Pei Xin, Liu Miao, Yu Shanshan
Department of Urology, China-Japan Union Hospital, Jilin University, Changchun, China.
Department of Cardiovascular Medicine, China-Japan Union Hospital, Jilin University, Changchun, China.
Front Cell Infect Microbiol. 2025 Jun 6;15:1602413. doi: 10.3389/fcimb.2025.1602413. eCollection 2025.
In recent years, the incidence of kidney stones has continued to rise worldwide, and conventional treatments have limited efficacy in treating stones associated with recurrent or metabolic abnormalities. The microbiome, as the 'second genome' of the host, is involved in the development of kidney stones through metabolic regulation, immune homeostasis and inflammatory response. Studies have shown that the urinary microbiome of healthy people is dominated by commensal bacteria such as Lactobacillus and Streptococcus, which maintain microenvironmental homeostasis, whereas patients with renal stones have a significantly reduced diversity of intestinal and urinary microbiomes, with a reduced abundance of oxalic acid-degrading bacteria (e.g., Bifidobacterium oxalicum, Bifidobacterium bifidum), and a possible concentration of pathogenic bacteria (e.g., Proteus mirabilis). The microbiome regulates stone formation through mechanisms such as metabolites (e.g., short-chain fatty acids), changes in urine physicochemical properties (e.g., elevated pH), and imbalances in the inflammatory and immune microenvironments. For example, urease-producing bacteria promote magnesium ammonium phosphate stone formation through the breakdown of urea, whereas dysbiosis of the intestinal flora increases urinary oxalic acid excretion and exacerbates the risk of calcium oxalate stones. Microbiome-based diagnostic markers (e.g., elevated abundance of Aspergillus phylum) and targeted intervention strategies (e.g., probiotic supplementation, faecal bacteria transplantation) show potential for clinical application. However, technical bottlenecks (e.g., sequencing bias in low-biomass samples), mechanistic complexity (e.g., multistrain synergism), and individual heterogeneity remain major challenges for future research. Integration of multi-omics data, development of personalised therapies and interdisciplinary research will be the core directions to decipher the relationship between microbiome and kidney stones.
近年来,肾结石的发病率在全球范围内持续上升,传统治疗方法在治疗与复发或代谢异常相关的结石方面疗效有限。微生物群作为宿主的“第二基因组”,通过代谢调节、免疫稳态和炎症反应参与肾结石的形成。研究表明,健康人的泌尿微生物群以乳酸杆菌和链球菌等共生细菌为主,它们维持着微环境的稳态,而肾结石患者的肠道和泌尿微生物群多样性显著降低,草酸降解菌(如草酸双歧杆菌、两歧双歧杆菌)丰度降低,并且可能存在病原菌(如奇异变形杆菌)的富集。微生物群通过代谢产物(如短链脂肪酸)、尿液理化性质的改变(如pH值升高)以及炎症和免疫微环境失衡等机制调节结石形成。例如,产脲酶细菌通过分解尿素促进磷酸镁铵结石的形成,而肠道菌群失调会增加尿草酸排泄,加剧草酸钙结石的风险。基于微生物群的诊断标志物(如曲霉门丰度升高)和靶向干预策略(如补充益生菌、粪便细菌移植)显示出临床应用潜力。然而,技术瓶颈(如低生物量样本的测序偏差)、机制复杂性(如多菌株协同作用)和个体异质性仍然是未来研究的主要挑战。整合多组学数据、开发个性化疗法和跨学科研究将是解读微生物群与肾结石之间关系的核心方向。