FGF-23 in dialysis patients: Ready for prime time?

Abstract

The discovery that fibroblast growth factor 23 (FGF-23) intimately connects skeletal biology and systemic mineral balance is one of the major breakthroughs of the last decade in renal medicine. In a recent observational study by Guti'errez et al. [2] high FGF-23 levels emerged as a much strong predictor of death and the predictive power of this peptide was maintained even when this relationship was analysed within serum phosphate levels quartiles. Because FGF-23 levels can be lowered by reducing phosphate intake, provided that the FGF-23-death link is causal, the perspective arises that patients with normal phosphate levels but high FGF-23may be targeted to a phosphate level lower than that currently recommended by guidelines. Replicating these novel findings in different populations and in diverse clinical settings would give strength to the hypothesis that high FGF-23 is causally involved in the high mortality of dialysis patients. Yet these studies would still remain insufficient proof for definitively establishing a causal link. Definitive proof of causality may only derive from intervention studies, i.e. from studies where FGF-23 is modified by an appropriate intervention. At this stage it is unjustified to measure FGF-23 in clinical practice. However, this nice observational study is an alert that we should stay tuned to this ebullient research area.