TMA syndromes are classified in four groups based on their underlying etiology: (1) autoantibodies against ADAMTS13 causing thrombotic thrombocytopenic purpura (TTP); (2) infections with E.Coli O157 producing Shiga toxin leading to hemolytic uremic syndrome (HUS); (3) mutations in the complement regulatory pathways causing atypical HUS (aHUS); and (4) drug-mediated TMA [1]. This evidence concerns the gene ADAMTS13 and hemolytic-uremic syndrome.