Download biomedica product list
Intact: C-terminal fragment FGF23 ratios explained
Why is it important to measure the ratio of active intact and inactive C-terminal FGF23 fragments?
FGF23 is an endocrine hormone regulating phosphate homeostasis by modulating renal phosphate reabsorption, vitamin D metabolism and parathyroid hormone (PTH) secretion. Epidemiological data suggests that higher FGF23 concentrations are associated with all-cause mortality, cardiovascular mortality, a higher risk of myocardial infarction, stroke and heart failure.
Levels of FGF23 and intact: C-terminal fragment FGF23 ratios can be altered in both genetic and acquired diseases. A primary excess in circulating intact FGF23 is the underlying cause of diseases like XLH, ADHR/ARHR or tumor-induced osteomalacia. The excessive FGF23 levels in these diseases cause renal phosphate wasting, low active vitamin D concentrations and defective mineralization of bones. By contrast, during iron deficiency FGF23 synthesis and cleavage are upregulated in a coupled manner, resulting in normal levels of intact FGF23 and high levels of cFGF23.
Therefore, different conditions result in varying characteristic iFGF23:cFGF23 ratios.
For more information on why iFGF23:cFGF23 ratios differ between diseases check out “Coupling Fibroblast Growth Factor 23 Production and Cleavage: Iron Deficiency, Rickets, and Kidney Disease” or check out out iFGF23 and cFGF12 ELISA.