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Table of Contents    
Year : 2018  |  Volume : 66  |  Issue : 5  |  Page : 1392-1393

BNP: Is it an ideal marker to assess volume status in patients with hyponatremia and natriuresis?

Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication17-Sep-2018

Correspondence Address:
Dr. Afzal Azim
Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.241391

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How to cite this article:
Azim A, Jena S. BNP: Is it an ideal marker to assess volume status in patients with hyponatremia and natriuresis?. Neurol India 2018;66:1392-3

How to cite this URL:
Azim A, Jena S. BNP: Is it an ideal marker to assess volume status in patients with hyponatremia and natriuresis?. Neurol India [serial online] 2018 [cited 2019 Feb 16];66:1392-3. Available from:

The 108-amino acid prohormone, B-type natriuretic peptide (BNP), is released during hemodynamic stress and, once in the circulation, it gets cleaved by endopeptidase, corin, into the inactive 76-amino acid and biologically active 32-amino acid BNP. BNP is removed from circulation via internalization by cells that express BNP receptors, while renal clearance is the main mechanism for NT-pro BNP excretion. BNP is primarily synthesized by cardiomyocytes in a short time and in large quantities.[1] It is released in response to volume or pressure overload conditions. BNPs have diuretic, natriuretic, hypotensive effects, as well as cardiac antihypertrophic and antifibrotic properties. They also inhibit the renin-angiotensin system, endothelin secretion, and systemic and renal sympathetic activity. A number of variables affect plasma brain natriuretic peptide and N-terminal pro brain natriuretic peptide levels, including the assay used, age (higher normal values are observed with increasing age), sex (higher values are observed in women), body mass index (lower levels are observed with a higher body mass index) renal dysfunction, inflammatory conditions, steroid therapy and diurnal variation. These variables can influence the reference range that is utilized to exclude or confirm a diagnosis.

The utility of measuring NT-pro BNP and BNP has been best validated in acute heart failure in the acute settings with a reassuringly high sensitivity.[2] Plasma BNPs concentrations are elevated in patients with pulmonary hypertension and pulmonary embolism. In such patients, they correlate positively with right atrial pressure, mean pulmonary artery pressure, pulmonary vascular resistance, and right ventricular mass, and inversely with cardiac index. Elevated BNP or NT-pro BNP level may prove to be a powerful predictor of mortality in patients with sepsis but the results are inconsistent with variations in sensitivity and the timing of measurements.[3] The elevation of BNPs in patients with sepsis can be considerably high, even though the cardiac depression may not be obvious.[4] Volume resuscitation in patients with circulatory shock is considered as one of the mechanisms for increased BNPs.[5]

Elevated BNPs may be seen in patients with acute neurological insults. It is also known that BNP is secreted in the brain, primarily the hypothalamus, and this release is induced by cerebral ischemia.[6] Plasma BNP levels are seen to be increased in the acute phase of stroke and can be used as a prognostic marker for assessing morbidity and mortality.[7] One of the proposed mechanisms of hyponatremia in subarachnoid haemorrhage is considered to be due to natriuresis as a result of the effect of elevated BNPs.[8]

In the study in focus, the authors have tried to use NT-pro BNP as a marker to assess the volume status in post-operative neurosurgical patients with hyponatremia and natriuresis.[9] The main cause of hyponatremia with natriuresis has been attributed to syndrome of inappropriate anti-diuretic hormone (SIADH) or cerebral salt wasting (CSW). While SIADH is associated with an euvolemic or a hypervolemic state, CSW is associated with a hypovolemic status. Accordingly, for correction of hyponatremia, fluid restriction is needed in SIADH and fluid repletion is required in CSW. The authors have conducted this study in two phases; phase-1 (n = 10 patients) and phase-2 (n = 21 patients). In phase-1, the central venous pressure (CVP) value was taken as a criterion to differentiate SIADH and CSW, and then it was correlated with the NT- ProBNP level. Those with SIADH (CVP >5cm H2O) had NT-ProBNP levels <125pg/ml, and those with CSW (CVP > 5cm H2O) had NT-ProBNP levels >125pg/ml. In phase-2, NT-ProBNP level was taken as a criterion to diagnose SIADH and CSW and then therapy (fluid restriction vs fluid restriction) was started in the respective conditions which correlated with the correction of hyponatremia. All the 11 patients who had NT-ProBNP <125pg/ml (SIADH) responded to fluid restriction, and 9 of 10 patients with NT-ProBNP >125pg/ml (CSW) responded to fluid repletion. Combining the results of both phase-1 and phase-2, in patients with CSW syndrome, NT-ProBNP could diagnose hypovolemia with a sensitivity of 87.5% and a specificity of 93.3%.

