Relationship between Fibroblast Growth Factor-23 and Mineral Metabolism in Chronic Kidney Disease

Abstract EN

Fibroblast growth factor- (FGF-)23 is a recently discovered regulator of calcium-phosphate metabolism.

FGF-23 appears to decrease in synthesis and accelerated degradation of 1,25(OH)2D.

Together with its cofactor Klotho, FGF-23 maintains serum phosphate levels within the normal range by increasing renal phosphate excretion.

In chronic kidney disease (CKD), FGF-23 levels rise in parallel with the decline in renal function long before a significant increase in serum phosphate concentration occurs.

Both Klotho and FGF-23, linked by a receptor mechanism, affect vitamin D synthesis and parathyroid hormone (PTH) secretion.

Previous studies have shown a close association between reduced FGF-23 or Klotho activities and vascular calcification.

The possible association of FGF-23 and left ventricular hypertrophy or vascular dysfunction has been proposed.

Finally, prospective studies have shown that high serum FGF-23 concentrations predict more rapid disease progression in CKD patients who were not on dialysis and increased mortality in patients on maintenance hemodialysis.

FGF-23 may therefore prove to be an important therapeutic target for the management of CKD.