Pathophysiology and treatment of the anemia of renal failure

Abstract

The pathophysiology of anemia associated with renal failure and the major pharmacologic agents used in the treatment of this anemia are reviewed. Patients with renal failure are often anemic primarily because of diminished circulating erythropoietin and suppressed erythropoiesis in the bone marrow. The anemia may cause malaise, fatiguability, aggravated angina, and decreased exercise tolerance. Many patients require frequent red blood cell transfusions. Therapy has included anabolic androgen administration, iron and vitamin supplementation, and the administration of red blood cells. These approaches generally have not resulted in sustained improvement of the anemia. The recent development of recombinant human erythropoietin may represent a major therapeutic advance for the treatment of anemia associated with renal failure. Previously, erythropoietin therapy was not possible because of lack of sufficient quantities of the purified hormone. Clinical trials indicate, however, that recombinant human erythropoietin may improve erythropoiesis in most patients. Adverse effects have generally been mild and easily managed; however, increases in blood pressure and arteriovenous fistula clotting have been reported. Although initial reports are encouraging, larger and longer clinical trials are needed to determine proper dosing and to understand more completely the potential adverse effects of recombinant human erythropoietin. Previous pharmacologic attempts to improve the anemia associated with renal failure have been largely unsatisfactory; initial reports on the use of recombinant human erythropoietin are promising.