Oxidative stress in uremia : The role of anemia correction

• Published in: Journal of the American Society of Nephrology Vol. 17; no. 12 Suppl 3; pp. S174 - S177
• Main Authors: LAHERA, Vicente, GOICOECHEA, Marian, GARCIA DE VINUESA, Soledad, OUBINA, Pilar, CACHOFEIRO, Victoria, GOMEZ-CAMPDERA, Francisco, AMANN, Raquel, LUNO, José
• Format: Conference Proceeding Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.12.2006
• Subjects: Anemia - complications; Anemia - physiopathology; Anemias. Hemoglobinopathies; Biological and medical sciences; Cardiovascular Diseases - etiology; Cardiovascular Diseases - physiopathology; Chronic Disease; Diseases of red blood cells; Hematologic and hematopoietic diseases; Humans; Kidney Diseases - complications; Kidney Diseases - physiopathology; Medical sciences; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Oxidative Stress - physiology; Renal failure; Risk Factors; Uremia - etiology; Uremia - physiopathology; Kidney disease; Human; Oxidative stress; Nephrology; Urinary system disease; Anemia; Pathogenesis; Renal failure; Hemopathy; Urology
• ISSN: 1046-6673; 1533-3450
• DOI: 10.1681/ASN.2006080911

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.