Nephrology and electrolytes: haemodynamic AKI with NSAID: practice question

A General Medicine question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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General Medicine · Nephrology and electrolytes: haemodynamic AKI with NSAID

Sample item

A 72-year-old man with hypertension takes an ACE inhibitor and furosemide and starts regular ibuprofen for back pain. After a diarrhoeal illness, his creatinine rises from 1.2 to 3.0 mg/dL with bland urine and urine sodium of 8 mmol/L. What is the main mechanism?

AImmune-mediated interstitial inflammation with eosinophiluriaBBilateral ureteric obstruction by crystalsCDirect tubular toxicity with muddy brown castsDLoss of afferent dilation and efferent constriction

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Loss of afferent dilation and efferent constriction

Prostaglandins dilate the afferent arteriole and angiotensin II constricts the efferent arteriole to preserve glomerular filtration during volume depletion. An NSAID removes the first and an ACE inhibitor the second, so GFR collapses. The low urine sodium and bland sediment support a pre-renal, haemodynamic process.

Option by option

A. Immune-mediated interstitial inflammation with eosinophiluria
Interstitial nephritis would show white cells, white cell casts and sometimes eosinophiluria.
B. Bilateral ureteric obstruction by crystals
Obstruction would not explain a low urine sodium and bland urine.
C. Direct tubular toxicity with muddy brown casts
Tubular necrosis would show muddy brown casts and a high urine sodium.
D. Loss of afferent dilation and efferent constriction (correct)
Correct. NSAID plus ACE inhibitor plus volume loss removes both compensatory mechanisms.

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.

Questions about this General Medicine question

What is the answer to this General Medicine question?

The best answer is D, Loss of afferent dilation and efferent constriction. Prostaglandins dilate the afferent arteriole and angiotensin II constricts the efferent arteriole to preserve glomerular filtration during volume depletion.

Why is "Immune-mediated interstitial inflammation with eosinophiluria" not the answer?

Interstitial nephritis would show white cells, white cell casts and sometimes eosinophiluria.

Why is "Bilateral ureteric obstruction by crystals" not the answer?

Obstruction would not explain a low urine sodium and bland urine.

Why is "Direct tubular toxicity with muddy brown casts" not the answer?

Tubular necrosis would show muddy brown casts and a high urine sodium.

What concept does this question test?

It tests Nephrology and electrolytes: haemodynamic AKI with NSAID in General Medicine. An NSAID removes the first and an ACE inhibitor the second, so GFR collapses. The low urine sodium and bland sediment support a pre-renal, haemodynamic process.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Nephrology and electrolytes: haemodynamic AKI with NSAID?

For each disease know the classic presentation, the best test, and the first-line treatment. Then use the flashcards and the other General Medicine questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.