Renal: autoregulation of GFR: practice question

A Physiology 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.

Try it

Physiology · Renal: autoregulation of GFR

Sample item

A 68-year-old man with bilateral renal artery stenosis starts an ACE inhibitor and within days his creatinine rises from 1.1 to 2.4 mg/dL. What is the mechanism?

AInterstitial nephritis from a type IV reactionBLoss of angiotensin II-mediated efferent constriction lowers glomerular capillary pressureCConstriction of the afferent arteriole by bradykininDDirect tubular toxicity of the drug

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

The answer and the reasoning

B. Loss of angiotensin II-mediated efferent constriction lowers glomerular capillary pressure

With reduced renal perfusion, angiotensin II constricts the efferent arteriole and keeps glomerular capillary pressure and GFR up. An ACE inhibitor removes this effect and the filtration pressure falls, causing acute kidney injury that is usually reversible on stopping the drug. Bilateral stenosis (or one stenosed solitary kidney) is the classic risk.

Option by option

A. Interstitial nephritis from a type IV reaction
Interstitial nephritis is rare with ACE inhibitors and does not explain the prompt rise.
B. Loss of angiotensin II-mediated efferent constriction lowers glomerular capillary pressure (correct)
Correct. Efferent dilatation lowers filtration pressure when afferent flow is already limited.
C. Constriction of the afferent arteriole by bradykinin
Bradykinin is a vasodilator and its rise would dilate arterioles.
D. Direct tubular toxicity of the drug
The ACE inhibitor is not directly nephrotoxic to tubules; the change is haemodynamic.

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 Physiology question

What is the answer to this Physiology question?

The best answer is B, Loss of angiotensin II-mediated efferent constriction lowers glomerular capillary pressure. With reduced renal perfusion, angiotensin II constricts the efferent arteriole and keeps glomerular capillary pressure and GFR up.

Why is "Interstitial nephritis from a type IV reaction" not the answer?

Interstitial nephritis is rare with ACE inhibitors and does not explain the prompt rise.

Why is "Constriction of the afferent arteriole by bradykinin" not the answer?

Bradykinin is a vasodilator and its rise would dilate arterioles.

Why is "Direct tubular toxicity of the drug" not the answer?

The ACE inhibitor is not directly nephrotoxic to tubules; the change is haemodynamic.

What concept does this question test?

It tests Renal: autoregulation of GFR in Physiology. An ACE inhibitor removes this effect and the filtration pressure falls, causing acute kidney injury that is usually reversible on stopping the drug. Bilateral stenosis (or one stenosed solitary kidney) is the classic risk.

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 Renal: autoregulation of GFR?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology 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.