Journal article
Association between serum hepcidin-25 and primary resistance to erythropoiesis-stimulating agents in chronic kidney disease: a secondary analysis of the HERO trial
Nephrology, Vol.22(7), pp.548-554
2017
Abstract
Background: Pentoxifylline has been shown to increase haemoglobin levels in patients with chronic kidney disease (CKD) and erythropoietin-stimulating agent (ESA)-hyporesponsive anaemia in the Handling Erythropoietin Resistance with Oxpentifylline multicentre double-blind, randomized controlled trial. The present sub-study evaluated the effects of pentoxifylline on the iron-regulatory hormone hepcidin in patients with ESA-hyporesponsive CKD. Methods: This sub-study included 13 patients in the pentoxifylline arm (400 mg daily) and 13 in the matched placebo arm. Hepcidin-25 was measured by ultra performance liquid chromatography/quadrupole time-of-flight mass spectrometry following isolation from patient serum. Serum hepcidin-25, serum iron biomarkers, haemoglobin and ESA dosage were compared within and between the two groups. Results: Hepcidin-25 concentration at 4 months adjusted for baseline did not differ significantly in pentoxifylline versus placebo treated patients (adjusted mean difference (MD) −7.9 nmol, P = 0.114), although the difference between the groups mean translated into a >25% reduction of circulating hepcidin-25 due to pentoxifylline compared with the placebo baseline. In paired analysis, serum hepcidin-25 levels were significantly decreased at 4 months compared with baseline in the pentoxifylline group (−5.47 ± 2.27 nmol/l, P < 0.05) but not in the placebo group (2.82 ± 4.29 nmol/l, P = 0.24). Pentoxifylline did not significantly alter serum ferritin (MD 55.4 mcg/l), transferrin saturation (MD 4.04%), the dosage of ESA (MD −9.93 U/kg per week) or haemoglobin concentration (MD 5.75 g/l). Conclusion: The reduction of circulating hepcidin-25 due to pentoxifylline did not reach statistical significance; however, the magnitude of the difference suggests that pentoxifylline may be a clinically and biologically meaningful modulator of hepcidin-25 in dialysis of patients with ESA-hyporesponsive anaemia.
Details
- Title
- Association between serum hepcidin-25 and primary resistance to erythropoiesis-stimulating agents in chronic kidney disease: a secondary analysis of the HERO trial
- Authors/Creators
- J. Gummer (Author/Creator)R. Trengove (Author/Creator)E.M. Pascoe (Author/Creator)S.V. Badve (Author/Creator)A. Cass (Author/Creator)P. Clarke (Author/Creator)S.P. McDonald (Author/Creator)A.T. Morrish (Author/Creator)E. Pedagogos (Author/Creator)V. Perkovic (Author/Creator)D. Reidlinger (Author/Creator)A. Scaria (Author/Creator)R. Walker (Author/Creator)L.A. Vergara (Author/Creator)C.M. Hawley (Author/Creator)D.W. Johnson (Author/Creator)J.K. Olynyk (Author/Creator)P. Ferrari (Author/Creator)
- Publication Details
- Nephrology, Vol.22(7), pp.548-554
- Publisher
- Blackwell Publishing
- Identifiers
- 991005542428007891
- Copyright
- © 2016 Asian Pacific Society of Nephrology
- Murdoch Affiliation
- School of Veterinary and Life Sciences
- Language
- English
- Resource Type
- Journal article
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- Collaboration types
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- Citation topics
- 1 Clinical & Life Sciences
- 1.184 Physiology & Metals
- 1.184.573 Iron Metabolism
- Web Of Science research areas
- Urology & Nephrology
- ESI research areas
- Clinical Medicine