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Pharmacology · Antibacterials: trimethoprim and hyperkalaemia
Sample itemA 35-year-old man with HIV receiving high-dose co-trimoxazole for Pneumocystis pneumonia has a potassium of 5.8 mmol/L and a creatinine rise from 0.9 to 1.3 mg/dL, with normal urine output and a bland urine sediment. What best explains the hyperkalaemia?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Trimethoprim blocks epithelial sodium channels in the collecting duct, like amiloride
Trimethoprim is structurally related to amiloride and blocks collecting duct ENaC, reducing potassium secretion, particularly at high doses and with renal impairment or ACE inhibitors. It also competes for tubular creatinine secretion, raising serum creatinine without a true fall in filtration. The sediment is bland, which makes crystal nephropathy less likely.
Option by option
A. Trimethoprim blocks epithelial sodium channels in the collecting duct, like amiloride (correct)
Correct. Amiloride-like ENaC block reduces potassium excretion.
B. Sulfamethoxazole causes adrenal insufficiency
Sulfamethoxazole does not cause adrenal insufficiency.
C. Sulfamethoxazole crystals obstruct the distal nephron
Crystal nephropathy would be expected to show crystals and reduced urine output, which is not seen here.
D. Trimethoprim inhibits the Na-K-ATPase in the proximal tubule
Trimethoprim does not inhibit the proximal Na-K-ATPase; the target is the collecting duct ENaC.
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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