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Role of fibroblast growth factor 23 in phosphate homeostasis and pathogenesis of disordered mineral metabolism in chronic kidney disease.
Semin Dial. 2007 Jul-Aug; 20(4):302-8.SD

Abstract

The discovery of fibroblast growth factor 23 (FGF23), a novel bone-derived hormone that inhibits phosphate reabsorption and calcitriol production by the kidney, has uncovered primary regulatory pathways and new systems biology governing bone mineralization, vitamin D metabolism, parathyroid gland function and renal phosphate handling. This phosphaturic hormone, which is made predominately by osteocytes in bone, appears to have a physiologic role as a counter-regulatory hormone for vitamin D. Evidence has also emerged to support the existence of a bone-kidney axis to coordinate the mineralization of bone with renal handling of phosphate. Pathologically, high circulating levels of FGF23 result in hypophosphatemia, decreased production of 1,25(OH)(2)D, elevated parathyroid hormone and rickets/osteomalacia in patients with functioning kidneys, whereas low levels are associated with tumoral calcinosis, hyperphosphatemia and elevated 1,25(OH)(2)D. In addition, patients with chronic kidney disease (CKD) exhibit marked elevations of circulating FGF23. While the significance of increased FGF23 levels in CKD remains to be defined, it might contribute to phosphate excretion and suppression of 1,25(OH)(2)D levels in CKD stages 3 and 4, as well as potentially contribute to secondary hyperparathyroidism through direct actions on the parathyroid gland in more advanced renal failure. As our knowledge expands regarding the regulation and functions of FGF23, the assessment of FGF23 will become an important diagnostic marker as well as a therapeutic target for management of disordered mineral metabolism in a variety of acquired and hereditary disorders.

Authors+Show Affiliations

The Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17635819

Citation

Stubbs, Jason, et al. "Role of Fibroblast Growth Factor 23 in Phosphate Homeostasis and Pathogenesis of Disordered Mineral Metabolism in Chronic Kidney Disease." Seminars in Dialysis, vol. 20, no. 4, 2007, pp. 302-8.
Stubbs J, Liu S, Quarles LD. Role of fibroblast growth factor 23 in phosphate homeostasis and pathogenesis of disordered mineral metabolism in chronic kidney disease. Semin Dial. 2007;20(4):302-8.
Stubbs, J., Liu, S., & Quarles, L. D. (2007). Role of fibroblast growth factor 23 in phosphate homeostasis and pathogenesis of disordered mineral metabolism in chronic kidney disease. Seminars in Dialysis, 20(4), 302-8.
Stubbs J, Liu S, Quarles LD. Role of Fibroblast Growth Factor 23 in Phosphate Homeostasis and Pathogenesis of Disordered Mineral Metabolism in Chronic Kidney Disease. Semin Dial. 2007 Jul-Aug;20(4):302-8. PubMed PMID: 17635819.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of fibroblast growth factor 23 in phosphate homeostasis and pathogenesis of disordered mineral metabolism in chronic kidney disease. AU - Stubbs,Jason, AU - Liu,Shiguang, AU - Quarles,L Darryl, PY - 2007/7/20/pubmed PY - 2007/10/19/medline PY - 2007/7/20/entrez SP - 302 EP - 8 JF - Seminars in dialysis JO - Semin Dial VL - 20 IS - 4 N2 - The discovery of fibroblast growth factor 23 (FGF23), a novel bone-derived hormone that inhibits phosphate reabsorption and calcitriol production by the kidney, has uncovered primary regulatory pathways and new systems biology governing bone mineralization, vitamin D metabolism, parathyroid gland function and renal phosphate handling. This phosphaturic hormone, which is made predominately by osteocytes in bone, appears to have a physiologic role as a counter-regulatory hormone for vitamin D. Evidence has also emerged to support the existence of a bone-kidney axis to coordinate the mineralization of bone with renal handling of phosphate. Pathologically, high circulating levels of FGF23 result in hypophosphatemia, decreased production of 1,25(OH)(2)D, elevated parathyroid hormone and rickets/osteomalacia in patients with functioning kidneys, whereas low levels are associated with tumoral calcinosis, hyperphosphatemia and elevated 1,25(OH)(2)D. In addition, patients with chronic kidney disease (CKD) exhibit marked elevations of circulating FGF23. While the significance of increased FGF23 levels in CKD remains to be defined, it might contribute to phosphate excretion and suppression of 1,25(OH)(2)D levels in CKD stages 3 and 4, as well as potentially contribute to secondary hyperparathyroidism through direct actions on the parathyroid gland in more advanced renal failure. As our knowledge expands regarding the regulation and functions of FGF23, the assessment of FGF23 will become an important diagnostic marker as well as a therapeutic target for management of disordered mineral metabolism in a variety of acquired and hereditary disorders. SN - 0894-0959 UR - https://www.unboundmedicine.com/medline/citation/17635819/Role_of_fibroblast_growth_factor_23_in_phosphate_homeostasis_and_pathogenesis_of_disordered_mineral_metabolism_in_chronic_kidney_disease_ L2 - https://doi.org/10.1111/j.1525-139X.2007.00308.x DB - PRIME DP - Unbound Medicine ER -