Investigators found no correlation between changes in intradialytic BNP values and other measured parameters

Investigators found no correlation between changes in intradialytic BNP values and other measured parameters. in the setting of renal dysfunction. We spotlight the potential divergence in the role of natriuretic peptides for assessment of volume status in a subset of patients with renal dysfunction who receive renal replacement therapy and call for future research to elucidate the power of the biomarkers in this setting. 1. Background Heart failure (HF) is usually a major public health problem because of its high prevalence, poor prognosis, and healthcare cost burden. The prevalence of HF in adults over 20 years of age in the United States was estimated to be 2.4% in 2008, and by 2030, an additional 3 million people are predicted to develop HF, which is a 25% increase in prevalence from 2010 [1]. Congestion is recognized as the major cause for hospitalization in the vast majority of patients with HF and contributes to adverse outcomes [2]. Nevertheless, a significant proportion of the patients admitted to the hospital for acute decompensated heart failure (ADHF) is usually discharged with unresolved congestion. A report of more than 50,000 patients in the ADHF National Registry revealed that about 33% of the patients lose as little as less than 2.3?kg and another 16% even gain weight during the course of hospitalization [3]. Congestion often remains unrecognized until conditions develop that warrant hospital admission. Elevated left ventricular filling pressures are present in a significant subset of HF patients with no obvious clinical signs; termed hemodynamic congestion in contrast to clinical congestion that constitutes constellation of signs and symptoms including shortness of breath, orthopnea, pulmonary rales, peripheral edema, and jugular venous distention [4]. In Peptide YY(3-36), PYY, human addition, congestion is one of the contributing factors for worsening renal function (WRF) in the setting of ADHF, which in turn is usually thought to adversely impact outcomes. Interestingly, WRF can also occur while patients are being treated for congestion especially with diuretic therapy. With acknowledgement of the importance of early detection of congestion, there has been renewed desire for investigating novel circulating serum and plasma biomarkers in patients with HF. An ideal biomarker should have the following three characteristics to be clinically useful. Firstly, it should be accurate with affordable cost and short turnaround Peptide YY(3-36), PYY, human occasions; secondly, it should provide additional information that is not obtainable from a thorough clinical assessment; and finally, its measurement should aid in clinical decision making [5, 6]. The role of various biomarkers has been analyzed in diagnosing, grading the severity, and predicting the progression of HF as an adjunct to clinical parameters and invasive screening. B-type natriuretic peptide (BNP) and N-terminal prohormone of BNP (NT-proBNP), which are a a part of natriuretic peptide system, are frequently used in the clinical practice for this purpose. In this article, we briefly discuss the power and performance characteristics of these biomarkers in the setting of HF and discuss the impact of concomitant renal dysfunction on its application in this setting. 2. The Natriuretic Peptide System Atrial natriuretic peptide (ANP), BNP, and C-type natriuretic peptide (CNP) constitute the human natriuretic-peptide family. Among these, ANP was the first to be discovered in the 1980s. It is a 28-amino acid polypeptide resulting from the C-terminal end of the prohormone proANP and secreted mainly by the atria. BNP was Rabbit polyclonal to Caspase 3.This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family.Sequential activation of caspases initially isolated from brain tissue, but is also found in the blood circulation, and the highest concentration is found in the cardiac ventricles. Prior to its activation, BNP is stored as a 108-amino acid polypeptide precursor, proBNP, in both cardiac ventricles and, to a lesser extent, Peptide YY(3-36), PYY, human in the atria. ProBNP is usually cleaved in response to volume growth and myocyte stretch to produce the biologically active 32-amino acid BNP and the 76-amino acid peptide, NT-proBNP. CNP is usually primarily found in the brain, and plasma concentrations are typically low. Despite its name, CNP does not possess natriuretic effect but does have vasodilatory properties and can be synthesized by vascular endothelial cells [7, 8]. Plasma ANP and BNP concentrations increase in Peptide YY(3-36), PYY, human response to volume overload and pressure overload in the heart and are considered as physiological antagonists for the effects of angiotensin II on vascular firmness, aldosterone secretion, renal-tubular sodium reabsorption, and vascular-cell growth, thereby producing diuretic, natriuretic, and antihypertensive effects [7, 9]. On the other hand, plasma CNP concentrations switch very little with.


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