Chronic renal failure: a cardiovascular risk factor.
The risk of developing cardiovascular disease is greatly increased in patients undergoing renal replacement therapy and, notably, morbidity and mortality due to therapy is much higher in these patients than in the general population. Minimal alterations in renal function, as evidenced by reduced glomerular filtration rate and the presence of albuminuria, have been described as potent cardiovascular risk factors. The classic risk factors only partly explain this difference; hence, we must admit the existence of known and emerging factors associated with increased cardiovascular risk in patients with renal disease. This article provides a review of these factors. It describes the role of hyperphosphoremia and elevated calcium-phosphorous product in the formation of cardiovascular calcifications, the contribution of anemia to left ventricular hypertrophy, and the consequences of accelerated atherogenesis with oxidative stress and a microinflammatory state resulting from endothelial dysfunction. Hyperhomocysteinemia, increased sympathetic nervous system activity, lipoprotein alterations with elevated lipoprotein A, and increases in the concentrations of asymmetrical dimethyl-arginine are other examples of the changes described in this population. Patients with renal disease should be considered to be at high risk for developing cardiovascular disease and candidates for implementation of secondary prevention strategies. It is for this reason that early identification of renal failure, which remains hidden in many cases, is of prime importance.
Fort
Joan
J
Servicio de Nefrología, Hospital General Universitario Vall d'Hebron, Universidad Autónoma, Barcelona, Spain. 9159jfr@comb.es
D000419:Albuminuria / Q000453:epidemiology / Q000503:physiopathology; D000740:Anemia / Q000503:physiopathology; D002114:Calcinosis / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000209:etiology* / Q000503:physiopathology; D005919:Glomerular Filtration Rate; D006710:Homocysteine / Q000502:physiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000503:physiopathology / Q000517:prevention & control; D024821:Metabolic Syndrome / Q000503:physiopathology; D018384:Oxidative Stress; D015995:Prevalence; D012307:Risk Factors; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014511:Uremia / Q000503:physiopathology
D006710:Homocysteine