We Give Too Much Intravenous Iron

Abstract

Dialysis patients have absolute and functional iron deficiencies. Traditionally, oral iron preparations have been insufficient to maintain iron stores to support erythropoiesis, especially in the setting of the ubiquitous use of erythropoiesis-stimulating agents. This has led to the widespread adoption of intravenous iron protocols designed to maintain iron stores at levels that are much higher than for patients not on dialysis. These protocols are often developed by dialysis providers and may be largely independent of the treating nephrologist. Concerns about multiple risks associated with the use of intravenous iron persist. Despite this, mean ferritin levels in the United States have risen, partly due to more intravenous iron use and partly due to reduced erythropoiesis-stimulating agent use. Questions about the relationship of intravenous iron to infection, cardiac, and hepatobiliary risks remain. The failure of oral iron preparations to maintain iron stores continues to prompt the use of intravenous iron. Recently, studies with oral ferric citrate as a phosphate binder have shown improved iron stores and maintenance of hemoglobin, and studies with soluble ferric pyrophosphate added to dialysate have shown both maintenance of iron stores and hemoglobin. With new iron options that affect iron stores in dialysis patients, the use of intravenous iron and its potential risks may wane.