Heme-induced kallikrein-kinin system activation in hemolytic uremic syndrome

The authors investigate the role of heme in activating the kallikrein-kinin system during hemolytic uremic syndrome (HUS) and its interaction with clotting factor XII (FXII). They find that heme induces FXII activation, leading to the degradation of high-molecular-weight kininogen and the release of bradykinin, which may contribute to inflammation in HUS. The study suggests that targeting this pathway could offer potential therapeutic strategies for managing hemolytic diseases.