Natriuretic Peptides

Natriuretic peptides (NPs) are markers of hemodynamic stress on the heart, denoting the neurohumoral activation of the myocardium. B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) are the two brain NPs that are derived from the prohormone, proBNP. BNP and NT-proBNP are produced in a 1:1 ratio when the left ventricle is stretched due to hemodynamic pressure.

BNP and NT-proBNP are synthesized mainly in the ventricular myocardium in response to myocardial wall stress. BNP is a neurohormone that acts to relieve the symptoms associated with volume expansion and pressure overload by promoting natriuresis and diuresis, vasodilation, and the suppression of the renin angiotensin aldosterone system. BNP is termed brain natriuretic peptide since it was initially discovered in the porcine brain.


Clinical Application

Blood levels of BNP and NT-proBNP are proportional to the severity of cardiac dysfunction and can be used for various applications such as:

  • Diagnosis of congestive heart failure (CHF)
  • Exclusion of heart failure (HF) in patients with HF-like symptoms due to the high negative predictive value of the marker1
  • Assessing the severity (grading) and prognosis of heart failure
  • Risk stratification of patients with acute coronary syndrome (ACS) and heart failure2,3
  • Differential diagnosis for cardiac and pulmonary diseases in patients with acute dyspnea4



The clinical and economic benefits of BNP and NT-proBNP make them essential tools in the diagnosis and treatment of heart failure. BNP and NT-proBNP assays provide several advantages, both to clinicians and patients, such as:

  • Helping to assess the patient’s condition with greater sensitivity and specificity along with clinical examination
  • Reducing the decision time, allowing quicker treatment initiation7
  • Eliminating unnecessary procedures or therapies, thereby reducing costs7-12
  • Decreasing the need for unwarranted electrocardiograms8,9,11
  • Reducing the number of hospital admissions6,7,10,12,13
  • Lowering median length of hospital stay6,7,10,12-14


Interpretation of BNP and NT-proBNP Results

BNP and NT-proBNP results can be interpreted accurately with the combination of:

  • good history and physical examination
  • clear understanding of the various factors influencing BNP or NT-proBNP levels such as age, gender, body mass index, thyroid function, anemia, and renal function
  • knowledge of differential diagnosis for elevated BNP or NT-proBNP levels15
Patient presenting
Patient symptoms

Impact on Management

BNP and NT-proBNP assays play a key role in improving the assessment of patients suspected of having heart failure. They also provide strong prognostic value in patients with diabetes, hypertension, and pre-HF. However, the exact implications of elevated BNP or NT-proBNP on the clinical management of these conditions remain unclear.


Preliminary studies on BNP or NT-proBNP-guided treatment for heart failure suggest that the markers;

  • Reduce total cardiovascular events
  • Delay the time to first event in comparison to intensive clinically guided treatment




Biological nature

Biologically inert

Biologically active


1 to 2 hours

22 minutes

Clearance mechanism

Reticuloendothelial system and renal system

Endocytosis and enzymatic degradation

Although there are certain differences between the two NPs, either one can be evaluated, as both deliver valuable clinical and economic benefits in the diagnosis and management of patients with heart failure. However, the results obtained from the respective markers cannot be compared or interchanged. 

 Reliable Answers to Critical Cardiac QuestionsSiemens Healthcare Diagnostics is the only company that offers a choice in natriuretic peptide testing across multiple instrument platforms. 

 Learn more about Natriuretic Peptides 

 Siemens offers you the option to choose the natriuretic peptide assay and the instrument solution that is right for you and your patients. 



1. Nielsen LS, et al. Eur J Heart Fail. 2004;6:63-70. 

2. Baggish AC, et al. Am J Cardiol. 2008;101(suppl):49A-55A. 

3. Omland T, et al. Am J Cardiol. 2008;101(suppl):61A-66A. DefaultReportPanel.Pubmed_RVDocSum 

4. Wu AH, et al. Eur J Heart Fail. 2004;6:309-12. 

7. Mueller C, et al. N Engl J Med. 2004;350:647-54. DefaultReportPanel.Pubmed_RVDocSum 

8. Maisel A, et al. Am Heart J. 2001;141:367-74. DefaultReportPanel.Pubmed_RVDocSum 

9. Galasko GIW, et al. Eur Heart J. 2006;27:193-200. DefaultReportPanel.Pubmed_RVDocSum 

10. Breidthardt T, et al. Clin Chem. 2007;53:1415-22. 

11. Collinson PO. Congest Heart Fail. 2006;12:103-7. 

12. Mueller C, et al. Arch Intern Med. 2006;166:1081-7. 

13. Siebert U, et al. Am J Cardiol. 2006;98:800-5. 

14. Seino Y, et al. Eur J Heart Fail. 2004;6:295-300. 

15. Jannuzzi JL, et al. Am J Cardiol. 2008;101(suppl):29A-38A. 

16. Silver MA, et al. Congest Heart Fail. 2004;10:1-30. 

17. van Kimmenade RRJ, et al. J Am Coll Cardiol. 2006;48:1621-7. DefaultReportPanel.Pubmed_RVDocSum 

18. Agency for Healthcare Research and Quality. Evidence Report/Technology Assessment No 142. September 2006. Accessed January 2009.

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