Intestinal Microbiota and Kidney Diseases

Ao Xie; Jie Sheng; Feng Zheng

doi:10.1007/s11655-017-2927-5

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Intestinal Microbiota and Kidney Diseases

OriginalPaper | Updated：2021-08-27

- Intestinal Microbiota and Kidney Diseases
- Intestinal Microbiota and Kidney Diseases
- 中国结合医学杂志（英文版） 2018年24卷第6期页码：406-408
- Affiliations：
  
  Advanced Institute for Medical Science, The Second Hosptial, Dalian Medical University,Dalian,China
- Author bio：
- Funds：
- DOI：10.1007/s11655-017-2927-5
  中图分类号：
- 纸质出版日期：2018，
  
  网络出版日期：2018-4-12，
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Xie, A., Sheng, J. & Zheng, F. Intestinal Microbiota and Kidney Diseases., Chin. J. Integr. Med. 24, 406–408 (2018). https://doi.org/10.1007/s11655-017-2927-5

Ao Xie, Jie Sheng, Feng Zheng. Intestinal Microbiota and Kidney Diseases[J]. Chinese Journal of Integrative Medicine, 2018,24(6):406-408.
Xie, A., Sheng, J. & Zheng, F. Intestinal Microbiota and Kidney Diseases., Chin. J. Integr. Med. 24, 406–408 (2018). https://doi.org/10.1007/s11655-017-2927-5 DOI：

Ao Xie, Jie Sheng, Feng Zheng. Intestinal Microbiota and Kidney Diseases[J]. Chinese Journal of Integrative Medicine, 2018,24(6):406-408. DOI： 10.1007/s11655-017-2927-5.

摘要

Kidney diseases are common and the incidence rate is increasing. Gut microbiota is involved in metabolic and immune regulation of the host. Genetic

alimentary and environmental disease factors may change gut flora and increase opportunistic and pathogenic bacteria

contributing to immune or non-immune mediated kidney diseases including IgA nephropathy and diabetic nephropathy. Additionally

bacterial metabolites may be a source of uremic toxins. Thus

identification of diversity

composition

and metabolic and immunologic features of gut bacteria in chronic kidney diseases may help understand pathogenetic mechanism and develop therapy for diseases.

Abstract

Kidney diseases are common and the incidence rate is increasing. Gut microbiota is involved in metabolic and immune regulation of the host. Genetic

alimentary and environmental disease factors may change gut flora and increase opportunistic and pathogenic bacteria

contributing to immune or non-immune mediated kidney diseases including IgA nephropathy and diabetic nephropathy. Additionally

bacterial metabolites may be a source of uremic toxins. Thus

identification of diversity

composition

and metabolic and immunologic features of gut bacteria in chronic kidney diseases may help understand pathogenetic mechanism and develop therapy for diseases.

关键词

microbiotaIgA nephropathychronic kidney diseaseuremia

Keywords

microbiotaIgA nephropathychronic kidney diseaseuremia

references

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Kiryluk K, Moldoveanu Z, Sanders JT, Eison TM, Suzuki H, Julian BA, et al. Aberrant glycosylation of IgA1 is inherited in both pediatric IgA nephropathy and Henoch-Schönlein purpura nephritis. Kidney Int 2011;80:79–87.

Kiryluk K, Li Y, Scolari F, Sanna-Cherchi S, Choi M, Verbitsky M, et al. Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens. Nat Genet 2014;46:1187–1196.

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Neal MD, Jia H, Eyer B, Good M, Guerriero CJ, Sodhi CP, et al. Discovery and validation of a new class of small molecule Tolllike receptor 4 (TLR-4) inhibitors. PLoS One 2013;8:e65779.

Vaziri ND, Wong J, Pahl M, Piceno YM, Yuan J, DeSantis TZ, et al. Chronic kidney disease alters the componsition of intestinal microbial flora. Kidney Int 2013;83:308–315.

Aronov PA, Luo FJ, Plummer NS, Quan Z, Holmes S, Hostetter TH, et al. Colonic contribution to uremic solutes. J Am Soc Nephrol 2011;22:1769–1776.

Lin CJ, Chen HH, Pan CF, Chuang CK, Wang TJ, Sun FJ, et al. p-Cresylsulfate and indoxyl sulfate level at different stages of chronic kidney disease. J Clin Lab Anal 2011;25:191–197.

Niwa T. Role of indoxyl sulfate in the progression of chronic kidney disease and cardiovascular disease: experimental and clinical effects of oral sorbent AST-120. Ther Apher Dial 2011;15:120–124.

Wang F, Zhang P, Jiang H, Cheng S. Gut bacterial translocation contributes to microinflammation in experimental uremia. Dig Dis Sci 2012;57:2856–2862.

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