Abstract
Anemia is a frequent and serious complication of end-stage renal disease (ESRD). Since the introduction of recombinant human erythropoietin (EPO) into clinical practice in the 1980s, our understanding of the importance of iron supply for optical erythropoiesis with EPO has increased. In the past decade we have clearly learned that anemia management can be optimized only if functional iron deficiency can be avoided1,2. During functional iron deficiency, erythropoietic capacity of the bone marrow to respond to epoetin is limited by iron release from storage sites and/or by a limited capacity to transport iron via transferrin3. The National Kidney Foundation–Dialysis Outcomes Quality Initiative (NKF-DOQI) guidelines advocate aggressive detection and management of functinoal iron deficiency4. The presence of functional iron deficiency is confirmed by the response to a course of parenteral iron that produces either a decrease in dose of EPO needed to maintain the terget hematocrit level or an increase in hemoglobin at the same dose of epoetin. Analysis of these "iron restoration" protocols, the most common of which administer 1000 mg of parenteral iron over five to ten consecutive dialysis treatments, indicates that ferritin increases from a pre-treatment mean of 209 ng/mL to a post treatment mean of 447 ng/mL3. The latter is higher than the upper limits for a normal population and is of concern to many physicians.
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