Jimbo Rika, Shimosawa Tatsuo
Department of Internal Medicine, Odaira-Memorial Tokyo Hitachi Hospital, 3-5-7 Yushima, Bunkyo-ku, Tokyo, Japan.
Department of Clinical Laboratory, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan.
Int J Hypertens. 2014;2014:381082. doi: 10.1155/2014/381082. Epub 2014 Jan 12.
Patients with chronic kidney disease (CKD) are at increased risk of mortality, mainly from cardiovascular disease. Moreover, abnormal mineral and bone metabolism, the so-called CKD-mineral and bone disorder (MBD), occurs from early stages of CKD. This CKD-MBD presents a strong cardiovascular risk for CKD patients. Discovery of fibroblast growth factor 23 (FGF23) has altered our understanding of CKD-MBD and has revealed more complex cross-talk and endocrine feedback loops between the kidney, parathyroid gland, intestines, and bone. During the past decade, reports of clinical studies have described the association between FGF23 and cardiovascular risks, left ventricular hypertrophy, and vascular calcification. Recent translational reports have described the existence of FGF23-Klotho axis in the vasculature and the causative effect of FGF23 on cardiovascular disease. These findings suggest FGF23 as a promising target for novel therapeutic approaches to improve clinical outcomes of CKD patients.
慢性肾脏病(CKD)患者的死亡风险增加,主要死于心血管疾病。此外,所谓的CKD-矿物质和骨异常(MBD),即矿物质和骨代谢异常,在CKD早期阶段就会出现。这种CKD-MBD给CKD患者带来了很大的心血管风险。成纤维细胞生长因子23(FGF23)的发现改变了我们对CKD-MBD的认识,并揭示了肾脏、甲状旁腺、肠道和骨骼之间更复杂的相互作用和内分泌反馈回路。在过去十年中,临床研究报告描述了FGF23与心血管风险、左心室肥厚和血管钙化之间的关联。最近的转化研究报告描述了血管系统中FGF23-klotho轴的存在以及FGF23对心血管疾病的致病作用。这些发现表明FGF23是改善CKD患者临床结局的新型治疗方法的一个有前景的靶点。