慢性肾脏疾病中FGF23如何影响多个器官。

IF 2.4 Q1 PEDIATRICS
Maren Leifheit-Nestler, Dieter Haffner
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引用次数: 8

摘要

慢性肾脏疾病(CKD)与儿童和成人矿物质代谢的明显改变相关,导致多器官功能障碍。患有晚期CKD的儿童经常遭受骨矿化受损,骨畸形和骨折,生长衰竭,肌肉无力,血管和软组织钙化,最近被称为CKD矿物质和骨骼疾病(CKD- mbd)。后者是这些患者心血管疾病合并症和死亡率增加的主要因素。循环中内分泌作用的磷酸化激素成纤维细胞生长因子(FGF) 23水平的升高是矿物质代谢的第一个可检测的改变,因此CKD-MBD。FGF23由骨细胞和成骨细胞表达和分泌,并随着肾脏功能下降以维持磷酸盐稳态而逐渐升高,这很可能是由于磷酸盐负荷增加所致。虽然尚未在临床常规中测量,但ckd介导的儿童FGF23循环水平升高与病理性心脏重构、血管改变和认知风险增加有关。针对其他fgf23介导的肾衰竭并发症(如高血压和骨矿化受损)的临床和实验研究显示,部分结果相互矛盾,而且因果关系并不总是完全清楚。这篇简短的综述总结了CKD中FGF23合成调节因子的改变以及与高FGF23水平相关的主要CKD介导的器官功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

How FGF23 shapes multiple organs in chronic kidney disease.

How FGF23 shapes multiple organs in chronic kidney disease.

How FGF23 shapes multiple organs in chronic kidney disease.

Chronic kidney disease (CKD) is associated with distinct alterations in mineral metabolism in children and adults resulting in multiple organ dysfunctions. Children with advanced CKD often suffer from impaired bone mineralization, bone deformities and fractures, growth failure, muscle weakness, and vascular and soft tissue calcification, a complex which was recently termed CKD-mineral and bone disorder (CKD-MBD). The latter is a major contributor to the enhanced cardiovascular disease comorbidity and mortality in these patients. Elevated circulating levels of the endocrine-acting phosphaturic hormone fibroblast growth factor (FGF) 23 are the first detectable alteration of mineral metabolism and thus CKD-MBD. FGF23 is expressed and secreted from osteocytes and osteoblasts and rises, most likely due to increased phosphate load, progressively as kidney function declines in order to maintain phosphate homeostasis. Although not measured in clinical routine yet, CKD-mediated increased circulating levels of FGF23 in children are associated with pathological cardiac remodeling, vascular alterations, and increased cognitive risk. Clinical and experimental studies addressing other FGF23-mediated complications of kidney failure, such as hypertension and impaired bone mineralization, show partly conflicting results, and the causal relationships are not always entirely clear. This short review summarizes regulators of FGF23 synthesis altered in CKD and the main CKD-mediated organ dysfunctions related to high FGF23 levels.

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