Prostacyclin-Like Activity and Bleeding in Renal Failure

Low Responsiveness to Clopidogrel Increases Risk among CKD Patients Undergoing Coronary Intervention

“…1 The mechanisms for decreased antiplatelet drug effects in patients with chronic kidney disease are poorly understood and could be explained by a number of disturbances found in chronic kidney disease and possibly leading to altered platelet function and reduced sensitivity to antiplatelet drugs. This includes an increase in the platelet turnover rate 18 by means of increased levels of thrombospondin 19,20 ; poor bioavailability of the active clopidogrel metabolite caused by impaired absorption or drug metabolization 21,22 ; procoagulant factors, such as thrombin-antithrombin III complex, D-dimer, fibrinogen, fibrinopeptide A, and von Willebrand factor 23,24 ; altered metabolism of prostaglandin 25 ; changes in thromboxane A2-dependent platelet activation and altered expression of platelet surface receptors 26,27 ; and extrinsic factors such as uremic toxin, anemia, and abnormality of nitric oxide synthesis. 28,29 We are aware of several limitations associated with this study.…”

Effect of 1-Deamino-8-D-Arginine Vasopressin on the Prolonged Bleeding Time in Chronic Renal Failure

“…This haemorrhagic diathesis is believed to be due to a qualita tive platelet disorder, and various defects in platelet func tion, as measured by platelet aggregation [2], adhesion [26], factor III availability [15], and bleeding time [27], have been described in association with advanced uraemia. Abnormalities of prostaglandin metabolism, which have more recently been identified in uraemic subjects, may also contribute to the platelet dysfunction [19,22], Of the tests available, the prolongation of bleeding time appears to correlate best with the risk of clinical haemorrhage [27].…”

Inhibitors of Coagulation in Terminal Renal Failure and during Hemodialysis

“…Hemostatic alterations in renal failure are certainly complex and involve abnormal platelet function [1], in creased release of vascular prostacyclin [2], impaired release of plasminogen activator [3], and abnormalities in Factor Vlll-von Willebrand complex [4], Low levels of circulating antithrombin III (AT III) have also been reported [1], Recently, Alegre et al [5] reported a decrease in immunoreactive protein C during hemodialysis and sug gested that this may contribute to the prothrombotic state observed in these patients.…”