HFE mutations modulate the effect of iron on serum hepcidin-25 in chronic hemodialysis patients
Articolo
Data di Pubblicazione:
2009
Citazione:
HFE mutations modulate the effect of iron on serum hepcidin-25 in chronic hemodialysis patients / L. Valenti, D. Girelli, G. Valenti, A. Castagna, G. Como, N. Campostrini, R. Rametta, P. Dongiovanni, P. Messa, S. Fargion. - In: CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY. - ISSN 1555-9041. - 4:8(2009 Aug), pp. 1331-1337.
Abstract:
Background and objectives: Increased serum hepcidin has been reported in patients receiving chronic hemodialysis, and hypothesized to contribute to the alterations of iron metabolism of end-stage renal disease. However, no quantitative assessment is available to date; the clinical determinants are still under definition; and the role of genetic factors, namely HFE mutations, has not yet been evaluated. The aim of this study was to quantitatively assess serum hepcidin-25 in hemodialysis patients versus controls, and analyze the relationship between hepcidin, iron indices, HFE genotype, and erythropoietic parameters.
Design, setting, participants & measurements: Sixty-five hemodialysis patients and 57 healthy controls were considered. Hepcidin-25 was evaluated by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry, HFE genotype by restriction analysis.
Results: Serum hepcidin-25 was higher in hemodialysis patients compared with controls. In patients, hepcidin-25 correlated positively with ferritin and C reactive protein, and negatively with serum iron after adjustment for confounders. Hepcidin/ferritin ratio was lower in patients with (n = 25) than in those without (n = 40) HFE mutations. At multivariate analysis, hepcidin-25 was independently associated with ferritin and HFE status. In a subgroup of 22 "stable" patients, i.e., with Hb levels on target, normal CRP levels, and absence of complications for at least 1 yr, hepcidin-25 was negatively correlated with Hb levels independently of confounders.
Conclusions: Serum hepcidin-25 is increased in hemodialysis patients, regulated by iron stores and inflammation, and relatively reduced in subjects carrying frequent HFE mutations. Hepcidin-25 may contribute to the pathogenesis of anemia by decreasing iron availability.
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
Chronic kidney-disease; hereditary hemochromatosis; renal-failure; anemia; ferritin; erythropoietin; inflammation; association; mortality; time
Elenco autori:
L. Valenti, D. Girelli, G. Valenti, A. Castagna, G. Como, N. Campostrini, R. Rametta, P. Dongiovanni, P. Messa, S. Fargion
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