Endothelial cell markers in chronic uremia: Relationship with hemostatic defects and severity of renal failure

Mezzano D.; Panes O.; Perez M.; Muñoz B.; Aranda, E; Pereira J.; Tagle, R; Pais, E; Downey P.; Barja P.; Thambo, S; González F; Mezzano S.

Keywords: endothelium, kidney, blood, cell, disease, markers, coagulation, activator, severity, humans, human, failure, fibrinolysis, inhibitor, progression, antigens, uremia, article, correlation, function, chronic, hemostasis, plasminogen, vascular, clinical, thrombomodulin, 1, priority, journal, biological, Endothelium,, Failure,, thrombocyte, thromboplastin


Plasma von Willebrand factor antigen, soluble thrombomodulin, and tissue factor were increased in 31 patients with severe chronic renal failure (creatinine clearance <20 ml/min) under conservative treatment, whereas plasminogen activator inhibitor antigen did not differ significantly from healthy controls. No correlation among plasma levels of these proteins was found. Three patterns of relationship between endothelial cell markers and hemostatic defects were identified: 1) Plasma thrombomodulin, a marker of endothelium damage, was found an independent predictor of bleeding time and platelet aggregation, and secretion defects, and was also related to the severity of renal failure; 2) yon Willebrand factor antigen, an index of endothelial cell activation and secretion, was significantly correlated with intravascular markers of thrombin and plasmin generation and with platelet adenosine triphosphate content, but not with plasma creatinine levels; and 3) tissue factor and plasminogen activator inhibitor antigen levels were not statistically correlated with the diverse hemostatic defects. Activation of coagulation and fibrinolysis, secondary to endothelial cell activation, appearing early during the evolution of chronic renal failure, is pathogenically related to the platelet dysfunction, and probably to development of atherosclerosis and thrombotic events in this disease. The progression of chronic renal failure, through endothelial cell damage, would lead to aggravation of the platelet functional defect potentiating the hemorrhagic risk.

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Título de la Revista: THROMBOSIS RESEARCH
Volumen: 88
Número: 6
Fecha de publicación: 1997
Página de inicio: 465
Página final: 472
URL: http://www.scopus.com/inward/record.url?eid=2-s2.0-0031574323&partnerID=q2rCbXpz