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成纤维细胞生长因子 23:在慢性肾脏病中新型心血管风险标志物的崛起。

FGF-23: the rise of a novel cardiovascular risk marker in CKD.

机构信息

Department of Internal Medicine IV—Nephrology and Hypertension, Saarland University Medical Center, Homburg/Saar, Germany.

出版信息

Nephrol Dial Transplant. 2012 Aug;27(8):3072-81. doi: 10.1093/ndt/gfs259.

Abstract

Elevated plasma levels of the phosphaturic hormone fibroblast growth factor 23 (FGF-23) are a hallmark of chronic kidney disease (CKD)-mineral and bone disorder. FGF-23 allows serum phosphate levels within physiological limits to be maintained in progressive CKD until end-stage renal disease is reached. Despite its seemingly beneficial role in phosphate homeostasis, several prospective studies in dialysis patients and in patients with less advanced CKD associated elevated FGF-23 with poor cardiovascular and renal outcome. Moreover, very recent evidence suggests an adverse prognostic impact of elevated FGF-23 even in subjects without manifest CKD. These epidemiological data are supplemented by laboratory findings that reveal a pathophysiological role of FGF-23 in the pathogenesis of myocardial injury. In aggregate, these clinical and experimental data identify FGF-23 as a promising target of novel therapeutic interventions in CKD and beyond, which should be tested in future clinical trials.

摘要

升高的血磷酸盐激素成纤维细胞生长因子 23(FGF-23)水平是慢性肾脏病(CKD)-矿物质和骨异常的标志。FGF-23 使进展性 CKD 中的血清磷酸盐水平保持在生理范围内,直到达到终末期肾病。尽管它在磷酸盐稳态中似乎具有有益的作用,但透析患者和 CKD 程度较低的患者的几项前瞻性研究表明,升高的 FGF-23 与心血管和肾脏不良预后相关。此外,最近的证据表明,即使在没有明显 CKD 的患者中,升高的 FGF-23 也具有不良的预后影响。这些流行病学数据得到了实验室发现的补充,这些发现揭示了 FGF-23 在心肌损伤发病机制中的病理生理作用。总的来说,这些临床和实验数据将 FGF-23 确定为 CKD 及其他疾病中新的治疗干预的有前途的靶点,应在未来的临床试验中进行测试。

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