Alterations of fibroblast growth factor 23 (FGF-23) and Klotho levels are considered to be the earliest biochemical abnormality of chronic kidney disease – mineral and bone disease (CKDMBD) syndrome. Moreover, emerging data suggests that the dysregulated FGF-23 and Klotho axis has many effects on the cardiovascular (CV) system and contributes significantly to the increased CV morbidity and mortality rates of CKD patients. This review examines recent evidence on the role of FGF-23 and Klotho in the development and progression of CV complications of uremia namely cardiac hypertrophy, uremic cardiomyopathy, and atherosclerotic and arteriosclerotic vascular lesions. Moreover, the available evidence on their associations with adverse clinical outcomes are summarized. Undoubtedly, more studies are needed to further elucidate the effects of FGF-23 and Klotho on the heart and vessels and to gain insights into their prognostic value as CV risk factors. Finally, large prospective studies are required to test the hypothesis that modification of their levels would have a favourable impact on the unacceptably high mortality rates of these patient populations.

成纤维细胞生长因子23（FGF-23）和Klotho水平的改变被认为是慢性肾脏疾病–矿物质和骨病（CKDMBD）综合征的最早生化异常。此外，新出现的数据表明，失调的FGF-23和Klotho轴对心血管（CV）系统有许多影响，并且对CKD患者的CV发病率和死亡率增加做出了重要贡献。这篇综述检查了关于FGF-23和Klotho在尿毒症的CV并发症（例如心脏肥大，尿毒症性心肌病以及动脉粥样硬化和动脉硬化性血管病变）的发生和发展中的作用的最新证据。此外，总结了与不良临床结局相关的现有证据。无疑，需要更多的研究来进一步阐明FGF-23和Klotho对心脏和血管的作用，并深入了解它们作为CV危险因素的预后价值。最后，需要进行大规模的前瞻性研究来检验以下假设：改变其水平将对这些患者群体的高死亡率产生有利影响。