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Annals of Clinical & Laboratory Science 36:299-306 (2006)
© 2006 Association of Clinical Scientists

Plasma BNP and NT-proBNP Assays by Automated Immunoanalyzers: Analytical and Clinical Study

Clara Bionda1, Cyril Bergerot2, Dominique Ardail1, Claire Rodriguez-Lafrasse1 and Robert Rousson1
1 Laboratoire de Biochimie et de Biologie Moléculaire, 2 Service de Cardiologie Unité 30, Hôpital Cardio-Vasculaire et Pneumologique Louis Pradel, Hospices Civils de Lyon, Lyon, France

Address correspondence to Dr Clara Bionda, Laboratoire de Biochimie et de Biologie Moléculaire, Hôpital Cardio-Vasculaire et Pneumologique L Pradel, Lyon, 28 Avenue Doyen Lépine, 69 677 Lyon, France; tel 33 04 72 11 80 30; fax 33 04 72 35 72 46; e-mail clara.bionda{at}chu-lyon.fr.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion.
 Acknowledgements
 References
 
The plasma concentrations of natriuretic peptides, BNP and NTproBNP, have been shown to be markers for the diagnosis of congestive heart failure (CHF). In this study, plasma BNP and NTproBNP concentrations were evaluated and stratified according to renal function, body mass index (BMI), and New York Heart Association (NYHA) classification. Comparison studies between the 2 natriuretic peptide markers were performed. Assays for BNP were performed with a Triage reagent pack (Biosite, Inc) on an Access 2 immunoanalyzer (Beckman-Coulter); NTproBNP assays were performed with a Roche reagent pack on an Elecsys 20.10 immunoanalyzer (Roche Diagnostics). Plasma samples were collected from consecutive patients hospitalized for cardiac disorders at our institution. Nonparametric tests were used for statistical analyses. The results show that alterations of renal function had less impact on BNP (p = 0.9) than on NTproBNP concentrations (p <0.0001). BNP and NTproBNP levels were lower in obese patients with CHF (515 ± 61 ng/L and 1652 ± 124 ng/L, respectively) than in lean patients (900 ± 85 ng/L and 6686 ± 749 ng/L). Although NTproBNP levels averaged about 10 times higher than BNP levels, there was significant correlation between these 2 markers (Deming regression r2 = 0.40, IC: 0.95). In conclusion, plasma BNP and NTproBNP assays are both useful for the diagnosis of CHF and left ventricular dysfunction. However, renal function and obesity must be taken into account for clinical interpretation. These assays have good analytical performance and the choice between them depends on local preference.

Keywords: brain natriuretic peptides, NTproBNP, BNP, left ventricular ejection fraction (LVEF)

Abbreviations: NTproBNP, N-terminal (1–76) probrain natriuretic peptide; BNP, brain natriuretic peptide (77–108) fragment; LVEF, left ventricular ejection fraction; NYHA, New York Heart Association; CHF, congestive heart failure; LVD, left ventricular dysfunction


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion.
 Acknowledgements
 References
 
Two major natriuretic peptides, BNP and NTproBNP, have been shown to be powerful plasma markers in clinical and laboratory practice for the diagnosis, screening, and treatment of heart failure [1–3]. According to the European Society of Cardiology’s guidelines, assays for these markers, in association with the clinical examination, electrocardiogram (ECG), chest X-rays, and echocardiography, aid in the assessment of patients presenting with suspected congestive heart failure (CHF) [4]. BNP and NTproBNP peptides are released into the blood circulation in response to pressure and volume overload of the cardiac chambers. Cleavage of pre-proBNP precursor within cardiomyocytes leads to the formation of proBNP, which is subsequently cleaved into N-terminal (NTproBNP) and C-terminal (BNP) fragments. Most biological effects of BNP are the result of its binding to the natriuretic peptide receptor (NPRA), which has guanylate cyclase activity and is expressed in vascular endothelium, kidney, and adrenal glands [5].

The functions of BNP vary among its sites of action: in peripheral vascular endothelium, BNP causes vasodilatation and increased vascular permeability; in the kidneys, BNP increases the glomerular filtration rate and enhances sodium excretion. These effects are reinforced by inhibition of renin and aldosterone release from adrenal glands [6]. NTproBNP is a biologically inactive molecule, with a half-life that is longer than BNP (90 to 120 min vs 20 to 22 min, respectively).

