FGF23 is a protein hormone produced by bone cells that can decrease the production of 1,25 (OH)2 Vitamin D and can increase the excretion of phosphate in the urine by the suppression of proximal tubular phosphate reabsorption. There are evidences of these actions in experimental studies (1) using Wistar-Kyoto rats with progressive nephritis explaining early stage of chronic renal disease (CRD). In these studies the increase of FGF23 is related with the reduction of active Vitamin D and its consequences: Hypocalcemia and secondary hyperparathyroidism. Recent published clinical studies have considered FGF23 an independent risk factor for mortality in early CRD as well as cardiovascular disease, allograft loss, and death in kidney transplant (2,3).

 

The Chronic Renal Insufficiency Cohort (CRIC) Study is a multicenter, prospective observational study (3) of risk factors for cardiovascular disease, progression of CRD, and mortality in adult patients with an estimated GFR of between 20 and 70 cc/min/1.73 m2. In this study FGF23 correlated negatively with estimated GFR and hemoglobin, and correlated positively with cystatin, serum phosphate, parathyroid hormone, and fractional excretion of phosphate. Apart from these results FGF23 is considered not only a marker to define the severity of CRD, but it could also act as a toxin to explain the mortality risk associated with cardiovascular injuries (3,4).

 

Children older than 9 years old in hemodialysis with a single pool of urea kinetic (Kt/V) of 1.3 or greater, using not reused polysulfone dialysers, were recently studied observing a significant higher value of FGF23 and serum phosphorus in those patients with coronary calcifications (5).

 

Levels of FGF23 have been also found increased in calcium nephrolithiasis being specifically more important in the recurrent condition. The increase of phosphates in the urine produces urinary calcium saturation, but it has not been explained why nephrolithiasis in patients with phosphaturia is associated with higher FGF23 levels (6).

 

More experimental studies and prospective clinical studies are needed to define the relation of FGF23 with other bone markers, with mineral metabolism, and with Bone Mineral Density Z scores to explain better its activity in CRD. FGF23 will only be considered a useful biomarker with a clear understanding of the pathophysiology associated to this hormone.