Summary: Thrombotic microangiopathies (TMAs) in renal transplant recipients are a wide group of diseases with a complex etiopathogenesis. The crucial point of the disease is endothelial damage in the microcirculation with the formation of thrombi and renal graft failure. Thrombotic microangiopathy is a morphological entity with clinical manifestation as a hemolytic uremic syndrome (HUS) with symptoms of hemolytic anemia, thrombocytopenia and acute renal graft failure. The current classification of TMA includes primary (complement-mediated TMA, C-TMA), secondary, and infectious background. There are two kinds of TMA in renal transplant recipients ‒ a recurrent TMA or de novo TMA with systemic or localized (allograft limited) clinical presentation. In renal transplant recipients a number of TMA triggers are identified ‒ ischemia-reperfusion injury, acute rejection, infections (CMV and others), drugs (calcineurin inhibitors, mTOR inhibitors and others); TMA may appear in a patient with missed HUS diagnosis in the native kidneys or as a phenotype shift of C3 glomerulopathy into post-transplant HUS. Recent years have demonstrated great advances in understanding the disease mechanisms and complement dysregulation. A therapeutic complement inhibition, anti-C5 treatment, for C-TMA is available for renal transplant recipients. New molecules affecting complement alternative pathway are investigated. This paper discusses the manage-ment of TMA in renal transplant recipients including diagnostics with clinical and genetic approach. The current strategies for targeted therapy (anti-C5) including modification of the immunosuppressive regimen are presented.