Intravenous iron increases labile serum iron but does not impair forearm blood flow reactivity in dialysis patients

Abstract

Background. There are concerns about adverse vascular effects of intravenous iron by inducing oxidative stress. We therefore examined the effect of a single high dose of intravenous iron on endothelial function and biochemical markers of iron homeostasis. Methods. In a randomized, placebo-controlled, double-blind, parallel-group study, forearm blood flow (FBF) was assessed by strain-gauge plethysmography in 38 peritoneal dialysis patients before and after a single intravenous infusion of 300 mg iron sucrose. Results. Iron infusion increased total (Δ 601 μg/100 mL, CI 507, 696) and non-transferrin-bound iron (Δ 237.2 μmol/L, CI 173.6, 300.8) approximately 10-fold, as well as redox-active iron nearly five-fold (Δ 0.76 μmol/L, CI 0.54, 0.98). After iron infusion basal FBF was 59% higher than after placebo. FBF response to acetylcholine before and after iron infusion was 263 ± 32% and 310 ± 33%, corresponding to 304 ± 43% and 373 ± 29% in the placebo group, respectively. Before and after iron or placebo infusion, glyceryl-trinitrate increased resting FBF to 232 ± 22% and 258 ± 21% in the iron group, and to 234 ± 18% and 270 ± 30% in the placebo group. L-N-monomethyl-arginine decreased FBF to 70 ± 4% and 72 ± 3% before and after iron, and to 74 ± 4% and 73 ± 4% before and after placebo infusions, respectively. Despite higher basal FBF after iron infusion, absolute and relative FBF changes in response to vasoactive substances were not significantly different between iron and placebo groups. Conclusion. Our data suggest that 300 mg intravenous iron sucrose has a vasodilatory effect, but does not impair vascular reactivity in dialysis patients, despite a significant increase in non-transferrin-bound and redox-active iron. © 2005 by the International Society of Nephrology.