Purpose of review: In recent years, there has been an increasing awareness of the central regulatory role of fibroblast growth factor 23 (FGF23) in mineral metabolism and its particular prominence in patients with chronic kidney disease (CKD).
Recent findings: FGF23 is a powerful predictor of adverse clinical outcomes in CKD that appears to be superior to existing mineral metabolism markers such as serum phosphate and parathyroid hormone. Interesting new data suggest a central role of bone health in the regulation of FGF23 secretion, whereas another important new study reported that virtually all circulating FGF23 in advanced renal failure is biologically intact. Finally, new data demonstrate the ability to alter FGF23 levels using common CKD therapies such as phosphate binders, active vitamin D, and cinacalcet.
Summary: Although FGF23 was originally discovered in studies of rare diseases, we expect that its primary utility in mainstream clinical practice will ultimately lie in the management of CKD. Emerging data highlight the potential of FGF23 as a novel diagnostic to identify CKD patients at the highest risk for disease progression, cardiovascular disease, and death, and those who might benefit from early phosphorus-related therapies before the onset of overt hyperphosphatemia.