Iron homeostasis in this vulnerable patient group differs substantially from the general population due to changes in erythropoietin production and consequent increased iron utilization after transplantation, decreased iron absorption (presumably due to increased hepcidin concentrations), and intracellular iron shifts.4 As a result, iron deficiency is common among KTRs and is associated with adverse outcomes independent of anemia.2,3 In addition, some KTRs receive iron supplementation. This evidence concerns the gene HAMP and nutritional disorder.