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CNI-Induced TMA Management Transplant — ESENeph MCQ

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ModerateTransplantationCNI-Induced TMA Management TransplantESENeph

A kidney transplant recipient develops calcineurin inhibitor-induced thrombotic microangiopathy 3 months post-transplant. Biopsy shows arteriolar thrombi with endothelial swelling. ADAMTS13 is normal. DSA are negative. What is the management?

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Correct answer: A — Reduce or switch CNI (Tacrolimus to Ciclosporin or to Belatacept/mTOR inhibitor) – CNI-induced TMA is dose-dependent and usually improves with dose reduction or CNI avoidance; plasma exchange may be used as bridge therapy

CNI-induced TMA is a dose-dependent complication where the CNI causes direct endothelial injury, complement activation, and microthrombi formation. It is localised to the graft (systemic TMA is rare). Management involves: (1) CNI dose reduction (trough target 3-5 ng/mL); (2) CNI switch (Tacrolimus to Ciclosporin or vice versa, or to CNI-free regimen with Belatacept or mTOR inhibitor); (3) plasma exchange as bridge therapy for severe cases; (4) Eculizumab has been used in refractory cases but evidence is limited. Unlike de novo aHUS post-transplant, CNI TMA typically responds to dose modification.

Reference: KDIGO 2009 – Transplant; Pham et al 2011 – CNI-Induced TMA