Purposes: Study the clinical characteristics of cases with thrombotic microangiopathy (TMA) in the renal allograft, identify the triggers of this disease and determine its impact on graft survival. Methods: We reviewed the records of 54 patients with TMA in the kidney allograft, diagnosed by biopsy at our institution between 2011 and 2015. Results: The median age was 37 years (range: 13-70) with 33 (61%) women. Three (6%) patients were recipients of simultaneous pancreas-kidney transplant, and among the recipients of kidney transplant alone, 33 (65%) received deceased donor grafts. The cause of end stage kidney disease was unknown (41%), chronic glomerulonephritis (31%), obstructive uropathy (9%), diabetes (9%), hemolytic uremic syndrome (2%), and others (7%). Induction with thymoglobulin or basiliximab was performed in 36 (66%) patients. Maintenance immunosuppression was prednisone (PRED), tacrolimus (TAC), and azathioprine in 20 (37%), PRED, TAC and mycophenolate sodium in 17 (31%), PRED, TAC and everolimus in 7 (13%) and PRED and TAC in 7 (13%) patients. Patients were diagnosed with TMA at a median of 117 days (range: 5-1645 days) after transplantation, wherein 30% patients developed TMA within 1 month of transplantation and 35% after 1 year. At the time of TMA diagnosis, mean serum creatinine was 4.5±3.2 mg/dL and 20 (38%) patients needed renal replacement therapy. TMA was renal-limited in 37 (69%) patients. Concomitant acute rejection was present in 20 (37%) cases and cellular rejection was the most common (85%) type of rejection related to TMA. Cytomegalovirus infection occurred in 9 (17%) and other infections were present in 22 (41%) patients. Pregnancy was associated with 6 (11%) cases. Following diagnosis of TMA, calcineurin inhibitor (CNI) withdrawal was the first step in the management of 36 (67%) patients and 12 (22%) also received fresh frozen plasma and/or plasmapheresis. The median follow-up was 72 days (range: 1-1452) where 26 (48%) patients had improvement of renal function and 18 patients (33%) had allograft failure. Conclusions: Post-transplant TMA was predominantly diagnosed in young women, whose etiology of renal disease was unknown and who had received maintenance immunosuppression with CNI. Infections and rejections were identified as the possible main triggers of TMA. Regardless the treatment given, graft survival was poor following TMA diagnosis.

CITATION INFORMATION: Teixeira C, Pietrobom I, Lima A, Tenório N, Basso G, Cristelli M, Viana L, Kirsztajn G, Tedesco-Silva H, Medina-Pestana J. Thrombotic Microangiopathy After Kidney Transplantation: A Rare but Serious Complication. Am J Transplant. 2016;16 (suppl 3).

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