Anemia of Renal Disease
Anemia of renal disease is a hypoproliferative anemia resulting primarily from deficient erythropoietin (EPO) or a diminished response to it; it tends to be normocytic and normochromic. Treatment includes measures to correct the underlying disorder and supplementation with EPO and sometimes iron.
(See also Overview of Decreased Erythropoeisis.)
Anemia in chronic renal disease is multifactorial.
The most common mechanism is
Other factors include
Less common is RBC fragmentation (traumatic hemolytic anemia), which occurs when the renovascular endothelium is injured (eg, in malignant hypertension, membranoproliferative glomerulonephritis, polyarteritis nodosa, or acute cortical necrosis).
The deficiency in renal production of EPO and the severity of anemia do not always correlate with the extent of renal dysfunction; anemia occurs when creatinine clearance is < 45 mL/min. Renal glomerular lesions (eg, from amyloidosis, diabetic nephropathy) generally result in the most severe anemia for their degree of excretory failure.
Diagnosis is based on demonstration of renal insufficiency, normocytic anemia, and peripheral reticulocytopenia. Bone marrow may show erythroid hypoplasia. RBC fragmentation on the peripheral smear, particularly if there is thrombocytopenia, suggests simultaneous traumatic hemolysis.
Therapy is directed at improving renal function and increasing RBC production. If renal function returns to normal, anemia is slowly corrected. In patients receiving long-term dialysis, EPO, beginning with 50 to 100 units/kg IV or sc 3 times/wk with iron supplements, is the treatment of choice. In almost all cases, maximum increases in RBCs are reached by 8 to 12 wk. Reduced doses of EPO (about ½ the induction dose) can then be given 1 to 3 times/wk. Transfusions are rarely necessary. Careful monitoring of the response is needed to avoid adverse effects when Hb increases to >12 g/dL.