Growing recognition of the gut–kidney axis has revealed that gut dysbiosis and altered mucosal immunity are intimately intertwined with acute kidney injury (AKI). Gut changes following AKI, including dysbiosis and associated altered metabolites, barrier disruption, and maladaptive immune responses, affect post-AKI outcomes in a bidirectional manner. Therefore, the gut is increasingly recognized as a previously underappreciated modifier of AKI, and recent research is beginning to dissect the causal relationships between microbial perturbations and AKI, as well as the mechanisms underlying these complex interactions. However, relevant data remain limited, underscoring the need for further mechanistic and translational studies to fully elucidate key pathways for the development of novel, gut-targeted therapeutics. In this review, we summarize the mechanisms by which gut dysbiosis contributes to AKI outcomes and discuss gut-based therapeutic options based on experimental and clinical studies as well as future perspectives.
Yang et al. (Wed,) studied this question.