@article{22136,
  author = {Hawley C. and Pascoe E. and Pedagogos E. and McDonald S. and Ferrari P. and Johnson D. and Walker R. and Cass A. and Reidlinger D. and Badve S. and Clarke P. and Morrish A. and Scaria A. and Vergara L. and Gummer J. and Trengove R. and Olynyk J. and Perkovic Vlado},
  title = {Association between Serum Hepcidin-25 and Primary Resistance to Erythropoiesis Stimulating Agents in Chronic Kidney Disease: A Secondary Analysis of the HERO Trial},
  abstract = {<p>
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 (HERO) multi-centre double-blind, randomized controlled trial. The present sub-study evaluated the effects of pentoxifylline on the iron-regulatory hormone hepcidin in ESA-hyporesponsive CKD patients. 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 vs. placebo treated patients (adjusted mean difference (MD) -7.9 nmol, P = 0.114), although the difference between the groups mean translated into a &gt;25% reduction of circulating hepcidin-25 due to pentoxifylline compared to the placebo baseline. In paired analysis serum hepcidin-25 levels were significantly decreased at 4 months compared to baseline in the pentoxifylline group (-5.47 +/- 2.27 nmol/l, P &lt; 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 55.4mcg/l), transferrin saturation (MD 4.04%), the dosage of ESA (MD -9.93 U/kg/week), or haemoglobin concentration (MD 5.75 g/l). CONCLUSIONS: 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 patients with ESA-hyporesponsive anaemia.
</p>
},
  year = {2016},
  journal = {Nephrology (Carlton)},
  edition = {2016/05/14},
  isbn = {1440-1797 (Electronic)<br/>1320-5358 (Linking)},
  note = {Gummer, Joel<br/>Trengove, Robert<br/>Pascoe, Elaine M<br/>Badve, Sunil V<br/>Cass, Alan<br/>Clarke, Philip<br/>McDonald, Stephen P<br/>Morrish, Alicia T<br/>Pedagogos, Eugenie<br/>Perkovic, Vlado<br/>Reidlinger, Donna<br/>Scaria, Anish<br/>Walker, Rowan<br/>Vergara, Liza A<br/>Hawley, Carmel M<br/>Johnson, David W<br/>Olynyk, John K<br/>Ferrari, Paolo<br/>HERO Study Collaborative Group<br/>Nephrology (Carlton). 2016 May 12. doi: 10.1111/nep.12815.},
  language = {Eng},
}