scholarly journals Serum Lipocalin 2 (Neutrophil Gelatinase–Associated Lipocalin) in Relation to Biomarkers of Inflammation and Cardiac Stretch During Activation of the Renin-Angiotensin-Aldosterone System in Human Immunodeficiency Virus

2019 ◽  
Vol 220 (9) ◽  
pp. 1420-1424 ◽  
Author(s):  
Milana Bogorodskaya ◽  
Kathleen V Fitch ◽  
Tricia H Burdo ◽  
Patrick Maehler ◽  
Rebecca M Easly ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cardiac Injury ◽  
Lipocalin 2 ◽  
Clinical Trial Registration ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Immunodeficiency Virus

Abstract Purpose To evaluate the relationship of lipocalin 2 to inflammation and cardiac injury with increased aldosterone in human immunodeficiency virus (HIV). Methods A standardized 6-day low-sodium diet was used to stimulate renin-angiotensin-aldosterone system (RAAS) activation, and serum lipocalin 2 and biomarkers of inflammation and cardiac stretch were assessed among persons with or without HIV. Results Lipocalin 2 levels increased with RAAS activation compared with suppression in the HIV group (median level [interquartile range], 71.3 [59.2–99.7] vs 67.0 [51.8–86.3] ng/mL; P = .01). During RAAS activation, lipocalin 2 was related to biomarkers of inflammation (tumor necrosis factor α [P = .007]), monocyte/macrophage activation (soluble CD163 [P = .005] and chemokine [C-C motif] ligand 2 [P = .03]), and markers of cardiac stretch (brain natriuretic peptide [P < .001] and N-terminal fragment of the prohormone brain natriuretic peptide [P = .001]) in HIV. Conclusion Lipocalin 2 may be important in modulating aldosterone-induced inflammation, monocyte activation, and cardiac stretch during RAAS activation in HIV. Clinical Trial Registration NCT01407237

Comparative Effects of Atrial Natriuretic Peptide and Brain Natriuretic Peptide on the Aldosterone and Pressor Responses to Angiotensin Ii in Man

1995 ◽  
Vol 88 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Robert I. Cargill ◽  
Allan D. Struthers ◽  
Brian J. Lipworth
Keyword(s):  
Steady State ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Aldosterone ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

1. Atrial natriuretic peptide and brain natriuretic peptide have similar vasodilator and natriuretic properties, although little information is available regarding their relative effects as antagonists of the renin—angiotensin—aldosterone system. We have therefore compared how atrial natriuretic peptide and brain natriuretic peptide affect the systemic pressor and aldosterone responses to angiotensin II in eight male subjects. 2. Each subject was studied on three separate occasions, when they received a 60-min infusion of placebo, atrial natriuretic peptide (10 pmol min−1 kg−1) or brain natriuretic peptide (10 pmolmin−1 kg−1), with a concomitant infusion of angiotensin II (6 ng min−1 kg−1) given for the final 30 min of the infusion period. The change in haemodynamic parameters and plasma aldosterone induced by angiotensin II was measured. Plasma concentrations of atrial natriuretic peptide (182 ± 23 pmol/l) and brain natriuretic peptide (193 ± 25 pmol/l) achieved at steady-state during the infusion on each study day were not significantly different. 3. Increases in mean arterial pressure in response to angiotensin II were significantly lowered by concomitant infusion of atrial natriuretic peptide (21.0 ± 1.7 mmHg) and brain natriuretic peptide (20.1 ± 1.9 mmHg) compared with placebo (29.0 ± 4.1 mmHg). There were similar effects on systolic and diastolic blood pressure. Cardiac output was decreased on each study day to the same extent by angiotensin II infusion. Total systemic vascular resistance showed a non-significant trend towards an attenuated response to angiotensin II when atrial natriuretic peptide or brain natriuretic peptide was infused concomitantly in comparison with placebo. 4. Plasma aldosterone increased by 326 ± 49 pmol/l when angiotensin II was infused with placebo. Both atrial natriuretic peptide and brain natriuretic peptide significantly blunted this response, although the increase with atrial natriuretic peptide (19 ± 35 pmol/l) was significantly lower than the increase with brain natriuretic peptide (133 ± 19 pmol/l). 5. Atrial natriuretic peptide and brain natriuretic peptide were therefore equally effective in blunting the systemic pressor response to angiotensin II. It was apparent, however, in view of similar plasma concentrations at steady state, that on a molar basis atrial natriuretic peptide was a more potent inhibitor of angiotensin II-induced aldosterone secretion than brain natriuretic peptide. These results suggest a dissociation between the haemodynamic and hormonal effects of atrial natriuretic peptide and brain natriuretic peptide in terms of antagonism of the renin—angiotensin—aldosterone system.

