Fig. 2

Hypothesis based on our case series: both recipients and donors carried the complement genetic abnormality, contributing to the continuous injury of endothelial cells and leading to early graft loss after activation of TMA by triggers in our case series. Advice for these patients: (1) before transplantation, recipients with kidney disease of unknown etiology may consider complement genetic testing. A deceased donor kidney transplant should be recommended if testing reveals complement genetic variant in both donor and recipient; (2) after transplantation, intensive monitoring and timely treatment of triggers are critical. Besides, surveillance allograft biopsy, more testing, and exome sequence may help to diagnosis; (3) since diagnosis of post-transplant TMA, early anti-complement treatment is necessary. LKT, living-relative kidney disease; DD, deceased donor; ABMR, antibody-mediated rejection; CNIs, calcineurin inhibitors; TMA, thrombotic microangiopathy; LDH, lactic dehydrogenase; PE, plasma exchange