Natriuretic peptides BNP and NT-pro-BNP: established laboratory markers in clinical practice or just perspectives?

Pfister, Rudolf; Schneider, C. A.

doi:10.1016/j.cccn.2004.06.018

Cited by 41 publications

(39 citation statements)

References 70 publications

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“…16 which enters the pleural space through the highly permeable visceral pleura. 17 Fluid accumulates when the entry of fluid into the pleural space overwhelms the capacity of the lymphatics in the parietal pleura to remove the fluid. Small amounts of fluid may enter the pleural space from the capillaries in either pleural surface.…”

Section: Uremic Pleural Effusionmentioning

confidence: 99%

A Study on Etiology and Profile of Pleural Effusion in Chronic Kidney Disease

A¹,

Pathrudu²,

N³

et al. 2015

jemds

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BACKGROUND:Chronic Kidney disease is characterized by decreased glomerular filteration rate. Most pleural effusions occurring in CKD are attributed to renal failure & heart failure and are left alone, but there are other causes responsible for many effusions such as parapneumonic effusion, atelectasis, tuberculosis and other infections and malignancies due to immunosuppression, hence presence of pleural effusion in CKD deserves further evaluation. Our study is conducted to find the etiology and profile of patients with chronic Kidney disease developing pleural effusion. MATERIALS AND METHODS: Study was conducted among 35 patients with CKD and pleural effusion who attended Government hospital for chest and communicable diseases affiliated to Andhra Medical College, from March 2013 to September 2014. The clinical course of pleural effusions and their biochemical characteristics were studied together with radiographs and other relevant investigations. Study design-hospital based prospective study. OBSERVATIONS AND RESULTS: Of the 35 patients, 57% developed unilateral effusion, 43% bilateral effusion. Among unilateral effusions-minimal effusions were 25%, moderate were 60%, massive were 15%. Patients with transudative effusion were 31%, exudative were 69%. Causes of effusion were as follows: Cardiac failure 31%, Tuberculosis 28%, Malignancy 9%, uremic effusion 14%, parapneumonic 11%, connective tissue disorders 2%. CONCLUSIONS: Apart from cardiac failure, tuberculosis is a major cause of pleural effusion in CKD patients, especially if the effusion is unilateral, exudative in nature, blood tinged, and lymphocyte predominant. ATT produced improvement in clinical and radiological status in these patients.

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Section: Uremic Pleural Effusionmentioning

confidence: 99%

A Study on Etiology and Profile of Pleural Effusion in Chronic Kidney Disease

A¹,

Pathrudu²,

N³

et al. 2015

jemds

View full text Add to dashboard Cite

show abstract

“…Therefore, it can be kept for later analysis and may serve as a better marker than BNP for assessment of ventricular dysfunction and volume overload. 17 BNP binds to the natriuretic peptide receptor type A causing increased intracellular guanosine monophosphate production. 18,19 The biological effects of BNP include diuresis, vasodilatation, inhibition of renin and aldosterone production and of cardiac and vascular myocyte growth.…”

Section: Introductionmentioning

confidence: 99%

N-terminal probrain natriuretic peptide and patent ductus arteriosus in preterm infants

Nuntnarumit

Khositseth

2008

J Perinatol

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Objective: To determine whether plasma N-terminal probrain natriuretic peptide (NT-proBNP) in premature infants could identify hemodynamically significant patent ductus arteriosus (HsPDA) and to determine the correlation between serial plasma NT-proBNP and echocardiographic assessment of ductal shunting.Study Design: An observational study involving 35 preterm infants who underwent echocardiographic assessment for PDA on day 2, 4 and 7 of life with simultaneous blood sampling for determination of NT-proBNP concentrations. HsPDA was diagnosed by left-to-right ductal shunt on color Doppler, measuring diameter >1.5 mm on two-dimensional echocardiography plus X2 clinical features of PDA.Result: Plasma NT-proNBP levels on day 2 in the HsPDA group (n ¼ 12) were significantly higher than in non-HsPDA group (n ¼ 23) with a median of 16 353 pg ml À1 (interquartile range (IQR), 12 360-33 459; range, 10 316-104 998) vs 3914 pg ml À1 (IQR, 2601-5782; range, 1535-19 516) (P<0.001), respectively. Eight infants (67%) in the HsPDA group responded to an initial course of indomethacin or ibuprofen and their NT-proBNP levels significantly decreased within 48 h after treatment compared with non-responders (P ¼ 0.007). NT-proBNP concentrations were significantly correlated with left atrial to aortic root ratio. A cut-off NT-proBNP on day 2 of 10 180 pg ml À1 offered the best predictive values for HsPDA with a sensitivity of 100% and a specificity of 91%.Conclusion: Plasma NT-proBNP on day 2 was found as a sensitive marker for predicting HsPDA in preterm infants. Successful closure of PDA was also correspondent with the decline in plasma NT-proBNP. Journal of Perinatology (2009) 29, 137-142; doi:10.1038/jp.2008 published online 20 November 2008 Keywords: preterm infant; patent ductus arteriosus; NT-proBNP Introduction It is of vital importance to recognize and properly treat hemodynamically significant patent ductus arteriosus (HsPDA) in preterm infants. PDA has been reported to be associated with morbidities in preterm infants as a result of ductal steal from systemic circulation, for example, pulmonary congestion, pulmonary hemorrhage, bronchopulmonary dysplasia, intraventricular hemorrhage and necrotizing enterocolitis. [1][2][3][4] Strategies for PDA closure involve prophylactic treatment, presymptomatic treatment for non-HsPDA, and treatment for HsPDA. 5,6 Although prophylactic treatment with indomethacin reduces incidence of PDA and severe intraventricular hemorrhage in preterm infants, 7,8 there are no differences in mortality and long-term neurodevelopment. 9,10 Recent studies have shown that only one-third of very low birth weight infants develops significant PDA. 10,11 Therefore, a number of infants, whose PDA would otherwise close spontaneously, will be exposed to the treatment unnecessarily if prophylaxis strategy is used. Clinical assessment for the diagnosis of PDA has been shown to be specific, but not sensitive. [12][13][14] Echocardiography is used to detect PDA and to assess the degree of shunting through vario...

