Hematologic aspects of end-stage renal failure

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Abstract
Renal dysfunction may give rise to a variety of hematologic disturbances, including anemia, leukocyte dysfunction, and coagulopathy. The anemia of renal failure has been attributed to a relative deficiency of erythropoietin, but absolute deficiencies of iron or folate may also play a role. Other contributing factors include heavy-metal toxicity, blood loss, and a reduction in red cell survival induced by toxic radicals. The treatment of the anemia of renal disease has advanced with the development of recombinant human erythropoietin. At subcutaneous doses of 50–75 IU/kg triweekly in selected patients, normalization of hemoglobin is presently possible. The coagulopathy of renal disease consists of an acquired qualitative platelet defect, best remedied by dialysis but also treated successfully by rHuEPO, cryoprecipitate or DDAVP, and conjugated estrogens. Uremia-induced leukocyte dysfunctions include diminished granulocyte chemotaxis, phagocytosis, and bactericidal activity. Cell-mediated immune defects and hypogammaglobulinemia have also been described. The pathophysiology of the hematologic manifestations of uremia is discussed. Therapeutic recommendations for dealing with anemia, bleeding, and infectious complications of renal failure are described.