Iron deficiency and supplementation in heart failure and chronic kidney disease.

Abstract Iron is a key element for normal cellular function and plays a role in many cellular processes including mitochondrial respiration. The role of iron deficiency (ID) in heart failure (HF) has been a subject of debate amid increasing advocacy for intravenous (IV) supplementation. Both the definition and the approach to treatment of ID in HF have been adapted from the experience in patients with chronic kidney disease (CKD). In this review, we highlight the differences in regulatory mechanisms as well as pathophysiology of ID in CKD and HF population both at the systemic and cellular levels. We will review the major clinical trials in HF patients that have shown symptomatic benefit from IV iron supplementation but without effect on clinical outcomes. Intravenous iron loading bypasses the mechanisms that tightly regulate iron uptake and can potentially cause myocardial and endothelial damage by releasing reactive oxygen species. By contrast, newer oral iron preparations do not have similar toxicity concerns and might have a role in heart failure.