In CKD, uremic toxins (e.g., urea, creatinine, and uric acid) accumulate, altering the gut’s biochemical milieu and fostering dysbiosis—evidenced by reduced Bifidobacterium and Lactobacillus and increased Prevotella and Clostridium IV.319 This disrupts tight junctions, heightening bacterial translocation and systemic inflammation, as observed in end-stage renal disease (ESRD), where circulating LPS drives cytokine storms (e.g., TNF-α and IL-6). This evidence concerns the gene TNF and chronic kidney disease.