Renal: tubular transport defects: 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: tubular transport defects

Sample item

A 4-year-old with failure to thrive and polyuria has normal blood pressure, hypokalaemia, metabolic alkalosis and hypercalciuria. Which transporter is most likely defective?

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

The answer and the reasoning

D. Na-K-2Cl cotransporter in the thick ascending limb

Loss of function of the Na-K-2Cl cotransporter (Bartter syndrome) mimics chronic loop diuretic use. Salt wasting, secondary hyperaldosteronism and increased distal flow produce hypokalaemia and alkalosis. Loss of the lumen-positive potential impairs paracellular calcium reabsorption, so urinary calcium is high.

Option by option

  • A. Epithelial sodium channel in the collecting duct, with gain of function

    Gain of function (Liddle syndrome) causes hypertension with hypokalaemia.

  • B. Na-H exchanger in the proximal tubule

    Proximal Na-H exchange defects give bicarbonate loss and acidosis, not alkalosis.

  • C. Na-Cl cotransporter in the distal convoluted tubule

    A defect here (Gitelman syndrome) gives hypocalciuria and hypomagnesaemia, like thiazides.

  • D. Na-K-2Cl cotransporter in the thick ascending limb (correct)

    Correct. This is the loop diuretic pattern: salt wasting, hypokalaemia, alkalosis and hypercalciuria.

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, Na-K-2Cl cotransporter in the thick ascending limb. Loss of function of the Na-K-2Cl cotransporter (Bartter syndrome) mimics chronic loop diuretic use.

Why is "Epithelial sodium channel in the collecting duct, with gain of functi…" not the answer?

Gain of function (Liddle syndrome) causes hypertension with hypokalaemia.

Why is "Na-H exchanger in the proximal tubule" not the answer?

Proximal Na-H exchange defects give bicarbonate loss and acidosis, not alkalosis.

Why is "Na-Cl cotransporter in the distal convoluted tubule" not the answer?

A defect here (Gitelman syndrome) gives hypocalciuria and hypomagnesaemia, like thiazides.

What concept does this question test?

It tests Renal: tubular transport defects in Physiology. Salt wasting, secondary hyperaldosteronism and increased distal flow produce hypokalaemia and alkalosis. Loss of the lumen-positive potential impairs paracellular calcium reabsorption, so urinary calcium is high.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. 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: tubular transport defects?

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.