July 15, 2025Open Access

Gut microbiome remodeling in chronic kidney disease: implications of kidney replacement therapies and therapeutic interventions

Key Points

Gut microbiome remodeling is crucial in chronic kidney disease, linking microbial dysbiosis to uremic toxin accumulation.
Hemodialysis is associated with specific microbial shifts, increasing Firmicutes and Proteobacteria while reducing beneficial butyrate producers.
Interventions like plant-based diets lower inflammatory markers and reduce mortality risk in peritoneal dialysis patients.
Future research must focus on standardized protocols and integrating dietary therapies to enhance precision medicine for chronic kidney disease.

Abstract

The escalating global burden of end-stage renal disease (ESRD), driven by aging populations and rising metabolic comorbidities, underscores the urgent need for innovative therapeutic strategies. Emerging evidence highlights the gut microbiome as a pivotal modulator of renal pathophysiology through the gut-kidney axis, with microbial dysbiosis exacerbating gut microbial metabolites (e.g., uremic toxins), systemic inflammation, and multi-organ damage. This narrative review explores the divergent impacts of kidney replacement therapies (KRT)—hemodialysis (HD) and peritoneal dialysis (PD)—on gut microbiota dynamics: HD is associated with Firmicutes and Proteobacteria enrichment, reduced butyrate-producing taxa (e.g., Faecalibacterium , Roseburia ), and systemic microbial translocation; whereas PD-driven glucose absorption and iron supplementation foster pathogenic proliferation (e.g., Enterobacteriaceae ) and impair short-chain fatty acid (SCFA) metabolism. Current interventions, including probiotics, prebiotics, plant-based diets (PBDs), and fecal microbiota transplantation (FMT), demonstrate potential in mitigating dysbiosis and uremic toxin accumulation. PBDs reduce inflammatory markers (IL-6, CRP) and lower all-cause mortality risk by 24% in PD patients; synbiotics (e.g., Lactobacillus casei + galactooligosaccharides) reduce serum p-cresyl sulfate by 20% in HD patients; and FMT increases levels of short-chain fatty acids (propionate, butyrate) and lowers trimethylamine N-oxide (TMAO) concentrations in streptozotocin-induced diabetic nephropathy mouse models. However, clinical translation remains challenged by small sample sizes, heterogeneous outcomes, and a lack of hard endpoints. Future research must prioritize standardized protocols, personalized microbial profiling, and synergistic integration of dietary and microbiome-targeted therapies. Bridging mechanistic insights with clinical validation will advance precision medicine in ESRD management, offering transformative potential for patients burdened by this therapeutic impasse.

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