Cardiovascular disease is a leading cause of death in patients with chronic kidney disease (CKD), for whom the cardiovascular mortality rate is 15 to 30 times higher than in the general population. The underlying pathological state is caused by a complex interplay of traditional and nontraditional risk factors that results in atherosclerosis, arteriosclerosis, and altered cardiac morphological characteristics. (Effat et al 2012) Several factors are associated with the onset and progression of CKD, such as obesity, hypertension and diabetes mellitus. Beyond these factors, there is evidence of a pathophysiological role for inflammation in CKD. Inflammation actively participates in the mechanisms of renal damage progression in diseases of several etiologies (Akchurin OM and Kaskel F, 2015). In glomerular diseases, for example, the following sequence is believed to occur: 1) persistent glomerular injury produces capillary hypertension, with increased glomerular filtration and passage of proteins into the tubular fluid; 2) glomerular proteinuria increases the production of angiotensin II and promotes liberation of inflammatory mediators (cytokines and chemokines), which induce the renal interstitial build-up of mononuclear cells; 3) the initial neutrophil recruiting is replaced by macrophages and T lymphocytes, which unleash the immune response producing interstitial nephritis; 4) tubular cells respond to this inflammatory process with injury to their basement membrane and with the epithelial-mesenchymal transition, becoming interstitial fibroblasts; 5) The formed fibroblasts produce collagen which, in turn, injuries the renal vessels and tubules, eventually generating a cellular scar (Vianna H R et al 2011).