Radmila Lyubarova1, Elvira O Gosmanova2,3. 1. Division of Cardiology, Department of Medicine, Albany Medical College, Albany, NY, USA. 2. Nephrology Section, Stratton VA Medical Center, 113 Holland Ave, Albany, NY, 12208, USA. elvira.gosmanova@va.gov. 3. Division of Nephrology and Hypertension, Department of Medicine, Albany Medical College, Albany, NY, USA. elvira.gosmanova@va.gov.
Abstract
PURPOSE OF REVIEW: The purpose of this study was to summarize recent findings about cardiovascular benefits and safety of aldosterone blockade in patients with end-stage renal disease (ESRD). RECENT FINDINGS: It is now well recognized that aldosterone's deleterious cardiovascular impact is not limited to its pressor effect arising from an increase in sodium reabsorption in the kidneys. Aldosterone has also been shown to increase blood pressure by a direct activation of the sympathetic nervous system, to cause endothelial and vascular smooth muscle cell dysfunction, myocardial remodeling and fibrosis, and to have pro-arrhythmogenic actions in the heart. These unconventional extra-renal effects of aldosterone make its blockade feasible and potentially beneficial for patients with ESRD. Accumulating data support the idea that aldosterone antagonism leads to a better blood pressure control, reduction in left ventricular (LV) mass, improved LV function, and reduced all-cause and cardiovascular mortality in ESRD patients. Reassuringly, rates of major adverse events, especially, significant hyperkalemia-the most feared adverse consequence-were low with careful patient selection and monitoring.
PURPOSE OF REVIEW: The purpose of this study was to summarize recent findings about cardiovascular benefits and safety of aldosterone blockade in patients with end-stage renal disease (ESRD). RECENT FINDINGS: It is now well recognized that aldosterone's deleterious cardiovascular impact is not limited to its pressor effect arising from an increase in sodium reabsorption in the kidneys. Aldosterone has also been shown to increase blood pressure by a direct activation of the sympathetic nervous system, to cause endothelial and vascular smooth muscle cell dysfunction, myocardial remodeling and fibrosis, and to have pro-arrhythmogenic actions in the heart. These unconventional extra-renal effects of aldosterone make its blockade feasible and potentially beneficial for patients with ESRD. Accumulating data support the idea that aldosterone antagonism leads to a better blood pressure control, reduction in left ventricular (LV) mass, improved LV function, and reduced all-cause and cardiovascular mortality in ESRDpatients. Reassuringly, rates of major adverse events, especially, significant hyperkalemia-the most feared adverse consequence-were low with careful patient selection and monitoring.
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