Abstract-Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease. Key Words: atherosclerosis Ⅲ hypertension Ⅲ kidney Ⅲ vasculature I t is increasingly apparent that individuals with chronic kidney disease (CKD) are more likely to die of cardiovascular (CV) disease (CVD) than to develop kidney failure. 1,2 A large cohort study comprising Ͼ130 000 elderly subjects showed that increased incidence of CV events could be in part related to the fact that persons with renal insufficiency are less likely to receive appropriate cardioprotective treatments. 3 However, beyond the effects of lack of appropriate therapy, it is clear that accelerated CVD is prevalent in subjects with CKD. The first part of the present review will therefore focus on the epidemiological links between impairment of renal function and adverse CV events, between albuminuria and CV events, and between serum cystatin C and CVD. The second part of the present review will address the mechanisms that lead to the association of renal and CVD, which include hypertension, dyslipidemia, activation of the renin-angiotensin system, endothelial dysfunction and the role of asymmetric dimethyl arginine (ADMA), oxidative stress, and inflammation. Finally, mechanisms that are involved in vascular calcification often found in CKD and end-stage renal disease (ESRD) will be described. Additionally, ESRD is associated with several specific complications caused by the uremic state per se, which can contribute to the development and progression of CVD through volume overload with consequent hypertension, anemia, uremic pericarditis, and cardiomyopathy. However, these issues will not be addressed because the emphasis will be on CKD before ESRD is reached. In addition, t...
Procedures to diagnose renal allograft rejection depend upon detection of graft dysfunction and the presence of a mononuclear leukocytic infiltrate; however, the presence of a modest cellular infiltrate is often not conclusive and can be detected in non-rejecting grafts. We have pursued a molecular approach utilizing reverse transcription (
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