Iron metabolism in solid‑organ transplantation: how far are we from solving the mystery?

Abstract

Iron is the most abundant transition metal in the human body and an essential element required for growth and survival. Our understanding of the molecular control of iron metabolism has increased dramatically over the past 10 years due to the discovery of hepcidin, which regulates the uptake of dietary iron and its mobilization from macrophages and hepatic stores. Although general practitioners and internists encounter iron deficiency and anemia in their everyday practice, little is known about iron metabolism in patients after solid-organ transplantation. The aim of this review was to summarize the current knowledge on iron metabolism in kidney, heart, and liver transplant recipients. Iron deficiency and/or anemia, as well as iron overload, are frequently observed but the precise mechanism of these disturbances have not been fully elucidated. Iron deficiency is more prevalent in kidney and heart transplant patients, while iron overload in liver transplant recipients. Secondary and potentially reversible causes of these disturbances should be considered such as inflammation, graft failure, and type of immunosuppression. Iron status check‑up should be a part of long term follow-up because disturbances in iron metabolism are a possible risk factor of infections and mortality in solid transplant recipients. Internists and general practitioners are often the first doctors to take care of organ transplant recipients (before they will present at outpatient transplant clinics or hospital transplant units); therefore, knowledge about the disturbances in iron metabolism in this specific population would be useful for better diagnosis and treatment both before and after transplantation.