Development of a thrombotic microangiopathy can arise as a complication of bacterial infections like EHEC, from genetic mutations in complement regulatory pathways (atypical HUS, aHUS), from deficiencies of regulatory ADAMTS13 enzyme (thrombotic thrombocytopenic purpura, TTP) or even secondarily as a consequence of autoimmune diseases such as systemic lupus erythematosus. This evidence concerns the gene ADAMTS13 and atypical hemolytic-uremic syndrome.