It may be related to the activation of the renin-angiotensin-aldosterone system and endothelial dysfunction,[10]leading to the formation of small blood vessels and intravascular thrombosis, red blood cell fragmentation, platelet hemolytic consumption, and elevated LDH.[11,12] Persistent TMA is associated with endothelial injury, fibrinoid necrosis, and occlusive vasculopathy, which may explain persistent renal failure and dependence on dialysis.[13]. This evidence concerns the gene REN and endothelial dysfunction.