Kallikrein-Kinin System in Patients With Shock. Comparison Between Septic and Cardiogenic Shock

Abstract

Alterations of the kallikrein-kinin system (KKS) consistent with activation and increased consumption have been reported in septic patients and it has been suggested that this activation could contribute to the development of septic shock. As similar alterations have been found in other critically ill patients, many of them prone to shock, we wonder if activation of the KKS could be a consequence rather than a cause of the hemodynamic instability. To answer this question we compared 12 patients with septic shock (8 fatal) with 10 cases of cardiogenic shock secondary to myocardial infarction (8 fatal) as a model of non septic shock. In adition 25 episodes of uncomplicated sepsis and 10 intra-intensive care unit controls were studied. A functional measure of factor XII, high molecular weight kininogen (HMWK) (coagulative methods), prekallikrein (PK), Cl-inhibitor (Cl-INH), α2-macroglobulin (α2-M)- Antithrombin III (AT-III) and kallikrein inhibitor activity (KIA) (chromogenic methods) was performedRESULTS: Patients with septic shock, specially in fatal cases, showed a highly significant decrease in activities of factor XII (P<0.001), PK (P<0.0001), HMWK (P<0.005), α2-M (P<0.001), AT-III (P<0.0001) and KIA (P<0.005). Cl-INH activity was increased in uncomplicated sepsis (P<0.001) but came back to normal or was slightly decreased in septic shock. Components and inhibitors of the KKS were within normal limits in all patients with cardiogenic shock.Our findings support the idea of a contribution of the KKS to the development of septic shock but this system neither seems to play a role in the pathogenesis of cardiogenic shock nor to be altered as a consequence of it.