BackgroundSepsis-associated acute kidney injury (SA-AKI) carries high morbidity and mortality, yet its pathogenesis remains incompletely understood. Emerging evidence underscores the gut-kidney axis as a critical pathway in SA-AKI development.ObjectiveThis review aims to synthesize current knowledge on how sepsis-driven gut dysbiosis compromises intestinal barrier integrity and contributes to SA-AKI, and to explore potential therapeutic strategies targeting the gut microbiota.MethodsA comprehensive literature search was conducted in PubMed, Web of Science, and Scopus databases for publications between 2005 and 2026.
Studies focusing on gut-kidney crosstalk mechanisms in sepsis/AKI were included. Key findings from human and animal studies were summarized.ResultsSepsis induces marked gut dysbiosis characterized by loss of microbial diversity and expansion of pathobionts.
This dysbiosis compromises intestinal barrier integrity, facilitating translocation of bacterial products such as lipopolysaccharide (LPS). Upon entering circulation, these mediators activate systemic inflammation and renal signaling cascades, including the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway, leading to tubular injury and impaired renal function.
Frontiers in Immunology published a clinical update in Infectious Disease on 02 Jun 2026.
The item focuses on Gut microbiota and sepsis-associated acute kidney injury: a narrative review.
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