Background: Hepcidin-25 is a peptide hormone involved in iron absorption and homeostasis and found at increased serum levels
in conditions involving systemic inflammation, renal dysfunction, and increased adiposity. Hepcidin may play a role in the
pathogenesis of anemia, but its role in kidney transplantation is undefined.
Methods: This study enrolled 100 stable
patients beyond 12 months after transplantation, from a large single United Kingdom center. Serum hepcidin-25 level, and relevant
demographic and laboratory data pertinent to posttransplantation anemia, were measured and collected. Independent predictors
of serum hepcidin were evaluated, and the relationship between hepcidin and hemoglobin, assessed.
associations were seen between higher hepcidin levels and allograft dysfunction (estimated glomerular filtration rate), increased
inflammation (high-sensitivity C-reactive peptide), higher transferrin saturation (a marker of iron stores), and the use of
marrow-suppressive medication (P<0.05 for all). Higher fat tissue index (whole-body multifrequency bioimpedance measurement)
was also associated with higher hepcidin levels, but this relationship did not persist after adjustment for inflammation (high-sensitivity
C-reactive peptide). In turn, inflammation was associated with increased fat tissue index (P=0.01) and male gender (P=0.04).
A nonlinear association between serum hepcidin level and hemoglobin was seen, with a progressive fall in hemoglobin as hepcidin
levels rose to 100 ng/mL, but little effect thereafter (P=0.009). This association was independent of renal dysfunction and
female gender, both of which were also independently associated with a lower hemoglobin level.
results highlight possible mechanisms of hemoglobin reduction in kidney transplantation patients, and the therapeutic opportunities
from understanding the role of hepcidin in this context.