Thrombotic microangiopathies (TMA) are defined as a triad combining mechanical hemolyticanemia, peripheral thrombocytopenia and ischemic organ damage.Mitomycin C is an alkylating agent used as chemotherapy in adenocarcinomas of the breast,lung, pancreas, rectum and anal carcinoma. Mitomycin-C-induced TMA (m-TMA) is apotentially serious complication of chemotherapy: its estimated incidence ranges from 4to 15% and its mortality exceeds 70%, with an estimated median survival of 2 months. Thiscan also be responsible for kidney failure, sometimes requiring hemodialysis. The time toonset of m-TMA varies from one week to 15 months after the last infusion and is believedto depend on the cumulative dose of mitomycin C.Eculizumab is a monoclonal antibody that binds to complement protein C5, blockingactivation of the terminal complement pathway and formation of the membrane attackcomplex. This therapy has significantly changed the prognosis of patients with atypicalhemolytic uremic syndrome (HUS), a disease in which complement activation plays a centralrole in TMA. Recently, a retrospective study suggested efficacy of eculizumab in TMAinduced by gemcitabine, another chemotherapy, with normalization of platelets and LDH in83% of patients, and partial or complete renal recovery in 67% and 17% of patients. Theseresults provided arguments in favor of a potential benefit of complement-targetedtherapies in TMA induced by certain chemotherapies. However, data on eculizumab in m-TMAremain extremely limited to date.The objective of this study is to describe the clinical, biological and histologicalpresentation of patients with m-TMA and their evolution after treatment with or withouteculizumab.