In this study, automated immunoassays for plasma BNP were performed using the Biosite Triage reagent pack (Biosite Inc., San Diego, CA, USA) with an Access 2 immunoanalyzer (Beckman-Coulter, Fullerton, CA, USA). NTproBNP assays were performed using the proBNP reagent pack (Roche Diagnostics, Meylan, France) with an Elecsys 20.10 immunoanalyzer (Roche). After the imprecision and stability of plasma BNP assays were evaluated using the Access 2 analyzer, a clinical study was conducted on patients admitted to our institution for cardiac reasons. BNP and NTproBNP levels were stratified according to the patients’ renal function, body mass index (BMI), and New York Heart Association (NYHA) classification. Correlation of BNP and NTproBNT levels was evaluated by regression analysis.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion.
 Acknowledgements
 References
 
Consecutive patients admitted to our institution for cardiac problems (eg, myocardiopathy, acute coronary syndrome, or cardiac surgery) from January to September 2004 were included in this study; the patients all gave informed consent to be investigated. Plasma BNP and/or NTproBNP were measured in all patients with suspected CHF. These parameters were added to the cardiological assessment and to the information collected from medical history and physical examination, with an estimation of the severity of CHF based on NYHA classification, ECG, chest X-rays, and, if needed, echocardiogram with estimation of LVEF (Echocardiograph Vivid V, General Electric Co.). Along with determinations of NTproBNP and/or BNP concentrations, several parameters were collected: age, sex, plasma creatinine, body mass index (BMI), and plasma cardiac troponin I concentration (cTnI determined on an Access 2 analyzer, (Beckman-Coulter, Inc., Fullerton, CA, USA), reference value: TnIc <0.1 ng/L).

Blood samples were collected from patients into lithium heparin tubes for NTproBNP measurements (the tubes used for electrolyte and enzyme determinations) or into EDTA tubes for BNP measurements (recommended by the manufacturers). After centrifugation, one aliquot of plasma was used for BNP and/or NTproBNP measurement, and additional aliquots were stored at –20°C. NTproBNP was determined with a Elecsys 20.10 bench top analyzer (Roche Diagnostics, Meylan, France) with proBNP reagent pack (Roche Diagnostics). BNP was measured with BNP Triage reagent pack (Biosite Inc., San Diego, CA, USA), carried out on an Access 2 immunoanalyzer (Beckman-Coulter, Inc., Fullerton, CA, USA). For BNP and NTproBNP, the cut-off values proposed in France by their respective manufacturers (BNP Triage assay, Biosite Inc.; 04/2004 notice proBNP assay, Roche Diagnostics) for the exclusion of CHF diagnosis were 100 ng/L and 250 pg/ml, respectively, with a reported negative predictive value of 98% for NTproBNP [7]. (We note that in USA, the manufacturer’s NTproBNP cutoff is different and depends on the patient’s age: 125 ng/L for <75 yr, and 450 for ≤75 yr).

A precision study (within-run imprecision and total imprecision) of the BNP assay on the Access 2 analyzer was performed with commercial controls (#321053, Biosite Inc). To evaluate the stability of BNP, EDTA plasmas were used; each plasma was separated into 3 aliquots that were stored respectively at room temperature (20–22°C), 4°C, and –20°C. At various times, one aliquot was analyzed in duplicate.

Influence of renal dysfunction on BNP values was studied in 69 patients, and on NTproBNP values in 692 patients. The Kruskal-Wallis H test was used to test the associations between plasma BNP, NTproBNP, and creatinine. Levels of BNP and NTproBNP were compared in obese and non-obese CHF patients (FEVG <0.5). Obesity was defined as a body mass index (BMI) ≤30 kg/m2. For the relationship between BNP and NYHA class, 36 plasma samples were collected and analyzed. The correlation study between BNP and NTproBNP levels was performed using 85 EDTA or heparinized plasmas measured at the same time on the Access 2 and Elecsys 20.10 analyzers, respectively. This study was analyzed by Deming regression. Data are presented as mean ± SD or as median (interquartile range) when appropriate.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion.
 Acknowledgements
 References
 
