Intravenous iron supplementation in the anaemia of renal and cardiac failure—a double-edged sword?
Division of Adult Nephrology, Shaare Zedek Medical Center, PO Box 3235, Jerusalem, 91031 Israel
Correspondence and offprint requests to: Dr Itzchak Slotki, Division of Adult Nephrology, Shaare Zedek Medical Center, PO Box 3235, Jerusalem, 91031 Israel. Email: islotki{at}szmc.org.il
The anaemia of chronic kidney disease (CKD) is efficiently corrected with a combination of recombinant erythropoietin (rhEPO) and intravenous iron supplementation. Recently, patients with severe cardiac failure and anaemia have also been shown to benefit from this treatment. However, iron excess may lead to the production of free radicals and has been incriminated in the pathogenesis of atherosclerosis and increased risk of infection, the two major causes of death in end-stage renal disease. The exact risk of excess iron supplementation has not been defined and, in the absence of sensitive and specific indicators of iron overload, the risk remains difficult to quantify. There is increasing epidemiological evidence incriminating iron overload as a risk factor in CKD, but direct evidence is still hard to obtain. The precise role of iron is complicated further by the complex inter-relationships between iron metabolism and the inflammatory process characteristic of CKD. The recent discovery of the antimicrobial peptide, hepcidin, may shed light on these inter-relationships. New methods for quantifying non-transferrin-bound (or labile plasma) iron may help in the future to identify patients at risk for toxicity from excess iron supplementation.
Keywords: anaemia; cardiac failure; end-stage renal disease; intravenous iron; labile plasma iron; oxidative stress