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Iron Metabolism, Iron Deficiency, Thrombocytosis, and the Cardiorenal Anemia Syndrome

^aWayne State University, Detroit, Michigan, USA; ^bHenry Ford Hospital, Detroit, Michigan, USA; ^cDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria; ^dDepartment of Nephrology, Tel Aviv Medical Center, Tel Aviv, Israel

Key Words. Iron metabolism • Erythropoiesis-stimulating agents • Iron deficiency • Cardiorenal anemia syndrome • Thrombocytosis • Coagulopathy

Correspondence: Anatole Besarab, M.D., Henry Ford Hospital, Division of Nephrology and Hypertension, Department of Internal Medicine, 2799 West Grand Blvd., CFP-511, Detroit, Michigan 48301, USA. Telephone: 248-916-2713; Fax: 248-916-2554; e-mail: abesara1{at}hfhs.org

Received February 25, 2009; accepted for publication May 18, 2009.

Disclosures: Anatole Besarab: Honoraria: Amgen, AMAG Pharma, Watson Pharma, Hoffmann-La Roche; Research funding/contracted research: AMAG Pharma; Walter Hermann Hörl: None; Donald Silverberg: Consultant/advisory role: Amgen.

The content of this article has been reviewed by independent peer reviewers to ensure that it is balanced, objective, and free from commercial bias. No financial relationships relevant to the content of this article have been disclosed by the independent peer reviewers.

In treating moderate to severe anemia of chronic kidney disease (CKD), oral iron is effective only in a minority of nondialysis patients. Intravenous iron is more effective and can raise levels of hemoglobin even without the use of erythropoiesis-stimulating agents (ESAs). Unfortunately, the current assays of iron status that are presently widely available are not especially helpful in predicting response. In patients on dialysis, i.v. iron is effective over a wide range of serum ferritin from <100 ng/ml to 800 ng/ml. None of the three available randomized controlled trials comparing oral with i.v. iron showed evidence of nephrotoxicity caused by i.v. iron.

Iron deficiency is a risk factor for thrombocytosis and should, wherever possible, be avoided. Optimal coadministration of iron may reduce the risk for ESA-driven cardiovascular events. Increased total body iron stores (imperfectly reflected by serum ferritin levels in CKD) do not appear to be related to such events or hospitalization in CKD; it is unclear what other risk factors and mechanisms need to be considered.

In the appreciable proportion of patients with both renal and cardiac dysfunction, management is further complicated by a vicious circle (which can be characterized as cardiorenal anemia syndrome) in which CKD, heart failure, and anemia exacerbate each other. In such patients, correction of anemia appears to improve cardiac function and quality of life without a greater risk for adverse events.

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