In renal failure, there are no consistent major alterations in coagulation factors or tests, no impairment of fibrinolysis, and no reduction in platelet production. However, prolongation of the bleeding time correlates with clinical bleeding, and impaired aggregation, adhesion, and interaction of platelets with the vessel wall underlie the primary hemostatic defect in uremia (Zach.ee.eLa.1 1994). The pathogenesis of this platelet dysfunction is multifactorial, and defects in calcium homeostasis, purine nucleotide metabolism, prostaglandin production, and secondary hyperparathyroidism have been implicated. The prolonged bleeding time can be shortened by elevation of the hematocrit above 0.35, infusion of cryoprecipitate (enriched in factor VIII), or the administration of deamino-D-arginine vasopressin (0.3 pg/kg intravenously over 30 min or subcutaneously) which increases levels of circulating von Willebrand factor but may be relatively contraindicated in patients with critical coronary or cerebrovascular disease. Conjugated estrogens, which produce a longer-lasting reduction in bleeding time, are also used.
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