The authors have not tried to correlate BNP values with sex and body mass index (BMI) of the patients, as both can affect the BNP value. As many patients are diagnosed to have tumour or space occupying lesions, they might be on steroid therapy, which can influence (increase) BNP levels. The authors have not mentioned the presence of sepsis, which can again be a confounding factor for an increase in BNPs. In phase-1 of this study, the patients were diagnosed as CSW (hypovolemia) on the basis of CVP <5cm of H2O. Other patients with CVP >5cm of H20 were thought to have SIADH (thus being euvolemic/hypervolemic), and hence, fluid non-responsive. Even the authors of this study agree that it is difficult to predict the volume status and the response to fluids based on a single CVP value. In a recent systematic review by Eskesen et al., that included 1148 patients from 51 studies that evaluated the response to a fluid bolus and reported CVP, the overall predictive value of CVP was poor.[10] However, one third of patients with CVP values greater than 12 mmHg also responded to fluids.

In phase-2 of this study, the patients were diagnosed to have CSW with elevated BNPs and were given fluid replacement, which is contrary to the current belief that high BNPs value are seen in patients with volume overload. One study by Lee et al., demonstrated that for end- stage renal disease, BNPs levels were elevated prior to dialysis.[11] The authors have explained the central and neuroendocrine mechanisms which can contribute to elevated BNP levels in non-cardiac conditions. Although, in this study, all of those patients who were diagnosed to have CSW responded well to the fluid replacement, fluid replacement only on the basis of BNPs value can be hazardous for some patients. It should be used in conjunction with clinical assessment, daily fluid balance and objective parameters like measurement of CVP or inferior vena cava diameter. Also, the serial monitoring of BNP levels should be considered both before therapy and after therapy. The presence of an “extreme” CVP value may be more helpful to guide in fluid administration than the presence of intermediate values. Therefore, the correlation of CVP <5cm of H2O combined with an elevated NT-ProBNP value to diagnose CSW may hold true but at present appears to be exploratory in status. Further research is required that incudes recruiting a large sample size.

  References Top

Azzazy HM, Cristenson RH. B-type natriuretic peptide: Physiologic role and assay characteristics. Heart Fail Rev 2003;8:315-20.  Back to cited text no. 1
Roberts E, Ludman AJ, Dworzynski K, Al-Mohammad A, Cowie MR, McMurray JJ, et al. NICE guideline development Group for Acute Heart Failure. The diagnostic accuracy of the natriuretic peptides in heart failure: Systematic review and diagnostic meta-analysis in the acute care setting. BMJ 2015;350:h910. doi: 10.1136/bmj.h910.  Back to cited text no. 2
Wang F, Wu Y, Tang L, Zhu W, Chen F, Xu T, et al. Brain natriuretic peptide for prediction of mortality in patients with sepsis: A systematic review and meta-analysis. Crit Care 2012;16:R74.  Back to cited text no. 3
Maeder M, Ammann P, Kiowski W, Rickli H. B-type natriuretic peptide in patients with sepsis and preserved left ventricular ejection fraction. Eur J Heart Fail 2005; 7:1164-67.  Back to cited text no. 4
Takahashi K, Totsune K, Sone M, Ohneda M, Murakami O, Itoi K, et al. Human brain natriuretic peptide-like immunoreactivity in human brain. Peptides 1992;13:121-3.  Back to cited text no. 5
Phua J, Lim TK, Lee KH. B-type natriuretic peptide: Issues for the intensivist and pulmonologist. Crit Care Med 2005;33:2094-13.  Back to cited text no. 6
Sayan S, Kotan D. Levels of brain natriuretic peptide as a marker for the diagnosis and prognosis of acute ischemic stroke. Arch Med Sci Atheroscler Dis 2016;1:e16-22.  Back to cited text no. 7
Berendes E, Walter M, Cullen P, Prien T, Van Aken H, Horsthemke J, et al. Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage. Lancet 1997;349:245.  Back to cited text no. 8
Tobin G, Chacko AG, Simon R. Evaluation of NT-ProBNP as a marker of the volume status of neurosurgical patients developing hyponatremia and natriuresis: A pilot study. Neurol India 2018;66:1383-88.  Back to cited text no. 9
  [Full text]  
Eskesen TG, Wetterslev M, Perner A. Systematic review including re-analyses of 1148 individual data sets of central venous pressure as a predictor of fluid responsiveness. Intensive Care Med 2016;42:324-32.  Back to cited text no. 10
Lee SW, Song JH, Kim GA, Lim HJ, Kim MJ. Plasma brain natriuretic peptide concentration on assessment of hydration status in hemodialysis patient. Am J Kidney Dis 2003; 41:1257-66.  Back to cited text no. 11


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