PURPOSE: Chronic kidney disease (CKD) remains a major global health burden despite advances in conventional therapies. This review synthesizes current clinical and experimental evidence on the bidirectional relationship between CKD and gut microbial dysbiosis, emphasizing mechanisms, measurable outcomes, and therapeutic interventions. METHODS: A narrative review of recent clinical and experimental studies was conducted to explore alterations in gut microbial composition, generation of uremic toxins, and the impact of CKD therapies on microbial balance. Emerging microbiota-targeted interventions were also examined. RESULTS: Studies consistently report reduced microbial diversity, loss of short-chain fatty acid (SCFA)-producing taxa, and enrichment of proteolytic, toxin-producing bacteria in CKD. Gut-derived metabolites such as indoxyl sulfate (IS), p-cresyl sulfate (pCS), and trimethylamine N-oxide (TMAO) are linked to oxidative stress, RAAS activation, and fibrogenesis. In human trials, microbiota-directed therapies show modest biochemical benefits: a meta-analysis of 21 randomized studies reported mean reductions in serum BUN (8.5 mg/dL) and CRP (1.4 mg/L) with probiotic or synbiotic supplementation, while inulin (10 g/day) in stage 3-4 CKD reduced serum pCS by 25% and increased fecal butyrate by 40%. However, most mechanistic data derive from animal and in vitro models, and human evidence remains heterogeneous and underpowered. Stage-specific differences are evident-early CKD shows subtler dysbiosis, while advanced CKD and dialysis populations exhibit profound microbial shifts and variable responsiveness. CONCLUSION: The gut microbiota is a promising, modifiable contributor to CKD pathophysiology. Stage-stratified longitudinal studies are needed to establish causality and therapeutic efficacy.
Ahsan et al. (Mon,) studied this question.
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