Abstract
Growing interest has been focused on the pathogenesis of chronic kidney disease-mineral and bone disorder (CKD-MBD) , which is not restricted to those with end-stage CKD and dialysis patients but also includes those with early-stage CKD. Recent evidence demonstrated that FGF23 levels increase early in CKD to maintain normal phosphate balance, but this results in suppression of renal production of 1,25 dihydroxyvitamin D and thereby triggers the early development of secondary hyperparathyroidism. Thus, it can be interpreted that elevated FGF23 in response to phosphate overload represent the beginning of CKD-MBD. Elevations in FGF23 may also suggest the presence of compensatory response to phosphate retention, underscoring the potential of FGF23 as a new biomarker of phosphate balance. It is hoped that further research in this area will establish the treatment strategy of predialysis CKD-MBD and improves the outcome of CKD patients.
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