Intravenous iron therapy maintains iron stores and decreases erythropoietin demand in patients undergoing regular dialysis therapy. Microbiology studies show a close relationship between the availability of iron and bacterial virulence. Iron is also an essential requirement of bacteria for multiplication in the host. Therefore, clinical conditions associated with iron excess in the host may increase the risk for infection. Parenteral iron has already been shown in human and animal studies to be harmful when administered during infection. There is now convincing evidence that hydroxyl radicals, produced either by the Fenton reaction or by the iron-catalyzed Haber-Weiss reaction, are species responsible for the damaging effects of iron. The unavailability of iron limits microbial growth but also impairs host resistance. In end-stage renal disease, patients' overtreatment with iron enhances the pre-existing risk for infectious complications caused by dialysis procedure per se, malnutrition, increased intracellular calcium, as well as low and high molecular weight uremic toxins. Intravenous iron therapy may not only adversely affect phagocytes in end-stage renal disease patients, but also T and B lymphocytes.