Numerous hemostatic abnormalities have been associated with acute and chronic renal disease. The most common abnormalities are defective platelet aggregation, decreased platelet adhesiveness, decreased platelet factor-3 availability, and prolongation of the bleeding time. Among the above platelet function tests, the bleeding time is the single test that most closely correlates with clinical bleeding. The nature of the platelet defect in uremia is still not well understood. The pathophysiologic mechanisms which have been implicated include platelet inhibition by plasma metabolites, eg, urea, guanidinosuccinic acid, phenolic acid; increased vessel wall prostacyclin; abnormal platelet arachidonic acid metabolism; increased levels of parathyroid hormone (PTH); defective binding of the Factor VIII complex to platelets or defective binding of platelets to vessel wall subendothelium by the Factor VIII complex; decreased platelet-vessel wall-interaction due to severe anemia; platelet storage pool deficiency; defective fibrinogen binding to platelets. Dialysis remains the mainstay of the prevention and treatment of uremic bleeding although it is not always immediately effective. The availability of cryoprecipitate and DDAVP offers an alternative and effective treatment for the temporary reversal of uremic bleeding in patients who require urgent invasive procedures.