title: Chronic kidney disease: effects on the cardiovascular system.
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.
authors.affiliation: Department of Medicine, Sir Mortimer B. Davis Jewish General Hospital, McGill University, Montreal, Quebec, Canada. ernesto.schiffrin@mcgill.ca
authors.forename: Ernesto L
authors.initials: EL
authors.lastname: Schiffrin
authors.forename: Mark L
authors.initials: ML
authors.lastname: Lipman
authors.forename: Johannes F E
authors.initials: JF
authors.lastname: Mann
mesh_terms: D000419:Albuminuria / Q000453:epidemiology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000378:metabolism; D050197:Atherosclerosis / Q000209:etiology / Q000503:physiopathology; D015415:Biomarkers; D001862:Bone Resorption / Q000209:etiology; D002114:Calcinosis / Q000209:etiology / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D002908:Chronic Disease; D002986:Clinical Trials as Topic; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D055316:Cystatin C; D015891:Cystatins / Q000097:blood; D048909:Diabetes Complications / Q000503:physiopathology; D018450:Disease Progression; D004285:Dogs; D050171:Dyslipidemias / Q000209:etiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D005919:Glomerular Filtration Rate; D006801:Humans; D006977:Hypertension, Renal / Q000209:etiology; D018836:Inflammation Mediators / Q000378:metabolism; D007674:Kidney Diseases / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology*; D018384:Oxidative Stress; D010710:Phosphates / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology; D012307:Risk Factors
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; C525030:CST3 protein, human; D055316:Cystatin C; D015891:Cystatins; D018836:Inflammation Mediators; D010710:Phosphates; C018524:N,N-dimethylarginine; D001120:Arginine; D003404:Creatinine; D002118:Calcium