Intravenous iron sucrose does not impair sonographic brachial vasodilation in peritoneal dialysis patients.

Serious concerns have been raised with respect to intravenous (i.v.) iron as a potential oxidative stress inducer in chronic kidney disease patients. Oxidative stress has been linked to uremia-related inflammation and endothelial dysfunction. Because i.v. iron promotes oxidative stress and because uremic patients have numerous defects of antioxidant defense unrelated to iron, we hypothesized that i.v. iron administration might increment oxidative stress and consequently endothelial dysfunction. We undertook a pilot study of 8 patients from our peritoneal dialysis (PD) program who were in stable clinical condition. We measured high-sensitivity C-reactive protein (hsCRP), von Willebrand factor antigen (vWFa), and fibrinogen in serum, and several sonographic parameters: left ventricular ejection fraction, left ventricular mass index, carotid intima media thickness, and the presence of carotid plaques. We also used a sonographic methodology to measure endothelium-dependent vasodilation (EDV) and endothelium-independent vasodilation (EIV) in the brachial artery. Three hours after i.v. administration of 200 mg iron sucrose, we repeated the biochemical measurements and the sonographic vasodilation parameter measurements in the brachial artery. None of the biochemical parameters were modified after administration of i.v. iron sucrose [hsCRP: < 0.5 mg/L (range: < 0.5 - 48 mg/L) vs. < 0.5 mg/L (range: < 0.5 - 37 mg/L), p = 0.46; vWFa: 192% +/- 39% vs. 189% +/- 32%; p = 0.40; fibrinogen: 449 +/- 127 mg/dL vs. 445 +/- 128 mg/dL, p = 0.80). Furthermore, i.v. iron stimulus did not affect either EDV (5.8% +/- 2.7% vs. 7.8% +/- 1.9%, p = 0.09) or EIV (15.3% +/- 2.9% vs. 21.4% +/- 2.2%, p = 0.11). Our data do not support an acute impact of i.v. iron in our PD patients with regard to endothelial-related biochemical parameters or sonographic vasodilation of the brachial artery.