A patient with sudden oliguria and rising creatinine after NSAID use. What is the most likely cause?

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Multiple Choice

A patient with sudden oliguria and rising creatinine after NSAID use. What is the most likely cause?

Explanation:
The key idea is that NSAIDs can precipitate acute kidney injury by blocking prostaglandin-mediated dilation of the afferent arteriole. Prostaglandins normally help keep the GFR adequate when kidney perfusion is stressed. By inhibiting COX and reducing prostaglandins, NSAIDs cause afferent arteriolar vasoconstriction, lowering renal blood flow and GFR. This leads to a rapid rise in creatinine and oliguria after NSAID use. Stopping the NSAID and providing supportive care allows the kidney function to recover as normal prostaglandin effects resume. Dehydration can cause prerenal AKI, but the temporal link to NSAID use with the described mechanism makes NSAID-induced afferent vasoconstriction the most likely cause. Post-renal obstruction would present with signs of obstruction; acute tubular necrosis from a toxin is a different pattern of injury.

The key idea is that NSAIDs can precipitate acute kidney injury by blocking prostaglandin-mediated dilation of the afferent arteriole. Prostaglandins normally help keep the GFR adequate when kidney perfusion is stressed. By inhibiting COX and reducing prostaglandins, NSAIDs cause afferent arteriolar vasoconstriction, lowering renal blood flow and GFR. This leads to a rapid rise in creatinine and oliguria after NSAID use. Stopping the NSAID and providing supportive care allows the kidney function to recover as normal prostaglandin effects resume.

Dehydration can cause prerenal AKI, but the temporal link to NSAID use with the described mechanism makes NSAID-induced afferent vasoconstriction the most likely cause. Post-renal obstruction would present with signs of obstruction; acute tubular necrosis from a toxin is a different pattern of injury.

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