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Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review)

  • Authors:
    • Chenxia Jin
    • Yanping Wang
  • View Affiliations / Copyright

    Affiliations: Department of Blood Purification, The Third Affiliated Hospital of Gansu University of Chinese Medicine, Baiyin, Gansu 730900, P.R. China
    Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 333
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    Published online on: October 15, 2026
       https://doi.org/10.3892/mmr.2026.14044
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Abstract

Gut dysbiosis is increasingly recognized as a potential contributor to poor outcomes in patients receiving dialysis, yet its mechanistic complexity and therapeutic implications remain incompletely understood in clinical practice. The uremic environment, dietary restrictions, polypharmacy and dialysis modality‑specific factors collectively reshape the gut microbial ecology, promoting the overproduction of deleterious metabolites such as indoxyl sulfate, p‑cresyl sulfate and trimethylamine N‑oxide while depleting protective short‑chain fatty acids. These alterations compromise intestinal barrier integrity, fuel systemic inflammation through endotoxemia and NOD‑like receptor family pyrin domain containing 3 inflammasome activation and have been associated with cardiovascular disease, immune dysfunction, peritonitis, protein‑energy wasting and cognitive impairment. Although probiotic, prebiotic, synbiotic and dietary interventions show promise, heterogeneous responses across trials underscore the inadequacy of one‑size‑fits‑all strategies. Multi‑omics profiling has revealed substantial interindividual variability in microbial composition and metabolic capacity, providing a rationale for personalized approaches. The present review synthesizes current evidence on the mechanisms underlying dysbiosis and complications in patients receiving dialysis and proposes a roadmap toward personalized microbiome‑based care to improve clinical outcomes.
View Figures

Figure 1

Key drivers of gut microbiota
dysbiosis in patients receiving dialysis, and differential
compositional effects of HD and PD in a cohort of 25 patients
receiving HD and 25 patients receiving PD (17). All comparisons were between HD and
PD groups (no healthy control group was included). Patients
receiving HD had 2.6-fold higher Proteobacteria relative abundance
compared with patients receiving PD (18.7% vs. 7.2%; P=0.013) and
elevated Firmicutes levels (42.1% vs. 30.5%; P=0.021). Patients
receiving PD showed a 61.3% reduction in butyrate-producing
Roseburia/Faecalibacterium relative abundance compared with
patients receiving HD (2.3% in PD vs. 5.9% in HD; P=0.007),
alongside depleted Bifidobacterium and Lactobacillus.
Pathogenic Enterobacteriaceae were 3.1-fold more abundant in
patients receiving HD compared with patients receiving PD (11.4%
vs. 3.7%; P<0.01). Statistical significance was indicated by
P<0.05 for HD vs. PD comparisons. HD, hemodialysis; PD,
peritoneal dialysis; LPS, lipopolysaccharide; IS, indoxyl sulfate;
PCS, p-cresyl sulfate; TMAO, trimethylamine-N-oxide; SCFAs,
short-chain fatty acids.

Figure 2

Schematic illustrating
pathophysiological cascades linking gut dysbiosis to systemic
complications in patients receiving dialysis. Uremia induces gut
microbial shifts, such as the overproduction of protein-bound
uremic toxins (for example, IS, PCS and TMAO) and depletion of
protective SCFAs. Diminished SCFA-mediated mucosal protection and
uremic damage disrupts intestinal tight-junctions, increasing gut
permeability and enabling LPS translocation into circulation.
Circulating microbial metabolites and endotoxins trigger oxidative
stress and activate the NLRP3 inflammasome-NF-κB inflammatory axis.
Persistent systemic inflammation drives major dialysis-associated
adverse outcomes, including cardiovascular disease and vascular
calcification, immune dysfunction, PD-related peritonitis,
protein-energy wasting and cognitive dysfunction via the
kidney-gut-brain axis. Solid arrows indicate process
activation/promotion; bar-ended lines represent inhibition. IS,
indoxyl sulfate; PCS, p-cresyl sulfate; TMAO,
trimethylamine-N-oxide; SCFAs, short-chain fatty acids; LPS,
lipopolysaccharide; NLRP3, NOD-like receptor family pyrin domain
containing 3; PD, peritoneal dialysis.

Figure 3

Translational roadmap for
personalized microbiome-based care among patients receiving
dialysis. Baseline factors including uremic milieu, dietary
restrictions, polypharmacy, dialysis modality (HD/PD) and
inter-individual variation drive gut microbiome-metabolome
heterogeneity. Integrated assessments comprising microbiome
profiling, metabolomics and clinical phenotyping feed into
machine-learning-assisted risk stratification, which stratifies
patients by their individual risk of cardiovascular events,
inflammation-immune defects, peritonitis, PEW and cognitive
impairment. Stratified subgroups receive tailored interventions,
including dietary adjustment, prebiotics, probiotics/synbiotics,
dialysis modality optimization and medication adjustments
considering drug-microbiome interactions. Longitudinal follow-up
enables adaptive management to improve clinical outcomes. Solid
arrows represent assessment and clinical guidance; dashed arrows
denote prospective, evolving translational applications. HD,
hemodialysis; PD, peritoneal dialysis; PEW, protein-energy
wasting.
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Jin C and Wang Y: Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review). Mol Med Rep 34: 333, 2026.
APA
Jin, C., & Wang, Y. (2026). Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review). Molecular Medicine Reports, 34, 333. https://doi.org/10.3892/mmr.2026.14044
MLA
Jin, C., Wang, Y."Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review)". Molecular Medicine Reports 34.6 (2026): 333.
Chicago
Jin, C., Wang, Y."Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review)". Molecular Medicine Reports 34, no. 6 (2026): 333. https://doi.org/10.3892/mmr.2026.14044
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Spandidos Publications style
Jin C and Wang Y: Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review). Mol Med Rep 34: 333, 2026.
APA
Jin, C., & Wang, Y. (2026). Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review). Molecular Medicine Reports, 34, 333. https://doi.org/10.3892/mmr.2026.14044
MLA
Jin, C., Wang, Y."Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review)". Molecular Medicine Reports 34.6 (2026): 333.
Chicago
Jin, C., Wang, Y."Gut microbiota in patients receiving dialysis: Mechanisms, complications and the road to personalized microbiome‑based care (Review)". Molecular Medicine Reports 34, no. 6 (2026): 333. https://doi.org/10.3892/mmr.2026.14044
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