期刊
BONE
卷 100, 期 -, 页码 41-49出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2017.01.017
关键词
AKI; CKD; Klotho; Phosphate; Uremic cardiomyopathy; Vascular calcification; Vitamin D
资金
- NIH [R01-DK091392, R01-DK092461, R01-DK092461-S1]
- George M. O'Brien Kidney Research Center [P30-DK-07938]
- Charles and Jane Pak Foundation
- Pak Center Innovative Research Support
- Ben J. Lipps Research Fellowship Program of American Society of Nephrology Foundation for Kidney Research
- Truelson Fellowship Fund at the Charles and Jane Pak Center of Mineral Metabolism and Clinical Research
The extracellular domain of transmembrane alpha-Klotho (alpha Klotho, hereinafter simply called Klotho) is cleaved by secretases and released into the circulation as soluble Klotho. Soluble Klotho in the circulation starts to decline early in chronic kidney disease (CKD) stage 2 and urinary Klotho possibly even earlier in CKD stage I. Therefore soluble Klotho could serve as an early and sensitive marker of kidney function decline. Moreover, preclinical animal data support Klotho deficiency is not just merely a biomarker, but a pathogenic factor for CKD progression and extrarenal CKD complications including cardiovascular disease and disturbed mineral metabolism. Prevention of Klotho decline, re-activation of endogenous Klotho production or supplementation of exogenous Klotho are all associated with attenuation of renal fibrosis, retardation of CKD progression, improvement of mineral metabolism, amelioration of cardiomyopathy, and alleviation of vascular calcification in CKD. Therefore Klotho is not only a diagnostic and/or prognostic marker for CKD, but the treatment of Klotho deficiency may be a promising strategy to prevent, retard, and decrease the burden of comorbidity in CKD. (C) 2017 Elsevier Inc. All rights reserved.
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