Imprecision and stability studies.  Within-run and total imprecision of BNP assays using the BNP Triage reagent pack and the Access 2 analyzer were evaluated using commercial controls (Biosite, CQ1, CQ2, or CQ3). The study of total imprecision was performed during a 10 day period, with the level 2 commercial control (mean: 388 ng/L, SD ± 11, n = 10) and the level 3 control (mean: 2079 ng/L, SD ± 45, n = 10). The calculated CVs for level 2 and 3 controls were 2.86 % and 2.18% respectively. The with-run imprecision was estimated from 20 repeated measurements of BNP in one run, using the level 1 commercial control. This yielded a CV of 1.71% (mean = 85.1 ng/L, SD ± 1.4, n = 20).

The stability of BNP at room temperature, 4°C, and –20°C, was tested using EDTA plasmas. Just after centrifugation, at time 0, BNP concentrations in 3 aliquots of 1 plasma were respectively 767.9, 760.4, 763.2 ng/L. As listed in Table 1Go, determination of BNP concentrations at 4 hr post-centrifugation showed a 17% decrease compared to the initial value when the sample was stored at room temperature. The sample stored at 4°C was more stable, with a decrease of only 6% at 4 hr post-centrifugation. The decrease in BNP concentration in samples stored at –20°C and defrosted successively at 1, 2, 3, and 4 weeks after centrifugation was <3%.


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  		Table 1. Stability of BNP in EDTA plasma sample #1 stored at room temperature, 4°C, and –20°C. After centrifugation, the BNP concentration was determined (767.9, 760.4 and 763.2 ng/l), and the plasma sample was aliquoted and stored at room temperature, 4°C, and –20°C for various time periods. At the indicated times, BNP was determined with the Triage BNP assay and Access 2 analyzer. Results are expressed as absolute values and as percentages of the initial BNP concentration.
 
BNP, NTproBNP, and renal failure.  Pertinent characteristics of the patient groups (BNP and NTproBNP groups) are summarized in Table 2Go. Consecutive patients were enrolled in this study, with a majority being men. For the BNP study, 69 patients were enrolled (age 62.1 ± 14 yr, 43 men and 26 women, plasma creatinine 257 ± 223 µmol/ L with median of 159 µmol/L (67 to 1035)). In this group, the mean plasma BNP value was 728.3 ± 944 ng/L with median of 299 ng/L (7 to 4842). Concerning the NTproBNP study, 692 patients were enrolled (age 67.7 ± 13 yr, 462 men, 230 women, plasma creatinine 121.8 ± 71 µmol/L with a median of 104 µmol/L (36 to 918)). In this group, the mean plasma NTproBNP value was 4652.1 ± 9337 ng/L with a median of 1571.5 ng/L (9 to 110,426). For each patient in these 2 groups, plasma creatinine concentrations were measured simultaneously with the assays of BNP or NTproBNP.


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  		Table 2. Characteristics of BNP and NTproBNP groups of patients, categorized by age (yr) and plasma creatinine (µmol/L).
 
Three different classes were defined according to the degree of renal insufficiency as indicated by plasma creatinine levels: (A) from 10 to 110 µmol/ L, patients without renal failure, (B) from 111 to 200 µmol/L, patients with renal insufficiency, and (C) >200 µmol/L, patients with severe renal failure. Fig. 1Go shows that mean and median log10 NTproBNP values increased with renal insufficiency (p <0.0001); the mean NTproBNP values were 2451.9 ± 491, 6572.2 ± 1221, and 11,057.2 ± 1251 ng/L for groups A, B, and C respectively. On the other hand, BNP concentrations were not statisically different in groups A, B, and C (497.0 ± 50, 890.6 ± 107, and 771.8 ± 104 ng/L; p = 0.9).


Figure 1
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  		Fig. 1. Influence of renal insufficiency on plasma BNP and NTproBNP concentrations. Groups of patients were defined based on renal failure level (see Materials and Methods). For graphic representation and statistical analysis, log10BNP and log10NTproBNP were represented, the mean in gray, dotted line and the median in black, continuous line. With the Kruskal-Wallis H test, no significant difference of log10BNP was observed among the 3 groups (p = 0.939), but a significant increase of log10NTproBNP was observed in the patients with renal failure (p <0.0001).

