Fibroblast Growth Factor 23 and Klotho in AKI

被引：60

作者：

Christov, Marta ^{[1
]}

Neyra, Javier A. ^{[2
,3
]}

Gupta, Sanjeev ^{[1
]}

Leaf, David E. ^{[4
]}

机构：

[1] New York Med Coll, Dept Med, Valhalla, NY 10595 USA

[2] Univ Kentucky, Dept Internal Med, Div Nephrol Bone & Mineral Metab, Lexington, KY USA

[3] Univ Texas Southwestern, Dept Internal Med, Div Nephrol, Dallas, TX USA

[4] Brigham & Womens Hosp, Div Renal Med, 75 Francis St, Boston, MA 02115 USA

来源：

SEMINARS IN NEPHROLOGY | 2019年 / 39卷 / 01期

基金：

美国国家卫生研究院;

关键词：

FGF23; klotho; AKI; mineral metabolism; ACUTE KIDNEY INJURY; DYSREGULATED MINERAL METABOLISM; TRANSCRIPTS ENCODING MEMBRANE; FAMILIAL TUMORAL CALCINOSIS; STAGE RENAL-DISEASE; ALPHA-KLOTHO; VITAMIN-D; FGF23; LEVELS; PHOSPHATE HOMEOSTASIS; IRON-DEFICIENCY;

D O I：

10.1016/j.semnephrol.2018.10.005

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

Acute kidney injury (AKI) is associated with many of the same mineral metabolite abnormalities that are observed in chronic kidney disease. These include increased circulating levels of the osteocyte-derived, vitamin D-regulating hormone, fibroblast growth factor 23 (FGF23), and decreased renal expression of klotho, the co-receptor for FGF23. Recent data have indicated that increased FGF23 and decreased klotho levels in the blood and urine could serve as novel predictive biomarkers of incident AKI, or as novel prognostic biomarkers of adverse outcomes in patients with established AKI. In addition, because FGF23 and klotho exert numerous classic as well as off-target effects on a variety of organ systems, targeting their dysregulation in AKI may represent a unique opportunity for therapeutic intervention. We review the pathophysiology, kinetics, and regulation of FGF23 and klotho in animal and human studies of AKI, and we discuss the challenges and opportunities involved in targeting FGF23 and klotho therapeutically. (C) 2018 Published by Elsevier Inc.

引用

页码：57 / 75

页数：19

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