ArticleFrontiers in cellular and infection microbiology2022
Altered gut microbiota and gut-derived p-cresyl sulfate serum levels in peritoneal dialysis patients.
Article in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 20 citations in OpenAlex.
- Protecting peritoneal dialysis patients: evaluation and prevention strategies for noninfectious risk factors.Renal failure · 2026Review
- Article
- Integrative profiling of gut microbiome, bacteriophagenome, and predicted metabolome in obese adults: novel insights into intervention targets.BMC microbiology · 2026Article
- Gut microbiota as a therapeutic target in sepsis-induced multi-organ dysfunction: a review.Frontiers in cellular and infection microbiology · 2026Review
- Gut microbiota and gut-kidney axis in kidney diseases: therapeutic potential and perspectives of natural products.Frontiers in pharmacology · 2026Review
- Integrated multi-omics reveals dysbiosis in hemodialysis patients: A multi-center study.PloS one · 2026Observational
- Gut dysbiosis and constipation in patients with end-stage renal disease: pathogenic associations and therapeutic interventions.Frontiers in cellular and infection microbiology · 2026Review
- Differences in gut microbiota composition are an important reason for lower serum p-cresol sulfate levels in anuric peritoneal dialysis patients compared to hemodialysis patients.Current research in microbial sciences · 2026Article
- Microbiota-derived metabolites and cognitive dysfunction in dialysis patients: mechanisms and targeted therapeutic strategies.Frontiers in microbiology · 2026Review
- Microbiota-Gut-Kidney Axis and Targeted Therapeutic Strategies in Kidney Diseases.International journal of biological sciences · 2026Review
- Article
- The gut-kidney axis in chronic kidney disease: a vicious cycle of microbial dysbiosis and uremic toxin accumulation.Frontiers in immunology · 2026Review
- Gut microbiota-derived TMAO drives the kidney-bone-vascular axis in chronic kidney disease complications.Renal failure · 2025Review
- Spatial metabolic and phenotypic characterization of the germ-free mouse model.Annals of the New York Academy of Sciences · 2025Article
- Microbial Metabolites and Cardiovascular Dysfunction: A New Era of Diagnostics and Therapy.Cells · 2025Review
- Unraveling the mysteries of the gut-kidney axis: the protective role of traditional Chinese medicine in chronic kidney disease.Frontiers in microbiology · 2025Review
- LC-MS/MS identifies elevated imidazole propionate and gut-derived metabolite alterations in peritoneal dialysis patients.Computational and structural biotechnology journal · 2025Article
- The gut-kidney axis in chronic kidney disease: mechanisms, microbial metabolites, and microbiome-targeted therapeutics.Frontiers in medicine · 2025Review
- The microbial metabolite trimethylamine N-oxide and the kidney diseases.Frontiers in cellular and infection microbiology · 2025Review
- Gut microbiome dynamics of patients on dialysis: implications for complications and treatment.Frontiers in pharmacology · 2025Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peritoneal dialysis (PD) is a renal replacement therapy for end-stage renal disease. Gut microbiota-derived uremic solutes, indoxyl sulfate (IS), p-cresyl sulfate (PCS), and trimethylamine-N-oxide (TMAO) accumulate in PD patients. The objective was to explore the gut microbiota and their influence on uremic toxins in PD patients and healthy controls (HC). Fecal samples were collected from PD patients (n = 105) and HC (n = 102). 16S rRNA gene regions were sequenced for gut microbiota analysis. IS, PCS, and TMAO levels were measured using HPLC-MS. PD patients exhibited lower alpha diversity and altered gut microbiota composition compared to HC. At the genus level, PD patients showed increased abundance of opportunistic pathogenic bacteria, and decreased abundance of beneficial bacteria. Three Operational Taxonomic Units discriminated PD patients from HC. Phenylalanine metabolism increased in PD, whereas tryptophan metabolism was unaltered. Low serum PCS did not necessarily mean healthier due to the loss of alpha diversity, increased Proteobacteria and opportunistic pathogenic bacteria. High serum PCS was mainly caused by elevated p-cresol-producing bacteria, enriched amino acid related enzymes, and enhanced sulfur metabolism, rather than declined residual renal function. In patients with different urine volumes, the gut microbiota alpha diversity and composition were unaltered, but serum IS and TMAO were significantly elevated in anuric patients. In conclusion, the gut microbiota abundance, composition, and function were altered in PD patients, which increased the PCS levels. We provided a better understanding of the microbiota-metabolite-kidney axis in PD patients. Targeting certain bacteria could decrease the PCS levels, whereas preserving the residual renal function could reduce the IS and TMAO levels.
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