 
BNP, NTproBNP, and body mass index.  To evaluate the influence of obesity on plasma natriuretic peptide levels, BMI and BNP or NTproBNP values were collected in patients with CHF (FEVG <0.5). Two groups were defined according to BMI level: lean and overweight patients (BMI <30 kg/m2) and obese patients (BMI ≥30 kg/m2). The BMI values of 30 patients selected for NYHA/BNP study were collected (21 men, 9 women, age 64 ±13 yr, plasma creatinine 141 ± 27 µmol/L, BNP 835 ± 68 ng/L). Then, BMI and NTproBNP of 31 patients were collected (19 men, 12 women, age 67 ± 11 yr, plasma creatinine 98 ± 49 µmol/L, NTproBNP 5224 ± 672 ng/L). As listed in Fig 2Go, plasma BNP levels were lower in obese patients than in lean/overweight subjects (515 ± 61 ng/L vs 900 ± 85 ng/l, p ≤ 0.05). The effect of obesity was similar for NT proBNP (1652 ± 125 ng/L and 6686 ± 749 ng/L, p ≤ 0.05, respectively, in obese and lean/overweight patients). Thus, lower natriuretic peptide levels were observed in both groups of obese patients with CHF.


Figure 2
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  		Fig. 2. Influence of body mass index (BMI) on BNP and NTproBNP concentrations. Two groups of patients with CHF (FEVG <0.5) were defined based on BMI: lean/ overweight patients with BMI <30 kg/m2 and obese patients with BMI ≥30 kg/m2.

 
BNP and NYHA classification.  At admission, 36 patients (28 men, 11 women, age 65 ±12 yr, plasma creatinine 133 ± 23 µmol/L, BNP 733.1 ± 74 ng/L) were categorized according to the severity of their exercise limitation. According to NYHA classes (I/ II, III, and IV), BNP values were respectively 190 ± 116 ng/L, 709 ± 619 ng/L, and 1257 ± 1087 ng/L (Fig. 3Go). Using the nonparametric Kruskal Wallis H test, a significant difference (p = 0.012) was found between each of the 3 groups.


Figure 3
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  		Fig. 3. Distribution of plasma BNP levels in patients according to the severity of their exercise limitation based on NYHA classification. Mean values of BNP concentrations were 190, 709, and 1257 ng/L (in gray, dotted line), respectively, for NYHA I/II (n = 7), III (n = 13), and IV (n = 16) patients; the medians are indicated in black, continuous line. Study of BNP vs NYHA class shows significant differences (p = 0.012) among the 3 groups.

 
Correlation of plasma BNP and NTproBNP levels.  Comparison studies were performed using 85 samples. For each patient, an EDTA tube for BNP measurement and a heparinized tube for NTproBNP measurement were collected at the same time. Plasma BNP assays were performed with the Biosite Triage pack and the Access 2 analyzer; NTproBNP assays were performed with the Roche reagent pack and the Elecys 20.10 analyzer. Comparison between the 2 peptide levels (BNP and NTproBNP) was performed using Deming regression. Fig. 4Go shows the distribution of NTproBNP values (mean 6804 ± 7256 ng/L, range 27 – 30,601 ng/L) compared to BNP values (mean 493 ± 397 ng/L, range 20–1498 ng/L). The Deming regression analysis for the 85 paired values showed the regression equation: NTproBNP = 11.53 (BNP) + 1112; the correlation coefficient r2 was 0.40 (IC = 0.95). Among the 85 samples, 6 showed high NTproBNP values (>1200 ng/L), whereas the corresponding BNP values were close to or lower than the reference value (100 ng/ L). Two plasma samples had high BNP values (>200 ng/L) with NTproBNP values <100 ng/L, but the reason is unclear.


Figure 4
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  		Fig. 4. Correlation study of the concentrations of NTproBNP (Roche assays on Elecsys 20.10 analyzer) and BNP (Biosite Triage assays on Access 2 analyzer) in 85 plasma samples,

 

   Discussion.
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion.
Acknowledgements
 References
 
Imprecision studies of Biosite Triage assay for BNP performed on the Access 2 analyzer yielded total CVs (1.71 % to 2.86%) that are lower than the CVs (9.9 % to 14.6 %) reported with BNP Biosite assay on a Biosite Triage Meter (Biosite, Inc., San Diego, CA, USA) [8]. The present study indicates that the precision of the BNP assay on the Access 2 analyzer is similar to that reported for the Roche NTproBNP assay on the Elecsys 20.10 analyzer, which yielded CVs from 1.0 % to 2.5 % [9,10].

