Etiologically, TMA includes a spectrum of disorders: Thrombotic thrombocytopenic purpura (TTP), primarily caused by severe deficiency of the metalloprotease ADAMTS13, leading to accumulation of ultra-large von Willebrand factor multimers and platelet clumping; Hemolytic uremic syndrome (HUS), classically triggered by Shiga toxin-producing Escherichia coli infection; Atypical HUS (aHUS), a complement-mediated TMA resulting from genetic mutations or acquired dysregulation of the alternative complement pathway. This evidence concerns the gene ADAMTS13 and hemolytic-uremic syndrome.