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“…It is now generally accepted that cardiac natriuretic peptide concentrations in the peripheral blood are augmented by factors that increase cardiac pressure and volume overload (1)(2)(3). An intracellular prohormone containing 108 amino acids (proBNP) is split into B-type natriuretic peptide (BNP; 4 amino acids 77-108), which is considered the biologically active hormone, and an inactive aminoterminal fragment (NT-proBNP; amino acids 1-76) (2,3 ).…”

mentioning

confidence: 99%

“…An intracellular prohormone containing 108 amino acids (proBNP) is split into B-type natriuretic peptide (BNP; 4 amino acids 77-108), which is considered the biologically active hormone, and an inactive aminoterminal fragment (NT-proBNP; amino acids 1-76) (2,3 ). Although BNP and NT-proBNP are secreted on an equimolar basis, their molar ratio in plasma is not 1:1 because BNP has a shorter plasma half-life than does NT-proBNP (2,3 ).…”

mentioning

confidence: 99%

“…The diagnostic value of circulating BNP and NT-proBNP is well established in symptomatic patients with suspected heart failure, but their utility as a screening tool for cardiac structural disease in the general population appears to be limited (1)(2)(3). However, in populations at high risk for the development of symptomatic heart failure, the role of the 2 analytes for the detection of asymptomatic cardiac dysfunction remains to be clarified.…”

mentioning

confidence: 99%

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Capability of B-Type Natriuretic Peptide (BNP) and Amino-Terminal proBNP as Indicators of Cardiac Structural Disease in Asymptomatic Patients with Systemic Arterial Hypertension

Mueller¹,

Gegenhuber

Dieplinger³

et al. 2005

Clinical Chemistry

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Background:The aim of the present study was to prospectively evaluate the diagnostic utility of B-type natriuretic peptide (BNP) and amino-terminal proBNP (NT-proBNP) measurements for the detection of cardiac structural disease in asymptomatic patients with systemic arterial hypertension and to test the hypothesis that the 2 analytes are equally useful in this clinical setting. Methods: We studied a consecutive series of 149 asymptomatic patients referred for echocardiographic evaluation of the cardiac effects of systemic arterial hypertension. Diagnosis of cardiac structural disease was based on the presence of systolic or diastolic dysfunction, left atrial dilatation, left ventricular dilatation or hypertrophy, pulmonary hypertension, and wall motion or valvular abnormalities. Blood concentrations of BNP and NT-proBNP were measured by 2 commercially available assays (Abbott AxSYM and Roche Elecsys, respectively). Diagnostic accuracies of BNP and NT-proBNP were assessed by ROC curve analysis. Areas under the curves were compared by analysis of equivalency. Results: In distinguishing between hypertensive patients with cardiac structural disease (n ‫؍‬ 118) and hypertensive patients without (n ‫؍‬ 31), areas under the curves were 0.740 (95% confidence interval, 0.662-0.808) for BNP and 0.762 (0.685-0.828) for NT-proBNP and

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Natriuretic peptides BNP and NT-pro-BNP: established laboratory markers in clinical practice or just perspectives?

Cited by 41 publications

References 70 publications

A Study on Etiology and Profile of Pleural Effusion in Chronic Kidney Disease

A Study on Etiology and Profile of Pleural Effusion in Chronic Kidney Disease

N-terminal probrain natriuretic peptide and patent ductus arteriosus in preterm infants

Capability of B-Type Natriuretic Peptide (BNP) and Amino-Terminal proBNP as Indicators of Cardiac Structural Disease in Asymptomatic Patients with Systemic Arterial Hypertension

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