A case-control study indicates that coagulation imbalance is associated with arteriosclerosis and markers of endothelial dysfunction in kidney failure

Endothelial dysfunction, one of many causes arterial changes in end-stage kidney disease (kidney failure), is a likely link between early vascular aging and the risk thrombosis or bleeding this condition. To evaluate this, we compared links stiffness endothelial/coagulation factors 55 patients receiving hemodialysis therapy 57 age-/sex-matched control individuals. Arterial was assessed from carotid-femoral pulse wave velocity, coagulation status endogenous thrombin generating potential. Markers endothelial dysfunction (von Willebrand factor, tissue factor pathway inhibitor), neutrophil extracellular traps factor-positive vesicles were higher with failure. Prothrombin fragments 1 2, D-dimer markers vivo activation also higher. However, vitro presence platelets, potential lower its downregulation by activated protein C impaired. Antiplatelet drugs did not affect these parameters. In multiple regression analysis, prothrombin D-dimer, VIII monocyte-derived correlated velocity. failure, hypercoagulability occurred reduced generation platelet-rich plasma, explaining opposing thrombotic tendencies Importantly, arteriosclerosis more closely related to prothrombotic state. Thus, plus highlight major therapeutic challenge for anticoagulant antiplatelet drug use. Coagulation anomalies, aortic stiffnessKidney InternationalVol. 99Issue 5PreviewIn chronic disease, wall undergoes complex remodeling, which leads stiffness. This increased cardiac workload enhanced pressure transmission into microcirculation, leading microvascular damage organ dysfunction. Beyond regulation tone, endothelium plays key role coagulation. patients, Tran et al. show that ongoing activity associated contrast, are increased, risk. Full-Text PDF