In thrombotic microangiopathy, glomerulopathy is triggered by the activation of the coagulation cascade in renal tissue due to the presence of antiendothelial antibodies, C3 and/or C4 components, resulting in morphological changes similar to those found in TG and hemolytic-uremic syndrome (HUS) [43, 45, 46]. This evidence concerns the gene C3 and hemolytic-uremic syndrome.