Fibroblast growth factor 23 and adverse clinical outcomes in chronic kidney disease.
Fibroblast growth factor 23 and adverse clinical outcomes in chronic kidney disease.
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DOI：
10.1097/mnh.0b013e328351a391
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发表时间：
2012-05
影响因子：
3.2
通讯作者：
Isakova T
中科院分区：
文献类型：
--
作者：
Isakova T
回顾成纤维细胞生长因子 23 (FGF23) 的流行病学数据和慢性肾脏病 (CKD) 的不良临床结果，并介绍对观察到的关系背后的病理生理学的最新见解。终末期肾病和心血管疾病是 CKD 患者的常见事件，心血管疾病是其死亡的主要原因。 FGF23（一种磷酸盐和维生素 D 调节激素）水平升高与终末期肾病、心血管疾病和死亡风险相关。 FGF23 过量也与左心室肥大有关，创新的转化实验最近确定了 FGF23 的直接终末器官毒性，可诱导动物左心室肥大。 FGF23 正在成为 CKD 的新危险因素。未来的研究应确定降低 FGF23 水平的干预措施是否可以改善 CKD 的临床结果。
To review data on the epidemiology of fibroblast growth factor 23 (FGF23) and adverse clinical outcomes in chronic kidney disease (CKD) and introduce recent insights into the pathophysiology behind the observed relationships. End-stage renal disease and cardiovascular disease are frequent events in patients with CKD, in whom cardiovascular disease is the leading cause of death. Elevated levels of FGF23, a phosphate and vitamin D regulating hormone, have been associated with risks of end-stage renal disease, cardiovascular disease and mortality. FGF23 excess has also been linked with left ventricular hypertrophy, and innovative translational experiments have recently established direct end-organ toxicity of FGF23, which induced left ventricular hypertrophy in animals. FGF23 is emerging as a novel risk factor in CKD. Future studies should determine whether interventions that lower FGF23 levels improve clinical outcomes in CKD.