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Elimination of the Cardiac Natriuretic Peptides B-Type Natriuretic Peptide (BNP) and N-Terminal proBNP by Hemodialysis

¹ Klinikum der Philipps-Universität Marburg, Department of Clinical Chemistry and Molecular Diagnostics, 35033 Marburg, Germany;² Klinikum Fulda, Department of Internal Medicine III, Fulda, Germany

^aauthor for correspondence: fax 49-6421-2865594, e-mail hg.wahl@med.uni-marburg.de

The first 20% of the full text of this article appears below.

The measurement of natriuretic peptides for the diagnosis of heart failure has been a major breakthrough in cardiology (1)(2). B-Type natriuretic peptide (BNP) is synthesized as preproBNP mainly in the ventricular myocardium. On ventricular myocyte stretch, preproBNP is enzymatically cleaved to proBNP and released in the form of the hormonally active BNP and the inactive N-terminal proBNP (NT-proBNP). Both BNP and NT-proBNP have been shown to reflect heart failure severity (1), but studies on their sensitivity and specificity for different degrees of heart failure produced conflicting results (3)(4)(5)(6). Both BNP and NT-proBNP can be used for the diagnosis of heart failure, but there are important differences between the two tests, particularly regarding influence of age and renal function (1). In addition to glomerular filtration, BNP is eliminated from plasma mainly through natriuretic peptide receptors and degraded by neutral endopeptidases (7)(8)(9). In contrast, NT-proBNP possibly is largely eliminated by glomerular filtration only (4). This explains the strong influence of renal function on NT-proBNP concentrations. Because of the normal decrease in glomerular filtration rate with increasing age, the diagnostic cutoff for NT-proBNP depends on age (1). This is also true for BNP(10), but to a much lesser extent. Importantly, both BNP and NT-proBNP concentrations can be increased in the setting of hemodialysis (11)(12)(13)(14). The prevalence of chronic heart failure is significantly increased in dialysis patients and is associated with left ventricular hypertrophy, which may be secondary to volume overload and hypertension (15)(16)(17). Reports on the effect . . . [Full Text of this Article]

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