In routine clinical laboratory operations, BNP assay has technical constraints, such as the need for EDTA tubes and sample instability at room temperature. Previous studies of BNP stability in whole blood with or without aprotinine have been reported, with different conditions of storage [11–14]. Based on our study of EDTA plasmas stored at 20–22°C, 4°C, or –20°C, we recommend centrifuging the blood sample at the time of collection, storing the plasma at 4°C, and performing the assay within 4 hr. During 4 hr after sample collection, BNP concentrations in samples stored at 4°C remained stable (maximum reduction of 6% of the initial concentration). When analysis cannot be performed within the first 4 hr, we recommend storing EDTA plasma at –20°C and performing the analysis in the following weeks to limit BNP degradation.

Clinical interpretation of natriuretic peptide results is somewhat difficult in patients with renal insufficiency. Increased BNP and NTproBNP levels observed in most renal failure situations can be explained either by a defect of elimination or an increase of peptide release. NTproBNP metabolism and its defective elimination by renal clearance may explain its increase. As for BNP, several factors may be implicated. Patients with renal insufficiency generally have left ventricular hypertrophy and diastolic heart dysfunction [15], followed by cardiac arrhythmias; complications of acute pulmonary edema leading to systolic dysfunction [16] are responsible for high cardiovascular morbidity and mortality. Although the complete mechanism of this cardiomyopathy is still unknown (weakness, arterial hypertension, hypervolemia), its prevalence depends on the level of renal failure [15]. Previous studies emphasized renal function as a determining factor for BNP concentration [17]. Nevertheless, these natriuric peptides have an important discriminating power for assessing heart failure. The level of renal dysfunction must be taken into account for BNP or NTproBNP interpretation, by adapting values even with mild renal insufficiency.

The influence of obesity on the development of cardiovascular disease has been well established [18]. Obesity impacts systolic and diastolic ventricular function [19] and is a major risk factor for the development of heart failure [20]. Obesity is associated with increased prevalence of most cardiovascular risk factors, including systemic hypertension, diabetes, hyperlipidemia, and LV hypertrophy [21]. Recent studies have shown that natriuretic peptide levels are reduced in obesity, partly related to altered clearance receptors and peptide degradation [22]. Physiologically, natriuretic peptides and lipolysis have been linked, and adipose tissues are intimately related to the natriuretic clearance receptor [22,23]). The natriuretic system promotes adipose tissue lipolysis mediated by the interactions of natriuretic peptides with receptors (NPRA and NPRB) [24]. A reduced natriuretic peptide level exists in obese patients with heart failure [25], underlining that clinical interpretation of BNP or NTproBNP results should take BMI into account, whatever the etiology of CHF.

As expected, the correlation between NYHA class and BNP level showed that the natriuretic peptide can be used as a marker for the diagnosis of LVD and as a tool to evaluate the severity of this dysfunction, taken together with LVEF and NYHA class [26], even in patients with renal insufficiency or obesity.

Our observation of the correlation between NTproBNP and BNP levels is in accordance with a previous report by Yeo et al. [8]. NTproBNP values are approximately 10 to 20 fold higher than BNP values, with a correlation coefficient of about 0.40. Other studies showed that the proportional and absolute increase of NTproBNP exceeds that of BNP, suggesting that NTproBNP may be a more sensitive marker of LVD [27]. Plasma concentrations of these 2 peptides are not directly comparable, because of the differences in their stability, half-life, physiological release, and clearance. The choice of which peptide to analyze will depend on local preferences; once the choice between these two tests is made, it is important to use the same assay to monitor patients, and to interpret the analytical results within the clinical context of each patient.


   Acknowledgements
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion.
 Acknowledgements
References
 
We thank Roche Diagnostics, Biosite Inc., and Beckman-Coulter Inc. for donations of reagents.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion.
 Acknowledgements
 References
 

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