title: [New Developments in CKD-MBD. Development and progression of CKD-MBD in predialysis period -when and how?].
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.
authors.affiliation: Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Japan./Department of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, USA.
authors.forename: Hirotaka
authors.initials: H
authors.lastname: Komaba
mesh_terms: D000818:Animals; D001851:Bone Diseases, Metabolic / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D002114:Calcinosis; D018450:Disease Progression; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism; D006801:Humans; D010710:Phosphates / Q000378:metabolism; D006435:Renal Dialysis; D051436:Renal Insufficiency, Chronic / Q000150:complications / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology
chemical_list: C000717427:FGF23 protein, human; D010710:Phosphates; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23