Beyond traditional cardiovascular risks, the CKD continuum fosters a unique pro-atherogenic triad: (1) sustained systemic inflammation evidenced by elevated CRP and IL-6 [45]; (2) oxidative stress amplification via nicotinamide adenine dinucleotide phosphate oxidase-2 upregulation [46]; (3) immune dysregulation characterized by monocyte expansion and endotoxin-tolerant macrophage phenotypes [47]. This evidence concerns the gene IL6 and chronic kidney disease.