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Abstract

Thrombotic microangiopathy refers to a spectrum of conditions that share a common underlying pathologic mechanism that result in endothelial damage and microangiopathic hemolytic anemia. De novo thrombotic microangiopathy after kidney transplant is often triggered by immunosuppressive drugs, and studies most often implicate calcineurin inhibitors and/or mammalian target of rapamycin inhibitors; however, muromonab and alemtuzumab also reportedly cause thrombotic microangiopathy. In addition, thrombotic microangiopathy may be triggered by acute antibody-mediated rejection and infections like cytomegalovirus and parvovirus.Here, we present a case series of 3 patients without any apparent risk factors (eg, acute antibody-mediated rejection) who developed de novo thrombotic microangiopathy immediately following kidney transplant, but before the introduction of calcineurin inhibitors. Two of these 3 patients were successfully managed with plasma exchange, and calcineurin inhibitors were successfully introduced without the recurrence of thrombotic microangiopathy.