Uremic bleeding: pathogenesis and therapy

We reviewed current understanding of the pathophysiology of the uremic bleeding diathesis and discuss accepted therapeutic interventions that minimize the risk of bleeding in the uremic patient.

Computerized literature searches and references from previous publications, including articles describing original research and reviews pertaining to the pathophysiology of and clinical approach to uremic bleeding.

The most common hemorrhagic manifestations in uremia are prolonged bleeding from puncture sites; nasal, gastrointestinal and genitourinary bleeding; and subdural hematomas. The most useful clinical laboratory test to assess both bleeding risk and response to therapy is bleeding time. It correlates better with clinical bleeding complications than indices of azotemia (eg, blood urea nitrogen [BUN], creatinine) or in vitro platelet aggregation tests. A low hematocrit is also correlated with increased bleeding risk. Anemia plays an important role in the bleeding diathesis of uremia and its correction with red cell transfusions or human recombinant erythropoietin is critical. Anticoagulation during hemodialysis may transiently exacerbate the bleeding diathesis. Hemodialysis and peritoneal dialysis improve the hemostatic defect and renal transplantation totally corrects it. Cryoprecipitate has been largely replaced by desmopressin acetate, which acts promptly (in less than 1 hour) but has a short duration of action (hours) and exhibits tachyphylaxis. Conjugated estrogens are slower in the onset of action (about 6 hours) but their effect lasts for about 2 weeks.

The pathophysiology of the bleeding diathesis of uremia is complex and incompletely understood but useful clinical tests and therapies have evolved empirically. Broadly available dialysis and the advent of erythropoietin are likely to reduce the magnitude of this problem.