慢性肾衰竭患者血清hepcidin水平改变

目的探讨铁稳态调节分子hepcidin在慢性肾衰竭患者中的表达，以及血hepcidm在判定机体铁贮存和功能性缺铁方面的价值，对EPO治疗反应的影响，为合理治疗肾性贫血提供依据。方法采用酶联免疫吸附法（ELISA）、放射免疫法等测定三组、共70例CKD不同分期患者的血清Hepcidin水平，以及铁代谢指标和相关血液学参数、hsCRP、生化指标。结果患者血清Hepcidin水平随着CKD3期、CKD4期、CKD5期的发展呈现逐渐升高的趋势，CKD5期血透组Hepcidin水平最高，平均120．81±6．65pg／l，各期Hepcidin水平有显著差异（P〈0．001）。血透组Hepcidin水平与血清铁蛋白、转铁饱和度呈正相关，相关系数分别为0．641和0．370，有显著相关性（P〈0．05）。在不考虑CKD分期的情况下，血清hepcidin水平与hsCRP呈正相关，相关系数为0．457，与GFR、红细胞、红细胞压积呈负相关，相关系数分别是-0．790，-0．483和-0．466，均有显著相关性（P〈0．001）。在血透组A、B亚组中，EP0≥9000IU的A组血清hepcidin水平高于EPO〈9000IU的B组，有显著差异（P〈0．001）。结论慢性肾衰竭时随着肾小球滤过率的下降，hepcidin清除减少，伴随CKD的微炎症状态，血清hepcidin水平增加，引起功能性铁缺乏，贮存铁利用障碍．EPO低反应，贫血难以纠正。

Changes in serum hepcidin in patients with chronic renal failure

Objective To study the expression of iron homeostasis regulator hepcidin, the value of serum hepcidin in evaluation of iron storage and functional iron loss, and the effect of hepcidin on EPO treatment in patients with chronic renal failure. Methods Seventy CKD patients were divided into 3 groups. ELISA and RI were used to measure the level of serum hepcidin and iron metabolic indicators and related blood parameters, hsCRP and biochemistry parameters. Results Hepcidin level increased with CKD development, with the highest level （120.81±6.65 ug/l） in CKD5 （P〈0.001）. Statistically significance differences were observed in all 3 CKD patient groups. Hepcidin level correlated positively with serum ferritin level and transferritin saturation, the correlation coefficient being 0.641 and 0.370 respectively （P〈0.05）. Irrespective of CKD stages, hepcidin correlated positively with hsCRP （correlation coefficient = 0.457 ） and negatively with GFR, RBC count and HCT （correlation coefficient -0.790, -0.483 and -0.466 respectively）. In patients on hemodialysis, hepcidin was higher in EPO≥ 9000IU than that in EPO 〈 9000IU, the difference being statistically significant （P〈 0.001）. Conclusion With GFR decline and microinflammation status in CRF, hepcidin clearance decreased and serum level increased, leading to functional iron loss, disordered utilization of iron storage, EPO low reactivity and increased difficulty in anemia correction.