ArticleNature microbiology2025
Segatella copri and gut microbial ammonia metabolism contribute to chronic kidney disease pathogenesis.
Article in Nature microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Revisiting gut microbiota-driven ammonia metabolism: from disease burden to physiological adaptation.Gut microbes · 2026Review
- Linkage of gut microbiota dysbiosis to chronic kidney disease in patients with graded proteinuria levels.Microbiology spectrum · 2026Article
- Review
- The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026Review
- Intestinal aging-related immune dysfunction: mechanisms and interventions.Acta biochimica et biophysica Sinica · 2026Review
- Microbiota-associated metabolic networks in gut-kidney communication and renal immune regulation: mechanisms and therapeutic potential.Frontiers in microbiology · 2026Review
- Integrative multi-omics analysis identifies microbial dysbiosis and functional metabolic reprogramming in acute kidney injury.Frontiers in medicine · 2026Article
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Authors and funding
23 authors.
Funding
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Abstract
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.
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Registered trials
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