Anemia is a frequent complication of CKD. In CKD, the main causes of anemia are deficiency of erythropoietin, iron-restricted erythropoiesis and anemia of the chronic disease (ACD). In ACD, pro-inflammatory cytokines upregulate hepcidin production in the liver which subsequently hampers iron uptake from the gut and iron release from the reticulo-endothelial system. This leads to functional iron deficiency that negatively affects erythropoiesis. Furthermore, increased iron utilization due to the use of erythropoiesis-stimulating agents (ESA), and iron loss as a result of dialysis-related blood loss, contribute to the high prevalence of anemia in patients with CKD.

Oral administration of iron has limited efficacy and is associated with gastrointestinal side effects. By means of intravenous (IV) iron, gastrointestinal absorption is bypassed and it is incorporated more rapidly. Several studies have established that IV iron supplementation, as a treatment for iron deficiency anemia, is superior to oral iron supplementation in nondialysis-dependent CKD, hemodialysis (HD) and peritoneal dialysis patients. Furthermore, ESA requirements have been shown to be decreased in patients receiving IV iron.

Nowadays, several IV iron supplementations are available. Recently (Hofman et al), real-life study in HD patients showed that the switch from iron sucrose to ferric carboxymaltose (FCM) was associated with improvement in iron status parameters. In addition, use of FCM resulted in an increase in hemoglobin levels, while ESA dose was decreased. Hence, FCM can be an appropriate strategy for better control of iron status in HD patients.