title: [Kidney disease: therapeutic implications in heart failure and coronary heart disease].
abstract: Heart failure (HF) is more prevalent and evolves more rapidly in patients with renal failure (RF). Renal failure not only produces myocardial damage, but also induces the development of clinical heart failure thus making the treatment of these patients more difficult. The incidence of HF in patients with RF is around 15%. Renal function in patients with RF is lower than in the general population. This is true for patients with preserved and depressed left ventricular ejection fraction (LVEF). HF mortality increases 30% for every 1-mg/dL increase in creatinine and renal function should always be considered when assessing the cardiovascular risk and therapeutic alternatives of cardiovascular patients. Angiotensin converting enzyme inhibitors, Angiotensin receptor blockers and aldosterone blockers may cause acute renal failure and serum creatinine and potassium should be closely monitored. Chronic RF is a human model of accelerated atherosclerosis. It induces a rapid progression of coronary atherosclerosis and make atherosclerotic plaques more vulnerable to acute coronary syndromes (ACS) because of coagulation changes inherent to RF. Ischemia is also more frequent due to the imbalance between oxygen requirements and supplies. Chronic RF is associated with a worse outcome in patients with ACS and increases the risk of bleeding, and is associated with a higher mortality in patients under surgical or percutaneous coronary revascularization. Of the patients treated with an interventional coronary procedure (ICP), 3,3% suffer acute RF. Saline administration at a dose of 1 ml/kg/h for 12 hours before and 12 hours after ICP prevents the development of acute RF. Although the role of N-acetylcysteine is under discussion, taking into account the favourable risk profile of this drug, it seems reasonable to administer N-acetylcysteine in addition to saline administration. In ACS patients with severe RF, the risk of severe bleeding depends upon the anticoagulation regimen, increasing particularly when unfractionated heparin is used in combination with GP IIb/IIIa inhibitors.
authors.affiliation: Servicio de Cardiología, Hospital Universitario La Paz, Madrid, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Fernández de Bobadilla
authors.forename: J
authors.initials: J
authors.lastname: López-Sendón
mesh_terms: D006333:Heart Failure / Q000150:complications* / Q000188:drug therapy / Q000453:epidemiology; D006801:Humans; D017202:Myocardial Ischemia / Q000150:complications* / Q000453:epidemiology; D051437:Renal Insufficiency / Q000150:complications* / Q000453:epidemiology