Lee Gavin, Krishnasamy Rathika, Hawley Carmel M, Johnson David W
a 1 Department of Nephrology, Princess Alexandra Hospital, Brisbane, Australia.
b 2 School of Medicine, The University of Queensland, Brisbane, Australia.
Expert Rev Endocrinol Metab. 2015 Nov;10(6):565-568. doi: 10.1586/17446651.2015.1079124. Epub 2015 Aug 27.
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.
慢性肾脏病与心血管（CV）死亡风险加速相关。过去十年的开创性研究已确定骨代谢异常是该队列中心血管负担增加的重要调节因素。特别是，成纤维细胞生长因子23（FGF23）是一种排磷激素，其血清水平在慢性肾脏病中显著升高，与全因死亡风险和心血管事件增加独立相关。本社论将讨论在慢性肾脏病中FGF23与心血管疾病之间的潜在联系机制，即直接心肌细胞毒性、内皮功能障碍和血管钙化。
