Clinically, TMA presents a Coombs‐negative HA with elevated serum lactate dehydrogenase (LDH) level, undetectable or markedly decrease serum haptoglobin and the presence of schistocytes, a thrombocytopenia, an AKI, a proteinuria or a hypertension, neurologic and gastrointestinal symptoms and a normal coagulation [1, 2, 3, 4, 6, 15, 16, 17]. This evidence concerns the gene HP and acute kidney injury.