De novo thrombotic microangiopathy in renal transplant recipients: a comparison of hemolytic uremic syndrome with localized renal thrombotic microangiopathy.

Thrombotic microangiopathy (TMA) is a well-recognized and serious complication of renal transplantation, affecting 3% to 14% of patients administered calcineurin-inhibitor-based immunosuppression. We reviewed 1,219 biopsy reports of 742 kidney and kidney-pancreas transplants performed during 15 years at our center and found 21 biopsy-confirmed cases of TMA. On presentation, the majority (62%) had systemic TMA with manifest hemolysis and thrombocytopenia, whereas a subset had TMA localized only to the graft (38%). There were no statistically significant differences in sex, type of transplant, age, race, or type of immunosuppression. Patients with systemic TMA were more likely to be treated with plasma exchange (38% versus 13%; P < 0.05), more often required dialysis therapy (54% versus 0%; P = 0.01), and had a greater rate of graft loss (38% versus 0%; P < 0.05). No patient with the localized variant had TMA-related graft loss. Patients with localized TMA often responded to reduction, conversion, or temporary discontinuation of calcineurin-inhibitor-based immunosuppression therapy and did not routinely require plasma exchange for graft salvage. We compare our findings with the literature regarding the prognosis of TMA. Classifying patients with post-renal transplantation TMA into those with localized and systemic disease is clinically useful because each group has distinct characteristics and clinical courses.