To synthesize current knowledge on how sepsis-driven gut dysbiosis compromises intestinal barrier integrity and contributes to sepsis-associated acute kidney injury (SA-AKI).
Key Findings:
Sepsis induces gut dysbiosis characterized by loss of microbial diversity and expansion of pathobionts.
Gut dysbiosis compromises intestinal barrier integrity, facilitating translocation of bacterial products like lipopolysaccharide (LPS).
LPS activates systemic inflammation and renal signaling pathways, leading to tubular injury and impaired renal function.
Specific microbial signatures associated with AKI include increased Clostridium asparagiforme and decreased Roseburia spp.
Gut-derived metabolites such as indoxyl sulfate, p-cresol sulfate, and trimethylamine N-oxide (TMAO) have been implicated in renal inflammation and fibrosis.
Renal dysfunction disrupts gut homeostasis, establishing a pathological gut–kidney feedback loop.
Interpretation:
The intestine-kidney crosstalk may provide a basis for further research into the treatment of sepsis-induced organ injury.
Limitations:
The review is based on literature published until 2026, which may not include the most recent studies.
Exclusion of case reports and non-English publications may limit the comprehensiveness of the findings.
Conclusion:
Sepsis-induced gut microbiota dysregulation plays a role in the development of SA-AKI.
