Thrombotic microangiopathies after kidney transplantation in modern era: nosology based on chronology

Background Thrombotic microangiopathies (TMAs) are rare but can be severe in kidney transplant. recipients (KTR). Methods We analysed the epidemiology of adjudicated TMA in consecutive KTR during the. 2009–2021 period. Results TMA was found in 77/1644 (4.7%) KTR. Early TMA ( n = 24/77 (31.2%); 1.5% of all KTR) occurred during the first two weeks ((median, IQR) 3 [1–8] days). Triggers included acute antibody-mediated rejection (ABMR, n = 4) and bacterial infections ( n = 6). Graft survival (GS) was 100% and recurrence rate (RR) was 8%. Unexpected TMA ( n = 31/77 (40.2%); 1.5/1000 patient-years) occurred anytime during follow-up (3.0 (0.5–6.2) years). Triggers included infections (EBV/CMV: n = 10; bacterial: n = 6) and chronic active ABMR ( n = 5). GS was 81% and RR was 16%. Graft-failure associated TMA ( n = 22/77 (28.6%); 2.2% of graft losses) occurred after 8.8 (4.9–15.5) years). Triggers included acute ( n = 4) or chronic active ( n = 14) ABMR, infections (viral: n = 6; bacterial: n = 5) and cancer ( n = 6). 15 patients underwent transplantectomy. RR was 27%. Atypical ( n = 6) and typical ( n = 2) haemolytic and uremic syndrome, and isolated CNI toxicity ( n = 4) were rare. Two-third of biopsies presented TMA features. Conclusions TMA are mostly due to ABMR and infections; causes of TMA are frequently combined. Management often is heterogenous. Our nosology based on TMA timing identifies situations with distinct incidence, causes and prognosis.