IS affects the progression of CKD through multiple mechanisms: IS induces oxidative stress and inflammation, increases reactive oxygen species (ROS), and reduces antioxidant responses, affecting various signaling pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), tumor protein p53 (p53), signal transducer and activator of transcription 3 (STAT3), transforming growth factor-beta (TGF-β) and Smad2/3 [31,32,33]. This evidence concerns the gene NFKB1 and chronic kidney disease.