Abstract
The quantitative variation among patients in their response to erythropoietin can be explained, in part, by factors that can independently cause anemia in patients with end-stage renal disease. Aluminum can blunt the effect of erythropoietin, in part by interfering with iron bioavailability. This inhibitory effect cannot be completely overcome by aggressive ferrotherapy, but can be reversed with aluminum chelation therapy. A patient is described who developed hematological evidence of aluminum excess after being treated with erythropoietin. The biochemical evidence of functional iron deficiency and the response to aluminum chelation therapy support the hypothesis that the inhibitory effect of aluminum on erythropoiesis is mediated by the interference of aluminum with the bioavailability of iron.
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