Cardiovascular complications in patients with end stage renal disease
(ESRD) constitute a problem of epidemic dimensions (Am J Kidney Dis 32,
Suppl 3:S1-S4, 1998). The Framingham risk factors that are age, sex,
hypertension, left ventricular hypertrophy (LVH), diabetes,
dislipidemia, contribute to this high morbidity and mortality in
addition to the traditional uraemic risk factors like
hyperparathyroidism, anaemia and some more recently emerging risk
factors like inflammation, malnutrition and hyperhomocysteinemia. In
particular, LVH increases the risk of cardiac ischemia, LV dysfunction
and sudden cardiac death and represents a very strong predictor of
all-cause and cardiovascular mortality in patients on chronic dialysis
treatment (Kidney Int 47:186-192, 1995). In routine clinical practice,
cardiac involvement in patients with ESRD currently is evaluated by
means of electrocardiography (ECG) that has in fact a low sensitivity,
and echocardiography that, viceversa, is the golden standard in the
diagnosis of LVH but it is felt it is applied less than required by
nephrologists and dialysis physicians.
The observation that the synthesis of atrial and ventricular natriuretic peptides is enhanced in the presence of alterations in left ventricular mass and function, and that this phenomenon reliably reflects the severity of left ventricular hypertrophy and systolic dysfunction have focused much attention on the potential diagnostic value of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in clinical practice (Hypertension 28:988-994, 1996). In particular BNP is primarily produced by ventricular myocytes and its generation rate is amplified by heart failure or LVH.
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