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作 者:许书添 刘志红 XU Shutian;LIU Zhihong(National Clinical Research Center of Kidney Diseases,Jinling Hospital,Nanfing University School of Medicine,Nanjing 210016,China)
机构地区:[1]东部战区总医院国家肾脏疾病临床医学研究中心全军肾脏病研究所,南京210016
出 处:《肾脏病与透析肾移植杂志》2018年第6期560-564,共5页Chinese Journal of Nephrology,Dialysis & Transplantation
基 金:东部战区总医院院管课题(2015029);国家精准医学重点研发计划项目课题(2016YFC0904103)
摘 要:成纤维细胞生长因子23(FGF-23)由骨细胞产生,参与磷代谢,是慢性肾脏病(CKD)和终末期肾病(ESRD)心血管疾病不良预后的生物标志物。急性肾损伤(AKI)患者循环中FGF-23迅速升高,甚至早于中性粒细胞明胶酶相关载脂蛋白(NGAL)和血清肌酐(SCr)。AKI中FGF-23升高不依赖于维生素D、维生素D信号通路及磷的摄入。可能的机制包括:(1)骨细胞产生FGF-23增多;(2)损伤肾小管细胞异位分泌;(3) FGF-23肾清除率下降。通过酶联免疫吸附(ELISA)方法检测AKI循环中的FGF-23标志物,全段FGF-23(iFGF-23)比C端FGF-23(包括C端FGF-23片段和iFGF-23总和)更加可靠。需要进一步研究FGF-23能否成为早期识别AKI的标志物,是否影响患者预后,以及AKI中FGF-23升高的生物学效应。Fibroblast growth factor 23( FGF-23),which is produced in bone,participates in the maintenance of phosphate metabolism and can serve as a biomarker for adverse cardiovascular outcomes in patients with chronic kidney disease and end-stage renal disease.Circulating FGF-23 rapidly increases after acute kidney injury( AKI),preceding other known markers such as neutrophil gelatinase-associated lipocalin and serum creatinine. The increase in FGF-23 in AKI appears to be independent of parathyroid hormone,vitamin D signaling pathways,and dietary phosphate. The potential mechanisms include:( 1) increased production of FGF-23 in the bone by yet-to-be-identified factors;( 2) ectopic production of FGF-23 by injured renal tubules;and( 3) decreased renal clearance of circulating FGF-23. Circulating FGF-23 determined by enzyme-linked immunosorbent assay( ELISA) is a more reliable biomarker of AKI than FGF-23 C-terminal ELISA( a mixed readout of C-terminal fragment and intact FGF-23). More clinical and experimental studies are required to validate circulating FGF-23 as a biomarker for the early identification of AKI and prediction of short-and long-term outcomes post-AKI. More importantly,the biologic effect of increased FGF-23 in AKI needs to be defined.
关 键 词:成纤维细胞生长因子23 急性肾损伤
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