Renal and acid–base: type 4 renal tubular acidosis: 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 and acid–base: type 4 renal tubular acidosis

Sample item

A 62-year-old man with long-standing diabetic nephropathy has serum potassium 6.2 mmol/L, bicarbonate 17 mmol/L, a normal anion gap and urine pH of 5.0. Plasma renin and aldosterone are both low. Which mechanism explains the acidosis?

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

The answer and the reasoning

D. Low aldosterone effect impairs distal K+ and H+ secretion, and hyperkalaemia suppresses ammoniagenesis

In hyporeninaemic hypoaldosteronism (type 4 RTA), the lack of aldosterone action reduces the distal potassium and hydrogen ion secretion that accompanies sodium reabsorption, causing hyperkalaemia and mild acidosis. Hyperkalaemia also suppresses renal ammoniagenesis, but the urine can still be acidified, so the urine pH stays below 5.5.

Option by option

  • A. Failure of bicarbonate reabsorption in the proximal tubule with a low renal threshold

    Proximal bicarbonate wasting is type 2 RTA, which usually causes hypokalaemia, not hyperkalaemia.

  • B. Defective hydrogen ion pump function in alpha-intercalated cells of the collecting duct

    Defective alpha-intercalated secretion causes type 1 RTA, with an alkaline urine and hypokalaemia.

  • C. Overproduction of unmeasured organic acids that accumulate in the circulation

    Organic acid overproduction would widen the anion gap, which is normal here.

  • D. Low aldosterone effect impairs distal K+ and H+ secretion, and hyperkalaemia suppresses ammoniagenesis (correct)

    Correct. Reduced aldosterone effect and hyperkalaemia explain both the acidosis and the high potassium.

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.

More Physiology questions

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is D, Low aldosterone effect impairs distal K+ and H+ secretion, and hyperkalaemia suppresses ammoniagenesis. In hyporeninaemic hypoaldosteronism (type 4 RTA), the lack of aldosterone action reduces the distal potassium and hydrogen ion secretion that accompanies sodium reabsorption, causing hyperkalaemia and mild acidosis.

Why is "Failure of bicarbonate reabsorption in the proximal tubule with a low…" not the answer?

Proximal bicarbonate wasting is type 2 RTA, which usually causes hypokalaemia, not hyperkalaemia.

Why is "Defective hydrogen ion pump function in alpha-intercalated cells of t…" not the answer?

Defective alpha-intercalated secretion causes type 1 RTA, with an alkaline urine and hypokalaemia.

Why is "Overproduction of unmeasured organic acids that accumulate in the cir…" not the answer?

Organic acid overproduction would widen the anion gap, which is normal here.

What concept does this question test?

It tests Renal and acid–base: type 4 renal tubular acidosis in Physiology. Hyperkalaemia also suppresses renal ammoniagenesis, but the urine can still be acidified, so the urine pH stays below 5.5.

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: type 4 renal tubular acidosis?

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.