Renal and acid–base: creatinine secretion and trimethoprim: 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.

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Physiology · Renal and acid–base: creatinine secretion and trimethoprim

Sample item

A patient with a urinary tract infection takes co-trimoxazole. Serum creatinine rises from 0.9 to 1.2 mg/dL, but serum cystatin C and the urine output are unchanged and the urinalysis is bland. What explains the creatinine rise?

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

The answer and the reasoning

D. Trimethoprim competes for tubular secretion of creatinine, without altering GFR

A small part of excreted creatinine is secreted by proximal tubular cells through organic cation transport. Trimethoprim (and cimetidine) block this secretion and raise the serum creatinine without any true fall in GFR, as the unchanged cystatin C shows.

Option by option

  • A. Trimethoprim damages the glomerular filtration barrier

    Glomerular damage would also change cystatin C and produce an abnormal urinalysis.

  • B. Trimethoprim lowers renal blood flow by afferent constriction

    Afferent constriction would lower the true GFR, which cystatin C would also reflect.

  • C. Trimethoprim causes rhabdomyolysis with release of creatinine

    Rhabdomyolysis would raise muscle enzymes and cause other signs, and it does not fit the unchanged cystatin C.

  • D. Trimethoprim competes for tubular secretion of creatinine, without altering GFR (correct)

    Correct. Reduced tubular secretion raises serum creatinine while the true GFR stays the same.

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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Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is D, Trimethoprim competes for tubular secretion of creatinine, without altering GFR. A small part of excreted creatinine is secreted by proximal tubular cells through organic cation transport.

Why is "Trimethoprim damages the glomerular filtration barrier" not the answer?

Glomerular damage would also change cystatin C and produce an abnormal urinalysis.

Why is "Trimethoprim lowers renal blood flow by afferent constriction" not the answer?

Afferent constriction would lower the true GFR, which cystatin C would also reflect.

Why is "Trimethoprim causes rhabdomyolysis with release of creatinine" not the answer?

Rhabdomyolysis would raise muscle enzymes and cause other signs, and it does not fit the unchanged cystatin C.

What concept does this question test?

It tests Renal and acid–base: creatinine secretion and trimethoprim in Physiology. Trimethoprim (and cimetidine) block this secretion and raise the serum creatinine without any true fall in GFR, as the unchanged cystatin C shows.

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 and acid–base: creatinine secretion and trimethoprim?

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.