Iron deficiency after kidney transplantation

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.

Keywords: fibroblast growth factor-23; heart failure; immunity; iron; kidney transplantation.

FIGURE 1

Causes of ID in KTRs. In KTRs, low-grade inflammation and mTOR inhibitors promote hepcidin upregulation. Hepcidin suppresses iron uptake from the gut by inhibiting iron exporter ferroportin on enterocytes. Hepcidin also reduces available iron by inhibiting iron export from monocytes. Meanwhile, iron usage/consumption is increased in KTRs: renewed EPO production promotes erythropoiesis. Usage of anticoagulant medication, frequent blood sampling and in some cases gastro-intestinal and urogenital malignancies result in blood loss. Female KTRs of reproductive age often have a return of their menstrual cycle, another cause of blood loss. Finally, PPIs decrease dietary iron uptake.