June 7, 2005
View Full PaperEffect of Compensated Renal Dysfunction on Approved Heart Failure Markers
Key Result
Compensated renal dysfunction significantly elevated BNP (132 vs 68 pg/mL) and NT-proBNP (535 vs 232 pg/mL) in stable outpatients after myocardial infarction (P<0.05).
Study Design
Type
Cross-Sectional (n=469)
Multicenter
No
Structured PICO
Does compensated renal dysfunction affect the plasma concentrations and predictive power of BNP and NT-proBNP for detecting left ventricular dysfunction in stable outpatients after myocardial infarction?
P
Population
469 stable outpatients after myocardial infarction from the MONICA register evaluated for the effect of renal dysfunction on BNP and NT-proBNP levels.
E
Exposure
Measurement of BNP and NT-proBNP
O
Outcome
Plasma concentrations of BNP and NT-proBNP and their predictive power for detecting left ventricular dysfunctionsurrogate
Mild-to-moderate renal dysfunction significantly elevates BNP and NT-proBNP levels independent of left ventricular dysfunction, necessitating renal function-stratified cut-offs for accurate heart failure diagnosis.
Main Result
p-value: p=<0.05
Abstract
Brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) are markers of heart failure. Although renal dysfunction may increase plasma concentrations, the magnitude of this effect has not been assessed in a head-to-head comparison between the clinically approved tests. We assessed the effect of compensated renal dysfunction on BNP (Triage BNP; Biosite) and NT-proBNP (elecsys proBNP; Roche) in 469 randomly selected stable outpatients after myocardial infarction (MI; Monitoring Trends and Determinants in Cardiovascular Diseases MONICA register Augsburg) who were characterized with respect to renal function (glomerular filtration rate GFR; Cockroft method) and left ventricular (LV) ejection fraction (EF) and mass (2D echocardiography). BNP and NT-proBNP were elevated in MI patients with LV dysfunction (LVD; EF 45%; BNP 139+/-27 pg/mL versus 75+/-6; NT-proBNP 816+/-237 pg/mL versus 243+/-20; both P <0.03). Among all MI patients, the prevalence of renal dysfunction (GFR <85 mL/min) was 24%. BNP and NT-proBNP were significantly elevated in MI patients with renal dysfunction (BNP 132+/-17 pg/mL versus 68+/-4 without renal dysfunction; NT-proBNP 535+/-80 pg/mL versus 232+/-19; both P <0.05), and both markers were correlated with GFR in univariate and multivariate analyses (all P <0.01). When binary cut-off values were stratified according to the absence or presence of renal dysfunction (BNP 75 pg/mL and 125 pg/mL, respectively; NT-proBNP 100 pg/mL and 350 pg/mL, respectively), the predictive power of both markers for the detection of LVD increased substantially. BNP and NT-proBNP are almost similarly influenced by mild-to-moderate renal dysfunction. Renal dysfunction is a potential cause of elevated marker concentrations in the absence of LVD, and cut-off concentrations should be stratified according to renal function.