Summary
This meta-analytic study of 130 participants with quantitative faecal metagenomics and cross-study validation (n=4,420) found that host factors—particularly intestinal transit time and medications—explained microbiome variation in chronic kidney disease more strongly than kidney function itself. Lower eGFR was associated with shifts towards proteolytic pathways and increased production of uremic metabolites (p-cresol, indole), patterns mediated largely by slowed intestinal transit and dietary factors. The findings suggest that interventions targeting intestinal motility and nutrition may offer mechanistic leverage in CKD management, though replication of specific microbial biomarkers across independent studies remained inconsistent.
Regional applicability
This international multi-centre study provides insights applicable to CKD management across healthcare systems, including the United Kingdom. The emphasis on intestinal transit time and medication-mediated dysbiosis as modifiable targets aligns with the UK National Health Service's interest in non-pharmacological interventions for CKD progression, though direct translation of microbiome biomarkers into UK clinical practice would require further validation.
Key measures
Estimated glomerular filtration rate (eGFR), intestinal transit time (ITT), faecal metagenomics, p-cresol and indole biosynthetic potential, plant-to-animal CAZyme ratios, saccharolytic-to-proteolytic microbiome transitions, intestinal inflammation markers, microbial taxa replication across 11 studies
Outcomes reported
The study identified microbiome compositional changes associated with chronic kidney disease progression and kidney function, specifically examining faecal metagenomics and metabolic pathway alterations. It evaluated whether kidney function (eGFR) or host factors such as intestinal transit time and medications better explained observed microbiome variation.
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