Co-trimoxazole Pseudo-Nephrotoxicity — SCE Infectious Diseases MCQ

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ModerateHIV MedicineCo-trimoxazole Pseudo-NephrotoxicitySCE Infectious Diseases

A 45-year-old man with HIV on ART (CD4 550, VL <50) develops acute kidney injury (creatinine rise from 90 to 250 µmol/L) while being treated with IV Co-trimoxazole for PJP. What should be considered regarding the creatinine rise?

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Correct answer: A — Co-trimoxazole inhibits renal tubular secretion of creatinine — causing a rise in measured creatinine WITHOUT true GFR decline; true renal function should be assessed with Cystatin C

Trimethoprim (the Trimethoprim component of Co-trimoxazole) inhibits the organic cation transporter (OCT2) in the renal proximal tubule, which is responsible for creatinine secretion. This causes a rise in serum creatinine of approximately 10–20% WITHOUT a true decline in GFR. Cystatin C is an alternative marker unaffected by this mechanism and can be used to assess true renal function. This pseudo-nephrotoxicity is clinically important because it may lead to unnecessary dose reductions or drug discontinuation. However, genuine nephrotoxicity (crystal nephropathy from Sulfamethoxazole) can also occur — clinical context matters.

Reference: BNF 2024 – Co-trimoxazole; BHIVA 2022 – OI guidelines