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Differences in coagulation in clotting of vascular access in hemodialysis patients
Chinedu Nweke1, Erika Martin, Todd Gehr
1Division of Nephrology, Department of Internal Medicine, School of Medicine, Virginia Commonwealth University, Richmond, Virginia, USA.
Arteriovenous graft (AVG) thrombosis is a frequent cause of graft failure. We evaluated coagulation protein concentrations, platelet function, and viscoelasticity factors in 20 hemodialysis (HD) patients with AVGs. The goal was to determine whether significant differences in protein concentrations, platelet function, and viscoelasticity factors exist among dialysis patients requiring frequent AVG declot procedures vs. those who do not. Twenty HD patients were enrolled: 10 frequent clotters (>3 declots in the previous year) and 10 were nonclotters. Patients on antiplatelets or chronic anticoagulation were excluded. Laboratories were drawn pretreatment and heparinase was added to counteract any potential heparin effect. Coagulation protein concentrations including tissue factor (TF), thrombin/antithrombin III complex (TAT), and prothrombin fragment 1 + 2 (F(1+2)) were assayed. The time to clot onset was measured by force onset time (FOT). Platelet contractile force (PCF) measured the force produced by platelets during clot retraction, whereas clot rigidity was measured as clot elastic modulus (CEM). FOT, CEM, and PCF were measured by Hemodyne. Both groups had upregulation of the TF pathway, as TF, TAT, and F(1+2) levels were similarly increased over baseline levels. Hemodialysis patients with frequent AVG clotting had higher levels of both PCF and CEM compared with nonclotters. Additionally, the frequent clotters had a lower FOT relative to nonclotters, although both were considered in the normal range. Our study suggests that HD patients with recurrent AVG thrombotic events form clots with higher tensile strength compared with HD patients without recurrent graft thrombosis.
Arteriovenous graft (AVG) thrombosis is a frequent cause of graft failure. We evaluated coagulation protein concentrations, platelet function, and viscoelasticity factors in 20 hemodialysis (HD) patients with AVGs. The goal was to determine whether significant differences in protein concentrations, platelet function, and viscoelasticity factors exist among dialysis patients requiring frequent AVG declot procedures vs. those who do not. Twenty HD patients were enrolled: 10 frequent clotters (>3 declots in the previous year) and 10 were nonclotters. Patients on antiplatelets or chronic anticoagulation were excluded. Laboratories were drawn pretreatment and heparinase was added to counteract any potential heparin effect. Coagulation protein concentrations including tissue factor (TF), thrombin/antithrombin III complex (TAT), and prothrombin fragment 1 + 2 (F(1+2)) were assayed. The time to clot onset was measured by force onset time (FOT). Platelet contractile force (PCF) measured the force produced by platelets during clot retraction, whereas clot rigidity was measured as clot elastic modulus (CEM). FOT, CEM, and PCF were measured by Hemodyne. Both groups had upregulation of the TF pathway, as TF, TAT, and F(1+2) levels were similarly increased over baseline levels. Hemodialysis patients with frequent AVG clotting had higher levels of both PCF and CEM compared with nonclotters. Additionally, the frequent clotters had a lower FOT relative to nonclotters, although both were considered in the normal range. Our study suggests that HD patients with recurrent AVG thrombotic events form clots with higher tensile strength compared with HD patients without recurrent graft thrombosis.
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