Gut microbiota and sepsis-associated acute kidney injury: a narrative review

Background Sepsis-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. Objective This 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. Methods A 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. Results Sepsis 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. Recent human metagenomic studies have identified specific microbial signatures associated with AKI, such as increased Clostridium asparagiforme and decreased Roseburia spp., alongside elevated uremic toxin-producing bacteria like Gordonibacter pamelaeae . Additionally, gut-derived metabolites including indoxyl sulfate, p-cresol sulfate, and trimethylamine N-oxide (TMAO) have been implicated in promoting renal inflammation and fibrosis. Importantly, renal dysfunction further disrupts gut homeostasis, establishing a pathological gut–kidney feedback loop. Targeting the gut-kidney axis via fecal microbiota transplantation, probiotic supplementation, or short-chain fatty acid administration may offer novel therapeutic avenues. Conclusions Sepsis induces gut microbiota dysregulation play an important role in the development of SA-AKI. The intestine-kidney crosstalk may provide a basis for the treatment of sepsis-induced organ injury and also provide new ideas for the treatment of SA-AKI.