Evidence map›Paper›PMID 41398611›Full record

ArticleMicrobiome2025

Dysbiosis of the gut microbiota in calcium oxalate nephrolithiasis is associated with impaired short-chain fatty acid production and systemic metabolomic disruptions.

Xi Chen, Fangxing Zhang, Lang Cheng, Decao Niu, Jianpei Hu, Shengzhu Huang, Fubo Wang, Guijian Pang, Caisheng Huang, Mingli Li and 2 more

Abstract read
In one paragraph

Article in Microbiome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Xi Chen *Center for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Fangxing Zhang *Center for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Lang Cheng *Center for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Decao Niu *Center for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Jianpei Hu *Center for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Shengzhu HuangCenter for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Fubo WangCenter for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China.
Guijian PangDepartment of Urology, The First People's Hospital of Yulin, Yulin, Guangxi, 37000, China.
Caisheng HuangDepartment of Urology, The Nanning Second People's Hospital, The Third Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China.
Mingli LiCenter for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China. limingligx@126.com.
Chao WangCenter for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China. siraowang@foxmail.com.
Zengnan MoCenter for Genomic and Personalized Medicine, Guangxi Key Laboratory for Genomic and Personalized Medicine, Guangxi Collaborative Innovation Center for Genomic and Personalized Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China. mozengnan@gxmu.edu.cn.

Funding

Guangxi key Laboratory for Genomic and Personalized Medicine 22-35-17Guangxi Key Research and Development Project Guike AB21196022Guangxi Science and Technology Major Project Guike AA22096032Major Project of Guangxi Innovation Driven AA18118016National Natural Science Foundation of China 62272065
6 · The paper itself

Abstract

backgroundThe prevalence of calcium oxalate (CaOx) kidney stones is increasing, yet the underlying mechanisms remain incompletely understood. Emerging evidence suggests that gut microbiota-particularly short-chain fatty acid (SCFA)-producing bacteria-may modulate host metabolism and inflammation, thereby influencing stone formation. However, the mechanistic links between gut dysbiosis, metabolic disturbances, and CaOx stone pathophysiology remain to be fully elucidated. This study investigates gut microbiota composition, SCFA levels, and metabolomic alterations in CaOx stone formers (CSF), aiming to uncover potential pathophysiological mechanisms and therapeutic targets.

resultsAmong 59 CSF and 60 healthy controls (HC), CSF exhibited significantly reduced microbial richness, with marked depletion of SCFA-producing bacteria such as Faecalibacterium prausnitzii and Eubacterium rectale. This dysbiosis was associated with decreased fecal and plasma SCFA levels, reduced 24-h urinary citrate, and widespread metabolic disturbances, particularly in tryptophan metabolism and the citrate cycle. Plasma SCFA levels were positively correlated with urinary citrate excretion, suggesting a regulatory link within the gut-kidney axis. Mendelian randomization analysis suggested that Bacteroides thetaiotaomicron may be a potential microbial risk factor for stone formation (OR = 1.26, 95% CI: 1.03-1.54, p = 0.028). In a hyperoxaluria rat model, interventions with F. prausnitzii, E. rectale, or sodium butyrate reduced renal CaOx crystal deposition and kidney injury.

conclusionsOur findings highlight the central role of SCFA-producing bacteria and their metabolites in maintaining metabolic balance and protecting against CaOx stone formation. Gut dysbiosis and reduced SCFA levels appear to drive metabolic changes that contribute to stone development. B. thetaiotaomicron may increase stone risk, while F. prausnitzii, E. rectale, and sodium butyrate show therapeutic potential. These insights support further exploration of microbiome-based strategies for the prevention and personalized management of kidney stones. Video Abstract.

Indexed as

Calcium OxalateDysbiosisFatty Acids, VolatileGastrointestinal MicrobiomeNephrolithiasisAdultAnimalsBacteriaFecesFemaleHumansKidney CalculiMaleMetabolomicsMiddle AgedRatsCalcium OxalateFatty Acids, VolatileCalcium oxalate kidney stonesMetabolomicsMicrobiomeMulti-omicsSCFA-producing bacteriaShort-chain fatty acids

Identifiers

PMID41398611
PMCPMC12822354

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.