Research progress on the relationship between intestinal microecology and chronic kidney disease and the intervention therapy

doi:10.3877/cma.j.issn.2095-3216.2022.01.007

Abstract

Abstract:

Intestinal microecology is an important part of human microecology, and is closely related to many diseases. Intestinal dysbiosis and gut-derived toxins produced from gut microbes-metabolized dietary proteins play an important role in the progression of chronic kidney disease (CKD). This article described the metabolic processes of indoxyl sulfate, p-cresol sulfate, phenylacetylglutamine, trimethylamine oxide, and indole-3-acetic acid as well as their relationship with both CKD and its complications. Improving the gut microecology and reducing the production of gut-derived toxins may delay the progression of CKD, providing a new direction for the treatment of CKD.

Key words: Intestinal microecology, Chronic kidney disease, Gut-derived toxins

Runxia Song, Xiaole Su, Lihua Wang. Research progress on the relationship between intestinal microecology and chronic kidney disease and the intervention therapy[J]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2022, 11(01): 39-43.

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References 48

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肠源性毒素	机制	作用
PCS	1.抑制Klotho基因表达、激活TGF-β 、增加NADPH活性	肾脏纤维化
	2.激活、损伤内皮细胞	CKD心血管并发症
	3.抑制中性粒细胞、树突状细胞	适应性免疫和先天性免疫受损
IS	1.增加炎症因子的产生、促进M1巨噬细胞的活化和抑制Klotho基因的表达	肾间质纤维化
	2.增加ICAM-1、MCP-1的表达	血管壁硬化
	3.增加ROS的产生、抑制Klotho基因的表达和与AhR结合	动脉粥样硬化
TMAO	1.激活NF-κB通路	动脉粥样硬化形成
	2.诱导心肌细胞的横小管网络损伤和心肌细胞的钙离子处理功能障碍	心力衰竭
PAG	与心肌和血管的肾上腺素受体结合	心脏毒性、心力衰竭
IAA	诱导内皮环氧化酶-1和内皮TF的表达、减少TF泛素化	血栓形成和血管壁硬化

肠源性毒素	机制	作用
PCS	1.抑制Klotho基因表达、激活TGF-β 、增加NADPH活性	肾脏纤维化
	2.激活、损伤内皮细胞	CKD心血管并发症
	3.抑制中性粒细胞、树突状细胞	适应性免疫和先天性免疫受损
IS	1.增加炎症因子的产生、促进M1巨噬细胞的活化和抑制Klotho基因的表达	肾间质纤维化
	2.增加ICAM-1、MCP-1的表达	血管壁硬化
	3.增加ROS的产生、抑制Klotho基因的表达和与AhR结合	动脉粥样硬化
TMAO	1.激活NF-κB通路	动脉粥样硬化形成
	2.诱导心肌细胞的横小管网络损伤和心肌细胞的钙离子处理功能障碍	心力衰竭
PAG	与心肌和血管的肾上腺素受体结合	心脏毒性、心力衰竭
IAA	诱导内皮环氧化酶-1和内皮TF的表达、减少TF泛素化	血栓形成和血管壁硬化

干预措施	疗效	不良反应
口服吸附剂	减少肠源性毒素吸收	胃肠道症状(恶心、呕吐、腹泻、腹胀)、
AhR和IAA拮抗剂	降低CKD患者心血管疾病发生率
膳食调节	改善肠道黏膜屏障和抑制机体微炎症状态
益生菌、益生元	降低血清毒素水平、延缓GFR下降	增加IL-6水平
粪便微生物移植	减少小鼠IS产生
肾康栓	降低血清IS、PCS水平
高硫氨基酸饮食	减少小鼠吲哚的产生
重组α-Klotho蛋白	延缓小鼠心、肾纤维化

干预措施	疗效	不良反应
口服吸附剂	减少肠源性毒素吸收	胃肠道症状(恶心、呕吐、腹泻、腹胀)、
AhR和IAA拮抗剂	降低CKD患者心血管疾病发生率
膳食调节	改善肠道黏膜屏障和抑制机体微炎症状态
益生菌、益生元	降低血清毒素水平、延缓GFR下降	增加IL-6水平
粪便微生物移植	减少小鼠IS产生
肾康栓	降低血清IS、PCS水平
高硫氨基酸饮食	减少小鼠吲哚的产生
重组α-Klotho蛋白	延缓小鼠心、肾纤维化

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