Vol.:(0123456789) 1 3 J Nephrol DOI 10.1007/s40620-017-0383-0 ORIGINAL ARTICLE A single dialysis session of hemodiafltration with sorbent- regenerated endogenous ultrafltrate reinfusion (HFR) removes hepcidin more efciently than bicarbonate hemodialysis: a new approach to containing hepcidin burden in dialysis patients? Nicola Tessitore 1  · Albino Poli 2  · Valeria Bedogna 1  · Luca Corazza 3  · Natascia Campostrini 4  · Mauro Atti 3  · Luisa Sereni 3  · Annalisa Castagna 4  · Domenico Girelli 4  · Giuseppina Pessolano 1  · Antonio Lupo 1   Received: 8 December 2016 / Accepted: 22 February 2017 © Italian Society of Nephrology 2017 Results HFR achieved a greater reduction in Hepcidin-25 levels than both LFBD [−72% (95% CI: −11 to −133), p = 0.022] and HFBD [−137% (95% CI: −2 to −272), p = 0.047], conceivably due to both a greater removal (because of its convective/adsorptive component) and a lower infammation-related Hepcidin-25 production. HFR also led to a greater decrease in TNF-α than LFBD [−277% (95% CI: −59 to −494), p = 0.014], while the two methods induced similar changes in Interleukin-6, CRP and Pen- traxin-3 levels. Conclusions Our fndings suggest that a single bicarbo- nate-dialysis session can upregulate Hepcidin-25 synthe- sis and that HFR can fully overcome this efect, enabling a greater Hepcidin-25 removal during dialysis. Adequately- designed studies are needed, however, to establish whether the benefcial efect of HFR emerging from our study could reduce Hepcidin-25 (and TNF-α) burden and improve clini- cally-relevant outcomes. Trial registration: ISRCTN15957905 Keywords Bicarbonate-dialysis · Hepcidin-25 · Hemo Filtrate Reinfusion (HFR) · Pro-infammatory cytokines Introduction High levels of Hepcidin-25 (Hep-25), the key iron homeostasis-regulating hormone [1], have been reported in the majority of hemodialysis patients [2–4], and are thought to play a crucial part in the pathogenesis of several uremic complications linked to an altered iron metabolism, including hyporesponsiveness to erythro- poiesis-stimulating agents (ESAs) and intravenous iron, infections, accelerated atherosclerosis, and a higher risk Abstract Background Most hemodialysis patients have high Hepci- din-25 levels, which may be involved in the pathogenesis of several uremic complications related to an altered iron biology. The hemodialysis procedure itself can infuence Hepcidin-25 levels by removing Hepcidin-25 and maybe stimulating its production due to a pro-infammatory efect. Methods To assess the relationship between dialysis- related infammation and intradialysis changes in Hepci- din-25, we performed a crossover trial in 28 hemodialysis patients to compare the efects on serum levels of Hepci- din-25 and infammatory markers activated during dialysis [Tumor Necrosis Factor-α (TNF-α), Interleukin-6, C-reac- tive protein (CRP), Pentraxin-3] of a single dialysis ses- sion using a technique capable of reducing infammation, HFR (Hemo Filtrate Reinfusion: a hemodiafltration system combining convection, difusion and adsorption) or bicar- bonate-dialysis using either the same low-fux membrane as in the difusion stage of HFR (LFBD) or a high-fux membrane (HFBD). Electronic supplementary material The online version of this article (doi:10.1007/s40620-017-0383-0) contains supplementary material, which is available to authorized users. * Nicola Tessitore nicola.tessitore@aovr.veneto.it 1 Emodialisi Borgo Roma, Nephrology Section, Department of Medicine, University of Verona, Piazzale LA Scuro 10, 37134 Verona, Italy 2 Department of Diagnostic and Public Health, University of Verona, Verona, Italy 3 Bellco srl, Mirandola, MO, Italy 4 Internal Medicine Section, Department of Medicine, University of Verona, Verona, Italy