Reduction of serum hepcidin by hemodialysis in pediatric and adult patients

Joshua Zaritsky, Brian Y Young, Barbara Gales, He Jing Wang, Anjay Rastogi, Mark Westerman, Elizabeta Nemeth, Tomas Ganz, Isidro B. Salusky

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

Background and objectives: Hepcidin, the principal regulator of iron homeostasis, may play a critical role in the response of patients with anemia to iron and erythropoiesis-stimulating agent therapy; however, the contribution of hepcidin to iron maldistribution and anemia in hemodialysis (HD) patients and the ability of HD to lower serum hepcidin levels have not been fully characterized. Design, setting, participants, & measurements: We measured serum hepcidin using a competitive ELISA in 30 pediatric and 33 adult HD patients. In addition, we determined serum hepcidin kinetics and calculated hepcidin clearance by measuring serum hepcidin before, during, and after HD in eight pediatric and six adult patients. Results: Hepcidin was significantly increased in pediatric (median 240.5 ng/ml) and adult HD patients (690.2 ng/ml) when compared with their respective control subjects (pediatric 25.3 ng/ml, adult 72.9 ng/ml). Multivariate regression analysis showed that serum hepcidin was independently predicted by ferritin and high-sensitivity C-reactive protein in the pediatric group and ferritin, percentage of iron saturation, and high-sensitivity C-reactive protein in the adult group. Hepcidin levels decreased after dialysis from 532 ± 297 to 292 ± 171 ng/ml. Hepcidin clearance by HD was 141 ± 40 and 128 ± 44 ml/min in pediatric and adult patients, respectively (NS). Conclusions: These findings suggest that hepcidin may mediate the negative effects of inflammation on both disordered iron metabolism and erythropoiesis in HD patients and that intensification of HD could be used therapeutically to reduce hepcidin concentrations and thereby improve erythropoiesis-stimulating agent responsiveness.

Original languageEnglish (US)
Pages (from-to)1010-1014
Number of pages5
JournalClinical Journal of the American Society of Nephrology
Volume5
Issue number6
DOIs
StatePublished - Jun 1 2010

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Hepcidins
Renal Dialysis
Pediatrics
Serum
Iron
Hematinics
Ferritins
C-Reactive Protein
Anemia
Erythropoiesis

ASJC Scopus subject areas

  • Nephrology
  • Transplantation
  • Epidemiology
  • Critical Care and Intensive Care Medicine
  • Medicine(all)

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Reduction of serum hepcidin by hemodialysis in pediatric and adult patients. / Zaritsky, Joshua; Young, Brian Y; Gales, Barbara; Wang, He Jing; Rastogi, Anjay; Westerman, Mark; Nemeth, Elizabeta; Ganz, Tomas; Salusky, Isidro B.

In: Clinical Journal of the American Society of Nephrology, Vol. 5, No. 6, 01.06.2010, p. 1010-1014.

Research output: Contribution to journalArticle

Zaritsky, J, Young, BY, Gales, B, Wang, HJ, Rastogi, A, Westerman, M, Nemeth, E, Ganz, T & Salusky, IB 2010, 'Reduction of serum hepcidin by hemodialysis in pediatric and adult patients', Clinical Journal of the American Society of Nephrology, vol. 5, no. 6, pp. 1010-1014. https://doi.org/10.2215/CJN.08161109
Zaritsky, Joshua ; Young, Brian Y ; Gales, Barbara ; Wang, He Jing ; Rastogi, Anjay ; Westerman, Mark ; Nemeth, Elizabeta ; Ganz, Tomas ; Salusky, Isidro B. / Reduction of serum hepcidin by hemodialysis in pediatric and adult patients. In: Clinical Journal of the American Society of Nephrology. 2010 ; Vol. 5, No. 6. pp. 1010-1014.
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AU - Westerman, Mark

AU - Nemeth, Elizabeta

AU - Ganz, Tomas

AU - Salusky, Isidro B.

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AB - Background and objectives: Hepcidin, the principal regulator of iron homeostasis, may play a critical role in the response of patients with anemia to iron and erythropoiesis-stimulating agent therapy; however, the contribution of hepcidin to iron maldistribution and anemia in hemodialysis (HD) patients and the ability of HD to lower serum hepcidin levels have not been fully characterized. Design, setting, participants, & measurements: We measured serum hepcidin using a competitive ELISA in 30 pediatric and 33 adult HD patients. In addition, we determined serum hepcidin kinetics and calculated hepcidin clearance by measuring serum hepcidin before, during, and after HD in eight pediatric and six adult patients. Results: Hepcidin was significantly increased in pediatric (median 240.5 ng/ml) and adult HD patients (690.2 ng/ml) when compared with their respective control subjects (pediatric 25.3 ng/ml, adult 72.9 ng/ml). Multivariate regression analysis showed that serum hepcidin was independently predicted by ferritin and high-sensitivity C-reactive protein in the pediatric group and ferritin, percentage of iron saturation, and high-sensitivity C-reactive protein in the adult group. Hepcidin levels decreased after dialysis from 532 ± 297 to 292 ± 171 ng/ml. Hepcidin clearance by HD was 141 ± 40 and 128 ± 44 ml/min in pediatric and adult patients, respectively (NS). Conclusions: These findings suggest that hepcidin may mediate the negative effects of inflammation on both disordered iron metabolism and erythropoiesis in HD patients and that intensification of HD could be used therapeutically to reduce hepcidin concentrations and thereby improve erythropoiesis-stimulating agent responsiveness.

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