Thrombotic microangiopathy (TMA) is a clinical‑pathological syndrome characterized by thrombotic changes in vessels, thrombocytopenia and hemolytic anemia. Hemolytic‑uremic syndrome (HUS), atypical hemolytic‑uremic syndrome (aHUS) and thrombotic thrombocytopenic purpura (TTP) are three different manifestations of TMA. Although the clinical course of these syndromes is sometimes confusingly similar, they differ in etiology. This knowledge affects the therapeutic process and the prognosis associated with it. Hemolytic‑uremic syndrome is caused by the action of bacterial verotoxin. Patients are mainly treated symptomatically by red cell concentrate transfusion and renal replacement therapy. The pathophysiology of the atypical hemolytic‑uremic syndrome involves incorrect activation of an alternative complement pathway. This process can be inhibited by targeted therapy with eculizumab, which is a monoclonal antibody directed against the complement C5 component. Thrombotic thrombocytopenic purpura is in turn characterized by inborn or acquired deficiency of plasma ADAMTS13 metalloproteinase activity. The basis for the treatment of patients with acquired TTP is a therapeutic plasma exchange, and in patients with inborn TTP – a infusion of fresh frozen plasma.