The impact of fibroblast growth factor-23 on the cardiovascular system in chronic kidney disease

被引：1

作者：

Lee, Gavin ^{[1
]}

Krishnasamy, Rathika ^{[1
,2
]}

Hawley, Carmel M. ^{[1
,2
,3
]}

Johnson, David W. ^{[1
,2
,3
]}

机构：

[1] Princess Alexandra Hosp, Dept Nephrol, Brisbane, Qld, Australia

[2] Univ Queensland, Sch Med, Brisbane, Qld, Australia

[3] Translat Res Inst, Brisbane, Qld, Australia

来源：

EXPERT REVIEW OF ENDOCRINOLOGY & METABOLISM | 2015年 / 10卷 / 06期

关键词：

cardiovascular disease; chronic kidney disease; endothelial function; fibroblast growth factor-23; klotho; left ventricular hypertrophy; secondary hyperparathyroidism; vascular calcification;

D O I：

10.1586/17446651.2015.1079124

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Chronic kidney disease is associated with an accelerated risk of cardiovascular (CV) mortality. Seminal work over the last decade has identified abnormal bone metabolism as an important modulator of the increased CV burden in this cohort. In particular, FGF23, a phosphaturic hormone with serum levels found to be markedly elevated in chronic kidney disease, is independently associated with increased risks of all-cause mortality and CV events. This editorial will discuss the proposed mechanisms linking FGF23 to CV disease in chronic kidney disease, namely, direct cardiac myocyte toxicity, endothelial dysfunction and vascular calcification.

引用

页码：565 / 568

页数：4

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