Both a bleeding diathesis and a tendency to hypercoagulability occur in the course of renal disease. More common and consistent in occurrence during the progression of renal failure to end-stage renal disease is the hemostatic defect. The principal cause of this abnormality is the uremic state and, as a rule, it is reversible following the institution of adequate renal replacement therapy and correction of the anemia with epoietin. By contrast, the tendency to hypercoagulability is usually encountered in patients with the nephrotic syndrome and shows a correlation to the degree of hypoalbuminemia, being more evident at serum albumin levels of < 2 g/dl. Although the coagulopathy is complex in pathogenesis, a defect in the fibrinolytic process plays a critical role in its development. A tendency to pro-thrombosis due to abnormal fibrinolysis has been identified also in patients on renal replacement therapy with continuous ambulatory peritoneal dialysis (CAPD). The observed coagulation abnormalities resemble those of the nephrotic syndrome. Although its etiology remains undefined, a role for the albumin losses in the peritoneal dialysate has been implicated in the prothrombotic state that occurs in some CAPD patients.
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