Emodialisi Borgo Roma, Nephrology Section, Department of Medicine, University of Verona, Piazzale LA Scuro 10, 37134, Verona, Italy.
Department of Diagnostic and Public Health, University of Verona, Verona, Italy.
J Nephrol. 2018 Apr;31(2):297-306. doi: 10.1007/s40620-017-0383-0. Epub 2017 Mar 28.
Most hemodialysis patients have high Hepcidin-25 levels, which may be involved in the pathogenesis of several uremic complications related to an altered iron biology. The hemodialysis procedure itself can influence Hepcidin-25 levels by removing Hepcidin-25 and maybe stimulating its production due to a pro-inflammatory effect.
To assess the relationship between dialysis-related inflammation and intradialysis changes in Hepcidin-25, we performed a crossover trial in 28 hemodialysis patients to compare the effects on serum levels of Hepcidin-25 and inflammatory markers activated during dialysis [Tumor Necrosis Factor-α (TNF-α), Interleukin-6, C-reactive protein (CRP), Pentraxin-3] of a single dialysis session using a technique capable of reducing inflammation, HFR (Hemo Filtrate Reinfusion: a hemodiafiltration system combining convection, diffusion and adsorption) or bicarbonate-dialysis using either the same low-flux membrane as in the diffusion stage of HFR (LFBD) or a high-flux membrane (HFBD).
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 inflammation-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 Pentraxin-3 levels.
Our findings suggest that a single bicarbonate-dialysis session can upregulate Hepcidin-25 synthesis and that HFR can fully overcome this effect, enabling a greater Hepcidin-25 removal during dialysis. Adequately-designed studies are needed, however, to establish whether the beneficial effect of HFR emerging from our study could reduce Hepcidin-25 (and TNF-α) burden and improve clinically-relevant outcomes.
ISRCTN15957905.
大多数血液透析患者的 Hepcidin-25 水平较高,这可能与多种与铁生物学改变相关的尿毒症并发症的发病机制有关。血液透析过程本身可以通过去除 Hepcidin-25 并由于炎症反应而可能刺激其产生来影响 Hepcidin-25 水平。
为了评估与透析相关的炎症与 Hepcidin-25 透析过程中变化之间的关系,我们在 28 名血液透析患者中进行了一项交叉试验,比较了使用能够减少炎症的技术(HFR,血液滤过再灌注:一种结合对流、扩散和吸附的血液透析滤过系统)或碳酸氢盐透析(LFBD,低通量膜扩散阶段的相同膜或 HFBD,高通量膜)进行单次透析时,Hepcidin-25 水平和炎症标志物(肿瘤坏死因子-α(TNF-α)、白细胞介素-6、C 反应蛋白(CRP)、五聚素-3)的血清水平的变化。
HFR 比 LFBD(-72%(95%CI:-11 至-133),p=0.022)和 HFBD(-137%(95%CI:-2 至-272),p=0.047)更能降低 Hepcidin-25 水平,这可能是由于其对流/吸附成分的去除作用更大,以及炎症相关 Hepcidin-25 产生的降低。HFR 还导致 TNF-α水平下降比 LFBD 更大[-277%(95%CI:-59 至-494),p=0.014],而两种方法诱导的白细胞介素-6、CRP 和五聚素-3 水平的变化相似。
我们的研究结果表明,单次碳酸氢盐透析可上调 Hepcidin-25 合成,而 HFR 可完全克服这一效应,使透析过程中 Hepcidin-25 的清除率增加。然而,需要进行设计合理的研究,以确定我们研究中 HFR 带来的有益效果是否可以降低 Hepcidin-25(和 TNF-α)负担并改善临床相关结局。
ISRCTN84064249。