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肾脏病与透析肾移植杂志 ›› 2018, Vol. 27 ›› Issue (6): 560-564.DOI: 10.3969/j.issn.1006-298X.2018.06.014

• 论文 • 上一篇    下一篇

成纤维细胞生长因子23与急性肾损伤

  

  • 出版日期:2018-12-28 发布日期:2019-01-21

Fibroblast grow factor 23 in acute kidney injury

  • Online:2018-12-28 Published:2019-01-21

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。

 

关键词: 成纤维细胞生长因子23, 急性肾损伤

Abstract:

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 production 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.