Complement-mediated TMA presents with thrombocytopenia, mechanical hemolysis, and acute renal failure, with severe arterial hypertension and ischemic damage due to activation and/or abnormal regulation of the alternative pathway of the complement system on cell surfaces: mutations in C3 and factor B; autoantibodies against factor H interfering with regulation; disturbed recognition by factor H, factor I, or CD46 of C3b; and disturbed recognition by factor H of self-cell surface molecules, such as sialic acid or glycosaminoglycans [42]. The gene discussed is C3; the disease is acute kidney injury.