Duodenal microbiome in chronic kidney disease.

Chronic kidney disease Duodenal microbiome Gut microbiome Metagenomics Pathway analysis

Journal

Clinical and experimental nephrology
ISSN: 1437-7799
Titre abrégé: Clin Exp Nephrol
Pays: Japan
ID NLM: 9709923

Informations de publication

Date de publication:
Apr 2024
Historique:
received: 27 09 2023
accepted: 06 11 2023
pubmed: 14 12 2023
medline: 14 12 2023
entrez: 14 12 2023
Statut: ppublish

Résumé

The intestinal microbiome is involved in the pathogenesis of chronic kidney disease (CKD). Despite its importance, the microbiome of the small intestinal mucosa has been little studied due to sampling difficulties, and previous studies have mainly focused on fecal sources for microbiome studies. We aimed to characterize the small intestinal microbiome of CKD patients by studying the microbiome collected from duodenal and fecal samples of CKD patients and healthy controls. Overall, 28 stage 5 CKD patients and 21 healthy participants were enrolled. Mucosal samples were collected from the deep duodenum during esophagogastroduodenoscopy and fecal samples were also collected. The 16S ribosomal RNA gene sequencing using Qiime2 was used to investigate and compare the microbial structure and metagenomic function of the duodenal and fecal microbiomes. The duodenal flora of CKD patients had decreased alpha diversity compared with the control group. On the basis of taxonomic composition, Veillonella and Prevotella were significantly reduced in the duodenal flora of CKD patients. The tyrosine and tryptophan metabolic pathways were enhanced in the urea toxin-related metabolic pathways based on the Kyoto Encyclopedia of Genes and Genomes database. The small intestinal microbiome in CKD patients is significantly altered, indicating that increased intestinal permeability and production of uremic toxin may occur in the upper small intestine of CKD patients.

Sections du résumé

BACKGROUND BACKGROUND
The intestinal microbiome is involved in the pathogenesis of chronic kidney disease (CKD). Despite its importance, the microbiome of the small intestinal mucosa has been little studied due to sampling difficulties, and previous studies have mainly focused on fecal sources for microbiome studies. We aimed to characterize the small intestinal microbiome of CKD patients by studying the microbiome collected from duodenal and fecal samples of CKD patients and healthy controls.
METHODS METHODS
Overall, 28 stage 5 CKD patients and 21 healthy participants were enrolled. Mucosal samples were collected from the deep duodenum during esophagogastroduodenoscopy and fecal samples were also collected. The 16S ribosomal RNA gene sequencing using Qiime2 was used to investigate and compare the microbial structure and metagenomic function of the duodenal and fecal microbiomes.
RESULTS RESULTS
The duodenal flora of CKD patients had decreased alpha diversity compared with the control group. On the basis of taxonomic composition, Veillonella and Prevotella were significantly reduced in the duodenal flora of CKD patients. The tyrosine and tryptophan metabolic pathways were enhanced in the urea toxin-related metabolic pathways based on the Kyoto Encyclopedia of Genes and Genomes database.
CONCLUSION CONCLUSIONS
The small intestinal microbiome in CKD patients is significantly altered, indicating that increased intestinal permeability and production of uremic toxin may occur in the upper small intestine of CKD patients.

Identifiants

DOI: 10.1007/s10157-023-02434-x PMID: 38095826
pubmed: 38095826
doi: 10.1007/s10157-023-02434-x
pii: 10.1007/s10157-023-02434-x
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

263-272

Subventions

Organisme : Japan Society for the Promotion of Science
ID : JP21K06783

Informations de copyright

© 2023. The Author(s), under exclusive licence to Japanese Society of Nephrology.

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Auteurs

Masahiro Kondo (M)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.

Takehiro Torisu (T)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan. torisu.takehiro.437@m.kyushu-u.ac.jp.
ORCID: 0000-0001-8256-2549

Tomohiro Nagasue (T)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.

Hiroki Shibata (H)

Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.

Junji Umeno (J)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.

Keisuke Kawasaki (K)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.

Shin Fujioka (S)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.

Yuichi Matsuno (Y)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.

Tomohiko Moriyama (T)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.
International Medical Department, Kyushu University Hospital, Fukuoka, Japan.

Takanari Kitazono (T)

Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Maida-Shi 3-1-1, Higashi-Ku, Fukuoka, 812-8582, Japan.

Classifications MeSH