HFRS represents a systemic inflammatory response syndrome, with a multifactorial pathogenesis [7], including increased cleavage of high molecular weight kininogen, higher enzymatic activities of FXIIa/kallikrein, and increased liberation of bradykinin from endothelial cells, resulting in overactivation of the kallikrein-kinin system and increased endothelial cell permeability [8]. This evidence concerns the gene KLK4 and hemorrhagic fever with renal syndrome.