In addition to proteins directly related to the complement cascade, increasing evidence highlights the role of coagulation factors in the pathogenesis of aHUS, including thrombomodulin (THBD), which regulates Factor I-mediated C3b inactivation, and plasminogen (PLG), which enhances plasmin-mediated fibrinolysis and thrombi degradation (11, 12). Here, PLG is linked to atypical hemolytic-uremic syndrome.