skip to main content

Recurrent IgAN Allograft Management — ESENeph MCQ

Instant feedback + full explanation. One question, done properly.

ModerateTransplantationRecurrent IgAN Allograft ManagementESENeph

A kidney transplant recipient 10 years post-transplant on Tacrolimus has developed new-onset proteinuria (1.5 g/day). His native disease was IgA nephropathy. Transplant biopsy shows mesangial IgA deposits consistent with recurrent IgAN. His eGFR is 45. How should recurrent IgAN in the allograft be managed?

Educational content. Not a substitute for clinical judgement or local policy.

Reveal the answer and explanation

Correct answer: D — Same as native IgAN – RASi, SGLT2i, consider disease-modifying therapy if proteinuria persists; immunosuppression optimisation may also help

Recurrent IgAN in the allograft is managed following the same principles as native IgAN: RASi for proteinuria reduction, SGLT2i for renoprotective benefit (with transplant-specific monitoring), BP optimisation, and consideration of disease-modifying therapy (e.g. Nefecon, systemic steroids) if proteinuria persists ≥0.5 g/day despite supportive care. Additionally, transplant-specific factors apply: immunosuppression optimisation (avoiding underimmunosuppression which may worsen IgAN), adherence assessment, and monitoring for concurrent rejection. The evidence base for disease-modifying IgAN therapy in the transplant setting is limited and largely extrapolated from native disease data.

Reference: KDIGO 2025 – IgAN; KDIGO 2009 – Transplant