Does bone structure accurately reflect serum FGF23 levels in patients with chronic kidney disease?

Abstract

Serum fibroblast growth factor 23 (FGF23) levels regulate serum phosphate levels and are thought to be related to systemic complications, including in the cardiovascular system,1 in patients with chronic kidney disease (CKD). Patients with autosomal dominant hypophosphatemic rickets (ADHR) develop hypophosphatemia because these patients harbor a mutation in FGF23 making it resistant to degradation. However, a high incidence of cardiovascular complications has not been reported in ADHR patients. Interestingly, serum levels of intact, biologically active FGF23 in patients with ADHR do not significantly differ from that in healthy controls.2 Changes in bone structure in ADHR patients are caused by a slight increase in FGF23 levels, which may indicate that serum FGF23 levels are not always related to the effects of FGF23 on bone.2 Therefore, we should consider the relationship between serum FGF23 levels and bone structure. Our point is that significant changes occur in serum FGF23 levels in patients with CKD who often develop Osteitis fibrosa yet bone turnover may have an influence on FGF23 secretion. In the paper by Pereira et al.,3 human bone cells cultured from adult patients with CKD were shown to be an ex vivo model to reflect gene expression in osteoblasts and osteocytes. This model may be appropriate to evaluate the pathophysiologic relation between bone lesions and serum FGF23 in patients with CKD. We suggest that it is necessary to consider bone structural changes in Osteitis fibrosa when evaluating FGF23 metabolism.4