Genomics and metabolomics-based research progress on the regulation of kidney stone formation and recurrence via the gut microbiota-metabolite axis
10.3760/cma.j.cn115396-20251002-00241
- VernacularTitle:基因组学与代谢组学视角下肠道菌群-代谢物轴调控肾结石形成与复发的研究进展
- Author:
Teng CUI
1
;
Kai DANG
;
Jing XIAO
Author Information
1. 首都医科大学附属北京友谊医院泌尿外科 北京市卫生健康委员会泌尿外科研究所，北京 100050
- Keywords:
Kidney calculi;
Gut microbiota;
Genomics;
Metabolomics;
Short-chain fatty acid;
Tryptophan
- From:
International Journal of Surgery
2025;52(10):713-720
- CountryChina
- Language:Chinese
-
Abstract:
Kidney stones are a disease with high incidence, high recurrence rate and heavy economic burden. Current clinical treatments clear formed stones but fail to target the pathophysiological core of recurrence. Beyond systemic risk factors like obesity and diabetes, diet-driven gut dysbiosis is a key potential mediator of stone recurrence. Moreover, the gut-kidney syndrome and gut-kidney axis theories reveal the bidirectional regulation between intestine and kidney, among these, the gut microbiota-metabolite axis as the core functional carrier of the gut-kidney axis has a regulatory mechanism key to resolving recurrence. Currently, 16S rRNA sequencing and metagenomic sequencing have identified gut microbiota differences between stone and non-stone groups: kidney stone patients show reduced alpha diversity, imbalanced Firmicutes/ Bacteroidetes ratio, significantly higher abundance of harmful bacteria (e.g., Escherichia- Shigella), and lower abundance of oxalate-degrading bacteria ( Oxalobacter formigenes, Lactobacillus) and short-chain fatty acid (SCFA)-producing bacteria ( Faecalibacterium). Notably, gut dysbiosis persists even after surgery.Meanwhile, targeted and non-targeted metabolomics show significant abnormalities in intestinal and urinary metabolites (e.g., SCFA tryptophan derivatives) in stone patients, along with downregulated pathways including purine metabolism, caffeine metabolism and aromatic amino acid metabolism. These abnormalities promote stone formation by disrupting the intestinal barrier, worsening renal inflammation and triggering renal oxidative stress. This article reviews the aforementioned gut microbiota, metabolites and related regulatory pathways with significant inter-group differences. Combined with advances in genomics and metabolomics, it aims to provide theoretical references for further clarifying the mechanism of gut microbiota-metabolite axis regulates kidney stone formation and recurrence, and for developing microecological interventions.
