INTENDED USE
This kit is intended for research use only in the determination of human FGF-23 levels in plasma or cell culture media. Reference ranges and clinical utility have not been established.
INTRODUCTION
Fibroblast growth factor 23 (FGF-23), which is produced by bone cells, is a novel member of a large family of related proteins. The amino-terminal portion of FGF-23 (aa 1-24) is hydrophobic and serves as a signal peptide allowing its secretion into the blood circulation. Its carboxyl-terminal portion (aa 180-251) shares only limited amino acid homology with other members of the FGF family of proteins.
Renal phosphate wasting disorders leading to hypophosphatemia are among the causes of defective mineralization of bone and growth plate development. Patients with autosomal dominant hypophosphatemic rickets (ADHR), a rare genetic disorder, carry one of several different FGF-23 mutations that make the protein resistant to proteolytic cleavage. Furthermore, tumors that cause oncogenic osteomalacia (OOM) have been shown to overexpress FGF-23 mRNA making it likely that elevated concentrations of FGF-23 in the blood are the cause of renal phosphate wasting in this group of patients. FGF-23 levels have been shown to be elevated in renal disease. The concentration appears to correlate with the degree of bone mineralization and increasing levels have been shown to be a predictor of mortality in these patients. All currently available data suggest that FGF-23 is either directly or indirectly involved in the regulation of phosphate homeostasis.
The measurement of human FGF-23 levels in the blood is likely to provide an important diagnostic tool for the laboratory evaluation of patients with a variety of different hypophosphatemic and hyperphosphatemic disorders. Furthermore, the sensitive measurement of FGF-23 is likely to provide novel insights into the regulation of bone and mineral homeostasis.
