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Iron sucrose promotes endothelial injury and dysfunction and monocyte adhesion/infiltration.

Abstract：

BACKGROUND/AIMS:Intravenous (IV) iron preparations are widely used in the management of anemia in ESRD populations. Recent changes in reimbursement policy have dramatically increased the use of IV iron to lower the use of costly erythropoiesis-stimulating agents. These preparations are frequently administered with insufficient attention to the total body iron stores or presence of inflammation which is aggravated by excess iron. Endothelial injury and dysfunction are critical steps in atherosclerosis, thrombosis and cardiovascular disease. IV iron preparations raise plasma non-transferrin-bound iron which can promote oxidative stress, endothelial damage and dysfunction. We explored the effect of an IV iron preparation on endothelial cells, monocytes and isolated arteries. METHODS:Primary cultures of human aortic endothelial cells (HAEC) were treated with pharmacologically relevant concentrations of iron sucrose (10-100 μg/ml) for 4-24 h. Endothelial cell morphology, viability, and monocyte adhesion were tested. Endothelial function was assessed by measuring the vasorelaxation response to acetylcholine in normal rat thoracic aorta rings preincubated with iron sucrose (200 μg/ml). RESULTS:In contrast to the control HAEC which showed normal cobblestone appearance, cells treated with iron sucrose (50-100 μg/ml) for 4 h showed loss of normal morphological characteristics, cellular fragmentation, shrinkage, detachment, monolayer disruption and nuclear condensation/fragmentation features signifying apoptosis. HAEC exposure to iron sucrose (10-100 μg/ml) increased monocyte adhesion 5- to 25-fold. Incubation in media containing 200 μg/ml iron sucrose for 3 h caused marked reduction in the acetylcholine-mediated relaxation in phenylephrine-precontracted rat aorta. CONCLUSION:Pharmacologically relevant concentration of iron sucrose results in endothelial injury and dysfunction and marked increase in monocyte adhesion.

journal_name

Am J Nephrol

journal_title

American journal of nephrology

authors

Kamanna VS,Ganji SH,Shelkovnikov S,Norris K,Vaziri ND

doi

10.1159/000334939

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

114-9

issue

eissn

0250-8095

issn

1421-9670

pii

000334939

journal_volume

pub_type

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Iron sucrose promotes endothelial injury and dysfunction and monocyte adhesion/infiltration.