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Atherosclerotic cardiovascular disease (CVD) is a significant cause of morbidity and mortality in patients with chronic kidney disease (CKD), particularly patients undergoing hemodialysis (HD). The death rate from CVD in patients with advanced stage CKD is 10 to 40 times higher than that in the general population (Iliou et al., 2001; Sarnak et al., 2003). A majority of patients with CKD have traditional CVD risk factors such as old age, diabetes mellitus, systolic hypertension, smoking, and dyslipidemia. However, the interventions to address these traditional risk factors have failed to decrease the risk for CVD in patients with CKD (Stenvinkel et al., 2008). Atherosclerotic lesions develop through chronic inflammatory processes, and chronic inflammation is a common feature of CKD. In addition, the metabolic milieu during the development of renal dysfunction appears to accelerate the atherosclerotic process by decades in patients with CKD. Given these findings, many researchers have emphasized that nontraditional risk factors such as oxidative stress and advanced glycation endproducts (AGEs), in combination with their receptor (RAGE), may play an important role in the development of CVD in patients with CKD. RAGE is a member of the immunoglobulin superfamily of cell surface molecules. Enhanced RAGE expression has been observed in peripheral blood monocytes of patients with CKD, suggesting that RAGE may amplify ligand-induced monocyte perturbation and contribute to monocyte-mediated vascular inflammation in patients with CKD. The major alteration of glycated protein in patients with CKD is decreased clearance of glycation-free adducts and their markedly increased levels in plasma. However, the change of plasma AGEs into proteins in patients with CKD is relatively modest. Therefore, ligands other than AGEs for RAGE may be more important in RAGE-mediated atherosclerosis of patients with CKD. Several RAGE ligands, including S100 proteins, the High Mobility Group Box proteins, and amyloid fibrils, have been identified. Among them, emerging evidence indicates that S100A12 is a proinflammatory cytokine (Pietzsch and Hoppmann, 2009). In this review, we

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Chronic Inflammation and S100A12/ Receptor for Advanced Glycation Endproducts Axis: A Novel Risk Factor for Cardiovascular Disease in Patients with Chronic Kidney Disease?