(See also Overview of Decreased Erythropoiesis.)
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 renal 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/minute. Renal glomerular lesions (eg, due to amyloidosis, diabetic nephropathy) generally result in the most severe anemia for their degree of renal excretory failure.
Diagnosis of anemia of renal disease is based on demonstration of renal insufficiency, normocytic anemia, and peripheral reticulocytopenia.
The bone marrow may show erythroid hypoplasia. RBC fragmentation identified on the peripheral smear, particularly if there is thrombocytopenia, suggests simultaneous traumatic hemolysis.
Treatment of anemia of renal disease is directed at
If renal function returns to normal, anemia is slowly corrected.
In patients receiving long-term dialysis, recombinant erythropoietin, beginning with 50 to 100 units/kg IV or subcutaneously 3 times a week with iron supplements, is the treatment of choice. In almost all cases, maximum increases in RBCs are reached by 8 to 12 weeks. Reduced doses of EPO (about one half the induction dose) can then be given 1 to 3 times a week. Transfusions are rarely necessary. Careful monitoring of the response is needed to avoid adverse effects when hemoglobin increases to > 12 g/dL (> 120 g/L).