Serum iron concentrations >42.3 μmol/L (>250 μg%) seen in childhood iron poisoning may be high enough to exceed the total number of transferrin binding sites in serum and are associated with marked toxicity (1)(2). Concerns over iron toxicity related to this “oversaturation” of transferrin have recently been applied to circumstances in which iron is given intravenously as either iron dextran (used in the US) or iron gluconate to patients on hemodialysis receiving erythropoietin therapy(3)(4). A recent study describing oversaturation of transferrin, as calculated by the measurement of high serum iron concentrations shortly after intravenous iron gluconate treatment, suggested that with this product, transferrin saturation is commonly >100% (serum iron/total iron binding capacity for transferrin binding sites × 100 = % saturation)(3). When transferrin is fully saturated, serum may contain “free” iron or iron loosely bound to other plasma proteins, a situation that can cause acute toxicity, including tissue damage, cardiac arrhythmias, and/or hypotension (1)(2). It has been suggested that this oversaturation soon after intravenous iron infusion in hemodialysis patients may account for these types of complications (3). However, parenteral iron is a necessary treatment in this patient population, and similar complications, particularly hypotension, are common during hemodialysis sessions even when iron is not given (4). Because iron bound to iron dextran or iron gluconate does not cause acute iron toxicity (5), we hypothesized that serum assays for iron measure the iron present in these complexes after intravenous infusion, which produces misleadingly high results for the oversaturation of transferrin. Pharmacokinetic studies have indicated that after infusion, serum concentrations of dextran-bound iron are distributed almost entirely in the plasma, with removal limited to the reticulo-endothelial system at a constant rate (3)(5)(6)(7). Previous studies in iron-deficient patients have …