TSUCHIYA Ken    Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine    Position   Professor (Fixed Term)
Article types	Original article
Language	English
Peer review	Peer reviewed
Title	Klotho/FGF23 Axis in CKD.
Journal	Formal name：Contributions to nephrology Abbreviation：Contrib Nephrol ISSN code：1662-2782(Electronic)0302-5144(Linking)
Domestic / Foregin	Foregin
Volume, Issue, Page	185,pp.56-65
Author and coauthor	Tsuchiya Ken†, Nagano Nobuo, Nitta Kosaku
Authorship	Lead author
Publication date	2015/07
Summary	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.
DOI	10.1159/000380970
Document No.	26023015