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Klotho/FGF23 Axis in CKD.
Contrib Nephrol. 2015; 185:56-65.CN

Abstract

The sequential bone disorders, serum parameter abnormalities and vascular calcification that are associated with chronic kidney disease (CKD) have come to be generally known as CKD-mineral bone disorder (MBD). Klotho, a causative protein of aging, and fibroblast growth factor 23 (FGF23), a bone-derived phosphaturic factor, have been reported to be involved in CKD-MBD, and their relationship to the pathophysiology of this disease is gradually being elucidated. Klotho functions as a cofactor of FGF receptors and has been reported to cause FGF23 action and specificity in the kidney. In addition, the presence of secreted Klotho in membrane protein fractions has been determined, and its specific actions are now garnering attention. FGF23, in cooperation with Klotho, inhibits phosphate reabsorption and vitamin D production at the kidney. Blood Klotho and FGF23 levels have been reported to increase beginning at the early stages of CKD, and these factors are receiving attention as new surrogate markers that are reported to be related to life expectancy. In this chapter, we summarize and outline the pathophysiology of Klotho and FGF23 in CKD-MBD as well as important points that are starting to influence clinical practice.

Authors+Show Affiliations

Department of Medicine IV, Tokyo Women's Medical University, Tokyo, Japan.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

26023015

Citation

Tsuchiya, Ken, et al. "Klotho/FGF23 Axis in CKD." Contributions to Nephrology, vol. 185, 2015, pp. 56-65.
Tsuchiya K, Nagano N, Nitta K. Klotho/FGF23 Axis in CKD. Contrib Nephrol. 2015;185:56-65.
Tsuchiya, K., Nagano, N., & Nitta, K. (2015). Klotho/FGF23 Axis in CKD. Contributions to Nephrology, 185, 56-65. https://doi.org/10.1159/000380970
Tsuchiya K, Nagano N, Nitta K. Klotho/FGF23 Axis in CKD. Contrib Nephrol. 2015;185:56-65. PubMed PMID: 26023015.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Klotho/FGF23 Axis in CKD. AU - Tsuchiya,Ken, AU - Nagano,Nobuo, AU - Nitta,Kosaku, Y1 - 2015/05/19/ PY - 2015/5/30/entrez PY - 2015/5/30/pubmed PY - 2016/2/26/medline SP - 56 EP - 65 JF - Contributions to nephrology JO - Contrib Nephrol VL - 185 N2 - The sequential bone disorders, serum parameter abnormalities and vascular calcification that are associated with chronic kidney disease (CKD) have come to be generally known as CKD-mineral bone disorder (MBD). Klotho, a causative protein of aging, and fibroblast growth factor 23 (FGF23), a bone-derived phosphaturic factor, have been reported to be involved in CKD-MBD, and their relationship to the pathophysiology of this disease is gradually being elucidated. Klotho functions as a cofactor of FGF receptors and has been reported to cause FGF23 action and specificity in the kidney. In addition, the presence of secreted Klotho in membrane protein fractions has been determined, and its specific actions are now garnering attention. FGF23, in cooperation with Klotho, inhibits phosphate reabsorption and vitamin D production at the kidney. Blood Klotho and FGF23 levels have been reported to increase beginning at the early stages of CKD, and these factors are receiving attention as new surrogate markers that are reported to be related to life expectancy. In this chapter, we summarize and outline the pathophysiology of Klotho and FGF23 in CKD-MBD as well as important points that are starting to influence clinical practice. SN - 1662-2782 UR - https://www.unboundmedicine.com/medline/citation/26023015/Klotho/FGF23_Axis_in_CKD_ L2 - https://www.karger.com?DOI=10.1159/000380970 DB - PRIME DP - Unbound Medicine ER -