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肠道微生物群干预以保留残余肾功能。

Gut Microbiota Interventions to Retain Residual Kidney Function.

机构信息

Graduate Program in Nutrition Sciences, Fluminense Federal University (UFF), Niteroi 24020-140, Brazil.

Graduate Program in Biological Sciences-Physiology, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro 21941-902, Brazil.

出版信息

Toxins (Basel). 2023 Aug 11;15(8):499. doi: 10.3390/toxins15080499.

DOI:10.3390/toxins15080499
PMID:37624256
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10467110/
Abstract

Residual kidney function for patients with chronic kidney disease (CKD) is associated with better quality of life and outcome; thus, strategies should be implemented to preserve kidney function. Among the multiple causes that promote kidney damage, gut dysbiosis due to increased uremic toxin production and endotoxemia need attention. Several strategies have been proposed to modulate the gut microbiota in these patients, and diet has gained increasing attention in recent years since it is the primary driver of gut dysbiosis. In addition, medications and faecal transplantation may be valid strategies. Modifying gut microbiota composition may mitigate chronic kidney damage and preserve residual kidney function. Although various studies have shown the influential role of diet in modulating gut microbiota composition, the effects of this modulation on residual kidney function remain limited. This review discusses the role of gut microbiota metabolism on residual kidney function and vice versa and how we could preserve the residual kidney function by modulating the gut microbiota balance.

摘要

对于慢性肾脏病(CKD)患者来说,残余肾功能与更好的生活质量和预后相关;因此,应采取措施来保护肾功能。在导致肾功能损害的多种因素中,由于尿毒症毒素产生增加和内毒素血症导致的肠道菌群失调值得关注。已经提出了多种调节这些患者肠道微生物群的策略,近年来,饮食作为肠道菌群失调的主要驱动因素,越来越受到关注。此外,药物和粪便移植可能是有效的策略。调节肠道微生物群组成可能减轻慢性肾脏损害并保留残余肾功能。尽管多项研究表明饮食在调节肠道微生物群组成方面具有重要作用,但这种调节对残余肾功能的影响仍然有限。本文综述了肠道微生物群代谢对残余肾功能的作用及其相反作用,以及我们如何通过调节肠道微生物群平衡来保留残余肾功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4569/10467110/8201a38558ed/toxins-15-00499-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4569/10467110/eeebd8f76772/toxins-15-00499-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4569/10467110/8201a38558ed/toxins-15-00499-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4569/10467110/eeebd8f76772/toxins-15-00499-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4569/10467110/8201a38558ed/toxins-15-00499-g002.jpg

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Front Endocrinol (Lausanne). 2024 Dec 13;15:1469165. doi: 10.3389/fendo.2024.1469165. eCollection 2024.
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