Brain Natriuretic Peptide Counteracting the Renin-angiotensin-aldosterone System in Accelerated Malignant Hypertension

2016 ◽  
Vol 352 (5) ◽  
pp. 534-539 ◽  
Author(s):  
Hitoshi Nakagawa ◽  
Yuji Mizuno ◽  
Eisaku Harada ◽  
Yoshinobu Morikawa ◽  
Koichiro Kuwahara ◽  
...  
Keyword(s):  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Malignant Hypertension ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

scholarly journals Serum NGAL, BNP, PTH, and albumin do not improve glomerular filtration rate estimating formulas in children

2021 ◽  
Author(s):  
Julie Mouron-Hryciuk ◽  
François Cachat ◽  
Paloma Parvex ◽  
Thomas Perneger ◽  
Hassib Chehade
Keyword(s):  
Glomerular Filtration Rate ◽  
Parathyroid Hormone ◽  
Serum Creatinine ◽  
Brain Natriuretic Peptide ◽  
Glomerular Filtration ◽  
Natriuretic Peptide ◽  
Cystatin C ◽  
Filtration Rate ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Neutrophil Gelatinase

AbstractGlomerular filtration rate (GFR) is difficult to measure, and estimating formulas are notorious for lacking precision. This study aims to assess if the inclusion of additional biomarkers improves the performance of eGFR formulas. A hundred and sixteen children with renal diseases were enrolled. Data for age, weight, height, inulin clearance (iGFR), serum creatinine, cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), parathyroid hormone (PTH), albumin, and brain natriuretic peptide (BNP) were collected. These variables were added to the revised and combined (serum creatinine and cystatin C) Schwartz formulas, and the quadratic and combined quadratic formulas. We calculated the adjusted r-square (r2) in relation to iGFR and tested the improvement in variance explained by means of the likelihood ratio test. The combined Schwartz and the combined quadratic formulas yielded best results with an r2 of 0.676 and 0.730, respectively. The addition of BNP and PTH to the combined Schwartz and quadratic formulas improved the variance slightly. NGAL and albumin failed to improve the prediction of GFR further. These study results also confirm that the addition of cystatin C improves the performance of estimating GFR formulas, in particular the Schwartz formula.Conclusion: The addition of serum NGAL, BNP, PTH, and albumin to the combined Schwartz and quadratic formulas for estimating GFR did not improve GFR prediction in our population. What is Known:• Estimating glomerular filtration rate (GFR) formulas include serum creatinine and/or cystatin C but lack precision when compared to measured GFR.• The serum concentrations of some biological parameters such as neutrophil gelatinase-associated lipocalin (NGAL), parathyroid hormone (PTH), albumin, and brain natriuretic peptide (BNP) vary with the level of renal function. What is New:• The addition of BNP and PTH to the combined quadratic formula improved its performance only slightly. NGAL and albumin failed to improve the prediction of GFR further.

BRAIN NATRIURETIC PEPTIDE (BNP) SEBAGAI BIOMARKER GAGAL JANTUNG KONGESTIF

2020 ◽  
Vol 10 (3) ◽  
pp. 130-138
Author(s):  
Budi Sembiring ◽  
◽  
Jekson Siahaan
Keyword(s):  
Heart Failure ◽  
Brain Natriuretic Peptide ◽  
Enzyme Immunoassay ◽  
Natriuretic Peptide ◽  
Fluorescence Immunoassay ◽  
Renin Angiotensin ◽  
Heart Ventricles ◽  
Immuno Assay

Brain Natriuretic Peptide (BNP) is mainly secreted by the heart ventricles and acts as antagonist to Renin-Angiotensin-Aldosterone. BNP is secreted as pre-proBNP which is broken down into BNP and proBNP in circulation. The BNP examination is done by measuring the levels of BNP or N-Terminal-proBNP depending on the method and the manufacturer. Increased levels of BNP and NT-proBNP indicate heart failure so that BNP and NT-proBNP are considered markers of heart failure. This examination is also indicated to help establish the diagnosis, monitoring, and prognosis of heart failure. Natriuretic peptide examination can be done by several methods such as radioimmunoassay (RIA), Enzyme immunoassay (EIA), Fluorescence immunoassay (FIA), and Sandwich Electro Chemiluminescence Immuno Assay (Sandwich ECLIA).

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