Thrombotic microangiopathies (TMA) include a heterogeneous group of syndromes that share common pathological characteristics, or rather endothelial cellular damage and microvascular thrombosis, and a clinical triad characterized by thrombocytopenia, haemolytic anaemia and signs of ischemic suffering in various body areas, mainly, but not limited to kidney and central nervous system.1 TMA are: Pre-eclampsia/Eclampsia, HELLP syndrome, thrombotic thrombocytopenic purpura (TTP), atypical haemolytic-uremic syndrome (a-HUS) and typical, disseminated intravascular coagulation (CID) and antiphospholipid antibody syndrome. TMA are classified in primary and secondary forms. In their primary forms, the disease is defined by the presence of a thrombotic microangiopathies, such as TTP, due to the deficiency of ADAMTS13, a metalloprotease that cleaves the von Willebrand Factor (Fv-W), and as a-HUS characterized by complement dysregulation.2 In their secondary forms, on the other hand, they present themselves as events in which TMA arises as a complication of an underlying medical condition: pregnancy is the typical one, but also malignant hypertension, as a complication of a Preeclampsia or HELLP syndrome, drug use, kidney transplan