The osteocyte in CKD: new concepts regarding the role of FGF23 in mineral metabolism and systemic complications.
The identification of elevated circulating levels of the osteocytic protein fibroblast growth factor 23 (FGF23) in patients with chronic kidney disease (CKD), along with recent data linking these values to the pathogenesis of secondary hyperparathyroidism and to systemic complications, has changed the approach to the pathophysiology and treatment of disordered bone and mineral metabolism in renal failure. It now appears that osteocyte biology is altered very early in the course of CKD and these changes have implications for bone biology, as well as for progressive cardiovascular and renal disease. Since circulating FGF23 values are influenced by therapies used to treat secondary hyperparathyroidism, the effects of different therapeutic paradigms on FGF23 have important implications for mineral metabolism as well as for morbidity and mortality. Further studies are critically needed to identify the initial trigger for abnormalities of skeletal mineralization and turnover as well as the potential effects that current therapeutic options may have on osteocyte biology.
David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. kwesseling@mednet.ucla.edu
Katherine
K
Wesseling-Perry
Harald
H
Jüppner
D000818:Animals; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000150:complications / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000097:blood / Q000378:metabolism*; D006801:Humans; D008903:Minerals / Q000378:metabolism*; D010011:Osteocytes / Q000378:metabolism* / Q000473:pathology*; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy
C000717427:FGF23 protein, human; D008903:Minerals; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23