Abstract
Fibroblast growth factor 23 (FGF23) is primarily produced in bones and mainly regulates calcium and phosphorus metabolism. The level of circulating FGF23 increases rapidly in the early stage of acute kidney injury (AKI). Recent studies have shown that FGF23 may serve as a biomarker for the diagnosis and poor prognosis of AKI. The mechanism of increased FGF23 in AKI may include increased production of FGF23, decreased renal clearance of FGF23, and some new regulatory factors, such as inflammation and glycerol 3-phosphate. However, the biological effects of elevated FGF23 in AKI are still unclear. It is also not known whether reducing the level of circulating FGF23 could alleviate AKI or its poor prognosis. Here, we review the pathophysiological mechanism and possible regulation of FGF23 in AKI and discuss the possibility of using FGF23 as a therapeutic target.