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Etiology and Pathogenesis

  • Reduced renal production of erythropoietin (EPO), inflammation, and hepcidin-induced iron restriction are the most significant factors in the development of anemia in renal insufficiency.

  • A modest reduction in red cell life span occurs in uremia, probably as a result of metabolic impairment of red cells.

  • Iron deficiency occurs from blood loss in dialysis tubing, laboratory testing, or external bleeding, sometimes as a result of uremia-induced platelet dysfunction. Furthermore, increased hepcidin blocks iron absorption in the gut and iron release from macrophage stores (in part ameliorated by therapy with EPO or other erythropoiesis-stimulating agents [ESAs]).

  • The plasma volume varies widely in renal failure, with consequent variations in the hemoglobin concentration.

Clinical and Laboratory Features

  • The anemia is normocytic and normochromic with a reduced blood concentration of reticulocytes relative to the degree of anemia and, in this special case, a loss of renal parenchyma, thereby decreasing the source of EPO. Gastrointestinal and gynecologic bleeding occurs in one-third to one-half of all patients with chronic renal failure from associated platelet dysfunction, contributing to the anemia (see Chap. 77).

  • Acanthocytes or schistocytes may be seen on the blood film.

  • Total and differential leukocyte counts and platelet count are usually normal.

  • Platelet function is abnormal, in relationship to the degree of uremia.

  • Cellularity and blood cell maturation sequences in the marrow are normal. Despite the anemia, there is no compensatory erythroid hyperplasia as a result of low EPO levels.

Therapy, Course, and Prognosis

  • Replacement therapy with EPO or other ESA corrects the anemia in nearly all patients. Amelioration of the anemia improves the quality of life for uremic patients.

  • EPO and iron are usually given intravenously in dialysis patients. A target hemoglobin level of 10 to 11 g/dL is recommended.

  • Adequate iron and folate supply should be maintained to achieve an optimal response with EPO or ESA therapy. Low serum ferritin concentrations are indicative of iron deficiency in anemia of chronic renal disease, but normal or even high ferritin concentrations do not preclude a clinical response (increased hemoglobin and/or decreased dosage of EPO derivatives) after parenteral iron therapy. In these settings, high ferritin levels may largely reflect inflammation, and augmented iron supply may be needed to overcome functional iron deficiency, that is, to provide sufficient iron supply for erythropoiesis stimulated by intermittently administered pharmacologic doses of EPO or its derivatives. If transferrin iron saturation is less than 30% and ferritin is less than 300 μg/L, intravenous iron therapy usually increases hemoglobin levels or decreases the ESA doses required, whether or not patients are on hemodialysis.

  • Long-acting EPO preparations (eg, darbepoetin) given subcutaneously are more convenient and, perhaps, safer for patients not undergoing dialysis because plasma ESA levels are lower but more sustained.

  • Complications of EPO therapy include hypertension, seizures, increased cardiovascular morbidity and mortality, and thrombosis of ...

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