Division of Nephrology and Hypertension, Department of Medicine, University of Miami, Miller School of Medicine, Florida 33136, USA.
Curr Opin Nephrol Hypertens. 2012 May;21(3):334-40. doi: 10.1097/MNH.0b013e328351a391.
The aim is 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.
目的是回顾成纤维细胞生长因子 23（FGF23）在慢性肾脏病（CKD）中的流行病学和不良临床结局的数据，并介绍对观察到的相关性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，其中心血管疾病是死亡的主要原因。FGF23 水平升高与终末期肾病、心血管疾病和死亡率的风险相关，FGF23 是一种调节磷和维生素 D 的激素。FGF23 过量还与左心室肥厚有关，最近的创新性转化实验已经确定 FGF23 的直接靶器官毒性，它在动物中诱导左心室肥厚。
FGF23 正在成为 CKD 的一个新的危险因素。未来的研究应确定降低 FGF23 水平的干预措施是否能改善 CKD 的临床结局。
