2007 JASN IMPACT FACTOR 7.111	HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP
advanced	CURRENT ISSUE	ARCHIVES	JASN Express	ONLINE SUBMISSION

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lahera, V. Articles by Luño, J. Search for Related Content PubMed PubMed Citation Articles by Lahera, V. Articles by Luño, J.

Oxidative Stress in Uremia: The Role of Anemia Correction

Vicente Lahera^*, Marian Goicoechea, Soledad García de Vinuesa, Pilar Oubiña^*, Victoria Cachofeiro^*, Francisco Gómez-Campderá, Raquel Amann and José Luño

^* Department of Physiology, School of Medicine, Universidad Complutense, and Department of Nephrology, Hospital General Universitario Gregorio Marañon, Madrid, Spain

Address correspondence to: Dr. Vicente Lahera, Department of Physiology, Facultad de Medicina, Universidad Complutense de Madrid, 28040 Madrid, Spain. Phone: +34-91-394-2287; Fax: +34-91-394-1628; E-mail: vlahera{at}med.ucm.es

Patients with chronic kidney disease (CKD) are prone to develop cardiovascular disorders. Numerous reports have shown the association between uremia and oxidative stress, which increases patients’ risk for cumulative injury to multiple organs. Anemia is a common and disabling feature of CKD and seems to be a main cause of oxidative stress; correction of anemia represents an effective approach to reduce oxidative stress and, consequently, cardiovascular risk. There is increasing evidence that correction of anemia with erythropoiesis-stimulating agents could protect from oxidative stress in patients with CKD and ESRD. However, iron deficiency frequently complicates anemia in patients with CKD, and ferrous iron cation is a co-factor that is needed for hydroxyl radical production, which can promote cytotoxicity and tissue injury. This has raised a justifiable concern that prescription of intravenous iron may exacerbate oxidative stress and, hence, endothelial dysfunction, inflammation, and progression of cardiovascular disease, which are widely known consequences of CKD. Correction of anemia represents an effective approach to reduce oxidative stress and, consequently, cardiovascular risk. Iron deficiency is a common cause of resistance to erythropoiesis-stimulating agents, and the overall risk-benefit ratio favors use of intravenous iron to treat iron deficiency in patients with CKD. Consecutive or combined treatment with intravenous iron and erythropoiesis-stimulating agents clearly is beneficial for patients with CKD and iron deficiency, and anemia and could contribute to prevent the risk for cardiovascular events in these patients.

This article has been cited by other articles:

				M. Chonchol, G. Lippi, M. Montagnana, M. Muggeo, and G. Targher Association of inflammation with anaemia in patients with chronic kidney disease not requiring chronic dialysis Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2879 - 2883. [Abstract] [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673