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Ticagrelor Creatinine Artefact ENT1 Inhibition — ESENeph MCQ

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HardChronic Kidney DiseaseTicagrelor Creatinine Artefact ENT1 InhibitionESENeph

A 62-year-old man with CKD G5D on haemodialysis has a functioning AV fistula. He develops acute ST-elevation MI requiring primary PCI with drug-eluting stent placement. The interventional cardiologist plans to use the standard post-PCI regimen of aspirin plus ticagrelor for 12 months. What specific CKD-related concern must be addressed regarding ticagrelor?

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Correct answer: C — Ticagrelor raises serum creatinine by inhibiting tubular secretion — this is not true AKI

Ticagrelor inhibits the equilibrative nucleoside transporter 1 (ENT1), which is involved in tubular creatinine secretion. This causes a predictable 10-15% rise in serum creatinine WITHOUT any change in true GFR — a pharmacological artefact similar to trimethoprim. In dialysis patients, this is less clinically relevant (no residual function to track), but in CKD G3-4, the creatinine rise can be misinterpreted as AKI, leading to inappropriate drug withdrawal or unnecessary investigation. Ticagrelor does NOT require dose adjustment in CKD/ESKD and is not dialysable. Awareness of this effect prevents misdiagnosis and inappropriate treatment changes.

Reference: Nolin 2014 – Ticagrelor Creatinine Effect; BNF 2024 – Ticagrelor