Iron overload in renal failure patients: Changes since the introduction oferythropoietin therapy

Iron overload was a common complication in patients with chronic renal fail ure treated with dialysis prior to the availability of recombinant human er ythropoietin (rHuEPO) therapy. Iron overload was the result of hypoprolifer ative erythroid marrow function coupled with the need for frequent red bloo d cell transfusions to manage symptomatic anemia. The repetitive use of int ravenous iron with or without the use of red blood cell transfusions also c ontributed to iron loading and was associated with iron deposition in liver parenchymal and reticuloendothelial cells; however, there were no abnormal liver function tests or evidence of cirrhosis unless viral hepatitis resul ted from the transfusions. With rHuEPO therapy, the excess iron stores were shifted back into circulating red blood cells as the anemia was partially corrected, and red blood cells were lost from circulation by the hemodialys is procedure. After several years of rHuEPO therapy, most hemodialysis pati ents required iron supplements to replace the continuing blood losses relat ed to hemodialysis. The potential complications of iron overload (parenchym al iron deposition, permanent organ damage, increased risk of bacterial inf ections, and increased free radical generation) are reviewed in the context of this setting.