Chronic kidney disease (CKD) is a global health epidemic that accelerates cardiovascular disease, increases risk of infection, and causes anemia and bone disease, among other complications that collectively increase risk of premature death. Alterations in calcium and phosphate homeostasis have long been considered nontraditional risk factors for many of the most morbid outcomes of CKD. The discovery of fibroblast growth factor 23 (FGF23), which revolutionized the diagnosis and treatment of rare hereditary disorders of FGF23 excess that cause hypophosphatemic rickets, has also driven major paradigm shifts in our understanding of the pathophysiology and downstream end-organ complications of disordered mineral metabolism in CKD. As research of FGF23 in CKD has rapidly advanced, major new questions about its regulation and effects continuously emerge. These are promoting exciting innovations in laboratory, patient-oriented, and epidemiological research and stimulating clinical trials of new therapies and repurposing of existing ones to target FGF23.

中文翻译：

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FGF23在慢性肾脏疾病中的调节作用和作用。

慢性肾脏病（CKD）是一种全球性的健康流行病，它会加速心血管疾病，增加感染风险并引起贫血和骨骼疾病，以及其他导致总过早死亡风险增加的并发症。长期以来，钙和磷稳态的改变一直被认为是许多CKD最病态结局的非传统危险因素。成纤维细胞生长因子23（FGF23）的发现，彻底改变了导致低磷酸盐血症性rick病的FGF23过量罕见遗传性疾病的诊断和治疗方法，也推动了我们对病理生理和下游矿物质终末器官并发症的认识的重大转变。 CKD中的新陈代谢。随着CKD中FGF23的研究迅速发展，关于其调控和作用的重大新问题不断出现。