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5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
[Brain natriuretic peptide (BNP) and N-terminal-pro BNP in chronic haemodialysed renal failure]
1Service de cardiologie, CHU Nîmes, Hôpital Caremeau. jean.pierre.bertinchant@chu-nimes.fr
Abstract:
Brain natiuretic peptide (BNP) and N-Terminal-pro BNP (NT-proBNP) are biological markers of left ventricular dysfunction. An increase of one of these peptides is commonly observed in patients with chronic renal failure (CRF) undergoing haemodialysis, in the absence of cardiac failure or acute myocardial ischaemia. The interpretation and clinical implications of this finding are not known. This is a problem because cardiovascular disease is the main cause of morbidity and mortality in patients undergoing haemodialysis. In these patients, left ventricular hypertrophy and left ventricular dysfunction were associated with increased mortality. A biological marker of left ventricular dysfunction enabling early identification of high risk patients would be very useful in this population. Chronic renal failure and haemodialysis do not explain increased levels of BNP and NT-proBNP. Expansion of extra-cellular volume causing myocardial stretching and increased left ventricular pressures is the principal cause of increased BNP and NT-proBNP in haemodialysis patients. The left ventricular hypertrophy and endothelial dysfunction in severe chronic renal failure, systolic and diastolic left ventricular dysfunction, the associated cardiac disease (usually ischaemic) also contribute to this increase. In view of the relationship with left ventricular hypertrophy, left ventricular dysfunction, ischaemic heart disease, BNP and NT-proBNP are predictive factors of total and/or cardiovascular mortality in asymptomatic haemodialysed patients. The BNP/NT-proBNP value should allow identification of high risk asymptomatic haemodialysed patients who would benefit from aggressive evaluation of left ventricular hypertrophy and dysfunction and appropriate, targeted therapeutic intervention.
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