Together, these findings highlight the multifactorial nature of CV burden in CKD, where inflammation, endothelial dysfunction, and metabolic abnormalities converge to accelerate myocardial and vascular injury [17]. Although NT-proBNP and ADMA levels appeared higher in patients with advanced CKD (stages IV-V), these differences did not reach statistical significance, possibly reflecting limited sample size and stage heterogeneity. This evidence concerns the gene NPPB and endothelial dysfunction.