Lin Shuchun, Sun Zhonghan, Zhu Xinna, Wang Mengjing, Zhang Qian, Qian Jing, Zhang Hui, Mei Zhendong, Pu Yanni, Kong Mengmeng, Guo Peifeng, Zhou Xiaofeng, Li Jin, Sun Xuehui, Ma Liang, Zhang Xueli, Zhao Fangqing, Nie Jing, Hong Shangyu, Chen Jing, Wang Xiaofeng, Li Xiao, Zheng Yan
Division of Nephrology, National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University, Shanghai, China.
State Key Laboratory of Genetics and Development of Complex Phenotypes, Human Phenome Institute, and School of Life Sciences, Fudan University, Shanghai, China.
Nat Microbiol. 2025 Jun 24. doi: 10.1038/s41564-025-02039-y.
Alterations in gut microbiota have been linked to chronic kidney disease (CKD), but large-scale studies and mechanistic insights are limited. Here we analysed gut metagenome data from 1,550 older individuals (aged 65-93 years) with comprehensive kidney function measurements. Segatella copri was positively associated with kidney function through microbial ammonia metabolism-related pathways and the asnA gene, which encodes an ammonia-assimilating enzyme. These associations were replicated in two external studies. In mice, ammonia supplementation increased serum levels of creatinine and blood urea nitrogen, accelerating CKD progression. In vitro cultures of S. copri or asnA-overexpressing Escherichia coli reduced ammonia concentrations, which was markedly attenuated in asnA-knockout S. copri. Gavage of either S. copri or asnA-overexpressing E. coli, but not asnA-knockout S. copri, mitigated ammonia-induced CKD progression in mice. These findings highlight the role of gut microbial ammonia metabolism in CKD pathogenesis and underscore the therapeutic potential of microbial-based interventions.
肠道微生物群的改变与慢性肾脏病(CKD)有关,但大规模研究和机制性见解有限。在此,我们分析了1550名老年个体(年龄65 - 93岁)的肠道宏基因组数据,并进行了全面的肾功能测量。通过微生物氨代谢相关途径和编码氨同化酶的asnA基因,发现Copri菌与肾功能呈正相关。这些关联在两项外部研究中得到了重复验证。在小鼠中,补充氨会增加血清肌酐和血尿素氮水平,加速CKD进展。Copri菌或过表达asnA的大肠杆菌的体外培养可降低氨浓度,而在敲除asnA的Copri菌中这种降低作用明显减弱。给小鼠灌胃Copri菌或过表达asnA的大肠杆菌,但不包括敲除asnA的Copri菌,可减轻氨诱导的CKD进展。这些发现突出了肠道微生物氨代谢在CKD发病机制中的作用,并强调了基于微生物的干预措施的治疗潜力。