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These perturbations not only compromise intestinal barrier integrity but also exacerbate microinflammatory cascades through lipopolysaccharide (LPS) translocation, establishing a pernicious gut-kidney axis deterioration cycle. Furthermore, gut microbial dysregulation constitutes a cardinal pathogenic determinant in CKD-associated cardiorenal syndrome (CRS), with microbial metabolites such as TMAO compromising cardiac and renal functionality, precipitating inflammatory cascades and fibrogenesis (Zhao B