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Physiology · Renal and acid–base: type 4 renal tubular acidosis
Sample itemA 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.
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