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磷酸盐和 FGF23 对 CKD 进展的贡献。

Contribution of phosphate and FGF23 to CKD progression.

机构信息

The Jared Grantham Kidney Institute.

Department of Internal Medicine, Division of Nephrology & Hypertension, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.

出版信息

Curr Opin Nephrol Hypertens. 2022 Jul 1;31(4):306-311. doi: 10.1097/MNH.0000000000000793. Epub 2022 Mar 11.

DOI:10.1097/MNH.0000000000000793
PMID:35283435
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9232955/
Abstract

PURPOSE OF REVIEW

Progressive forms of chronic kidney disease (CKD) exhibit kidney inflammation and fibrosis that drive continued nephron loss; however, factors responsible for the development of these common pathologic features remain poorly defined. Recent investigations suggest pathways involved in maintaining urinary phosphate excretion in CKD may be contributing to kidney function decline. This review provides an update on recent evidence linking altered phosphate homeostasis to CKD progression.

RECENT FINDINGS

High dietary phosphate intake and increased serum concentrations of fibroblast growth factor 23 (FGF23) both increase urinary phosphate excretion and are associated with increased risk of kidney function decline. Recent investigations have discovered high concentrations of tubular phosphate promote phosphate-based nanocrystal formation that drives tubular injury, cyst formation, and fibrosis.

SUMMARY

Studies presented in this review highlight important scientific discoveries that have molded our current understanding of the contribution of altered phosphate homeostasis to CKD progression. The collective observations from these investigations implicate phosphaturia, and the resulting formation of phosphate-based crystals in tubular fluid, as unique risk factors for kidney function decline. Developing a better understanding of the relationship between tubular phosphate handling and kidney pathology could result in innovative strategies for improving kidney outcomes in patients with CKD.

摘要

目的综述

慢性肾脏病(CKD)的进行性形式表现为肾脏炎症和纤维化,导致持续的肾单位损失;然而,导致这些常见病理特征发展的因素仍未得到明确界定。最近的研究表明,参与维持 CKD 中尿磷酸盐排泄的途径可能导致肾功能下降。本文综述了最近将磷酸盐稳态改变与 CKD 进展联系起来的证据。

最近的发现

高膳食磷酸盐摄入和血清成纤维细胞生长因子 23(FGF23)浓度增加均增加尿磷酸盐排泄,并与肾功能下降风险增加相关。最近的研究发现,高浓度的管状磷酸盐促进基于磷酸盐的纳米晶体形成,从而导致管状损伤、囊肿形成和纤维化。

总结

本文综述介绍的研究强调了重要的科学发现,这些发现改变了我们目前对磷酸盐稳态改变对 CKD 进展贡献的理解。这些研究的综合观察结果表明,磷酸尿和由此在管状液中形成的基于磷酸盐的晶体是肾功能下降的独特危险因素。更好地了解管状磷酸盐处理与肾脏病理之间的关系可能会为改善 CKD 患者的肾脏预后提供创新策略。

相似文献

1
Contribution of phosphate and FGF23 to CKD progression.磷酸盐和 FGF23 对 CKD 进展的贡献。
Curr Opin Nephrol Hypertens. 2022 Jul 1;31(4):306-311. doi: 10.1097/MNH.0000000000000793. Epub 2022 Mar 11.
2
Simultaneous management of disordered phosphate and iron homeostasis to correct fibroblast growth factor 23 and associated outcomes in chronic kidney disease.同时管理紊乱的磷酸盐和铁稳态,以纠正慢性肾脏病中的成纤维细胞生长因子 23 及其相关结局。
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Update on fibroblast growth factor 23 in chronic kidney disease.慢性肾脏病中成纤维细胞生长因子 23 的最新研究进展。
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Pharmacol Res. 2016 Apr;106:87-91. doi: 10.1016/j.phrs.2016.02.015. Epub 2016 Feb 18.
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Dietary phosphate restriction suppresses phosphaturia but does not prevent FGF23 elevation in a mouse model of chronic kidney disease.饮食磷酸盐限制抑制尿磷排泄,但不能预防慢性肾脏病小鼠模型中 FGF23 的升高。
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J Clin Invest. 2021 Aug 16;131(16). doi: 10.1172/JCI145693.
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Associations of dietary phosphorus intake, urinary phosphate excretion, and fibroblast growth factor 23 with vascular stiffness in chronic kidney disease.膳食磷摄入、尿磷排泄和成纤维细胞生长因子 23 与慢性肾脏病患者血管僵硬的关系。
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Direct evidence for a causative role of FGF23 in the abnormal renal phosphate handling and vitamin D metabolism in rats with early-stage chronic kidney disease.直接证据表明,在早期慢性肾脏病大鼠中,FGF23 在异常肾脏磷酸盐处理和维生素 D 代谢中起因果作用。
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J Bone Miner Res. 2012 Jan;27(1):38-46. doi: 10.1002/jbmr.516.

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