Abstract:

Fibroblast growth factor 23 (FGF23),which is produced in bone,participates in the maintenance of phosphate metabolism and can serve as a biomarker for adverse cardiovascular outcomes in patients with chronic kidney disease and endstage renal disease.Circulating FGF23 rapidly increases after acute kidney injury (AKI),preceding other known markers such as neutrophil gelatinaseassociated lipocalin and serum creatinine.The increase in FGF23 in AKI appears to be independent of parathyroid hormone,vitamin D signaling pathways,and dietary phosphate.The potential mechanisms include:(1) increased production of FGF23 in the bone by yettobeidentified factors; (2) ectopic production of FGF23 by injured renal tubules; and (3) decreased renal clearance of circulating FGF23.Circulating FGF23 determined by enzymelinked immunosorbent assay (ELISA) is a more reliable biomarker of AKI than FGF23 Cterminal ELISA (a mixed readout of Cterminal fragment and intact FGF23)More clinical and experimental studies are required to validate  circulating FGF23 as a biomarker for the early identification of AKI and prediction of shortand longterm  outcomes postAKIMore importantly,the biologic effect of increased FGF23 in AKI needs to be defined.