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Aluminum induced anemia: Pathogenesis and treatment in patients on chronic hemodialysis. The baseline hematologic status of 27 patients with modest degrees of aluminum overload was examined. In addition, hematologic data were evaluated in 19 of these patients during and after treatment with DFO. Although neither severe anemia nor microcytosis was observed pretreatment, there was a significant correlation between hemoglobin level and degree of aluminum burden as determined by bone surface aluminum staining (r = -0.58; P < 0.007). Following treatment with DFO, hemoglobin concentration increased dramatically by 1.3 to 4.4 g/dl in eight patients but did not change in the remaining eleven. Responders and nonresponders were similar with regard to the degree of aluminum overload both before and after chelation therapy but differed with regard to baseline levels of erythropoietin (higher in responders) and degree of iron overload (greater in nonresponders). Pretherapy levels of red cell ALA dehydratase were depressed in all patients (32 ± 4 vs. 56 ± 5 U/g Hb in normals) but did not correlate with the degree of aluminum overload and did not change with chelation therapy. Pretherapy levels of red cell protoporphyrin were elevated in 15 of 24 patients (62%) and were higher in responders than in nonresponders. Following DFO therapy, levels fell by 25 to 50% in 7 of 8 patients with elevated pretherapy values, despite the tendency in several patients to develop iron deficiency with treatment. These results suggest that: 1) even in the absence of severe anemia or microcytosis, aluminum contributes to anemia in dialysis patients, an effect which correlates with bone surface staining for aluminum but not with other measures of aluminum overload; 2) the mechanism of the decreased red cell production seems to involve, at least in part, a defect in iron utilization; 3) in the absence of iron deficiency and inflammation, elevated levels of RBC protoporphyrin may be a useful test to suggest aluminum induced anemia but activity of red cell ALAD is not; and 4) a positive hematopoietic response to DFO requires at least adequate endogenous levels of erythropoietin to stimulate erythropoiesis.