The rapid progression of atherosclerosis is a characteristic feature of cardiovascular abnormalities in the vast majority of chronic kidney disease (CKD) patients. The inflammatory network of numerous cytokines and pathological reactions underlying the primary kidney insult and progression to chronic disease accompanied by a loss of glomerular function is linked with the pathogenesis of enhanced oxidative stress in CKD. The generation of reactive oxygen species by endothelial nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) oxidase (Nox) enzyme isoforms elicits activation of the nuclear transcription factor kB, and downstream signaling leading to inflammation, proliferation, accumulation of extracellular matrix, endothelial dysfunction, atherosclerosis and thrombosis. Chronic systemic and low-grade inflammation enhanced oxidative stress, retention of oxidized uremic toxins, depletion of antioxidant and buffering pools are unified mechanisms responsible for the enhanced atherosclerosis, contributing to the increased cardiovascular risk of all age groups of CKD patients.