclerotic renal artery stenosis is a common scenario, making ACE inhibitors particularly risky. By contrast, acute tubular necrosis would arise from ischemia or toxins and is not the direct consequence of ACE inhibition in this setting; nephrotic syndrome wouldn’t explain a sudden AKI after starting the medication. If only one kidney were diseased, the other intact kidney often maintains GFR, so AKI would be less likely.

Subscribe

Get the latest from Passetra

You can unsubscribe at any time. Read our privacy policy