Hemostatic disturbances in patients with systemic inflammatory response syndrome (SIRS) and associated acute renal failure (ARF)

Endothelial damage plays a central role in the development of an SIRS-relat ed Multiple Organ Dysfunction Syndrome (MODS) as a consequence of the estab lishment of a hemostatic imbalance between coagulation and fibrinolysis sys tems. Until now, sepsis is the SIRS model that has been most studied. The a im of this study was to assess the endothelial damage and the hemostatic im balance in early stages of an SIRS of different origins, and to study if th ere are any differences in these disturbances between infectious and noninf ectious SIRS. The endothelial damage and hemostatic changes were studied in 40 patients with SIRS (with less than 12 h of evolution) and an acute rena l failure. Infectious SIRS was diagnosed in 19 cases and noninfectious SIRS in the remaining 21 patients. Patients with SIRS presented significantly h igher values (p<0.001) for factors related to endothelial damage [von Wille brand factor (VWF), thrombomodulin, tissue plasminogen activator (t-PA), an d plasminogen activator inhibitor type 1 (PAI-1) antigen], hypercoagulabili ty [prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complexes (TA T)I, and fibrinolysis (D-dimer and PAI activity) with respect to the contro l group. However, although the group with infectious SIRS presented higher values for all the factors except for the t-PA and D-dimer with respect to SIRS of other origins, none of these differences reached statistical signif icance (p>0.05). Our data show that patients with SIRS and associated acute renal failure, irrespective of the origin (infectious or noninfectious), s how signs of intense endothelial damage and hypercoagulability throughout t he process. (C) 2000 Elsevier Science Ltd. All rights reserved.