Abstract and Introduction
Abstract
Iron deficiency (ID) is highly prevalent in kidney transplant recipients (KTRs) and has been independently associated with an excess mortality risk in this population. Several causes lead to ID in KTRs, including inflammation, medication and an increased iron need after transplantation. Although many studies in other populations indicate a pivotal role for iron as a regulator of the immune system, little is known about the impact of ID on the immune system in KTRs. Moreover, clinical trials in patients with chronic kidney disease or heart failure have shown that correction of ID, with or without anaemia, improves exercise capacity and quality of life, and may improve survival. ID could therefore be a modifiable risk factor to improve graft and patient outcomes in KTRs; prospective studies are warranted to substantiate this hypothesis.
Introduction
Iron deficiency anaemia (IDA) affects approximately one billion individuals globally and has a particularly high prevalence among patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD),[1] including kidney transplant recipients (KTRs).[2] The presence of iron deficiency (ID) after kidney transplantation is strongly associated with an increased mortality risk.[2,3] Interestingly, this association is independent of co-existing anaemia, suggesting a specific pathogenic role for ID in kidney transplantation.[2] Although the potential mechanisms driving the association between ID and mortality have not been fully elucidated, ID has been implicated in both immunological and non-immunological pathological processes. In this review, we will discuss the definition, prevalence and clinical impact of ID after kidney transplantation, address potential underlying pathophysiological pathways and propose areas for future study.