Chronic kidney disease (CKD) is a growing health problem with increasing incidence. The annual mortality of end-stage renal disease patients is about 9%, which is 10–20 fold higher than the general population, approximately 50% of these deaths are due to cardiovascular (CV) disease. CV risk factors, such as diabetes, hypertension, and hyperlipidemia, are strongly associated with poor outcome. Many other nontraditional risk factors such as inflammation, infection, oxidative stress, anemia, and malnutrition are also present. In this review we will focus on the role of oxidative stress in chronic kidney disease. 1. Introduction Chronic kidney disease (CKD) is a growing health problem with increasing incidence. In the United States, approximately 8 million adults have stage 3 CKD and about 400？000 have end-stage renal disease (ESRD), with over 300？000 of them on maintenance dialysis (MHD). The annual mortality of ESRD patients is about 9%, which is 10–20-fold higher than the general population; approximately 50% of these deaths are due to cardiovascular (CV) disease [1]. CKD is associated with high cardiovascular risk which is not fully due to traditional CV risk factors. CV risk factors, such as diabetes, hypertension, and hyperlipidemia, are strongly associated with poor outcome; other nontraditional risk factors are also present such as renal-specific risk factors: uraemia or dialysis and extrarenal risk factors: proteinuria, chronic volume overload, increased renin-angiotensin system activity, inflammation, infection, oxidative stress, altered calcium and phosphorus metabolism, anemia, malnutrition, elevated levels of homocysteine, uraemic toxins, and thrombogenic factors [1]. Changes in serum cytokines begin at an early phase of renal dysfunction. High levels of cytokines lead to changes in the levels of many acute phase proteins like c-reactive protein (CRP), albumin, brain natriuretic peptide (BNP), adiponectin, fetuin, and asymmetric dimethylargainine. Changes in these proteins can predict intima-media thickness of carotid artery and left ventricular hypertrophy leading to accelerated cardiovascular mortality. Chronic inflammation is a possible mediator between microvascular and macrovascular disease. Oxidative stress may accelerate atherogenesis, and hence make a significant contribution to the increased CV disease burden in CKD patients. Oxidative stress may actually represent a new target for therapeutic intervention. In this review, first we will discuss the role and the biochemical burden of diabetes and dyslipidemia in CKD and then focus on
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