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Systemic inflammation in acute cardiorenal syndrome: an observational pilot study
AIMS: Acute cardiorenal syndrome (CRS) with and without consideration of the volume state was assessed with regard to inflammatory parameters. METHODS AND RESULTS: Blood samples from patients with acute CRS (Ronco type 1 or 3, Group 1, n = 15), end‐stage renal disease (Group 2, n = 12), hypertension...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6165938/ https://www.ncbi.nlm.nih.gov/pubmed/30015388 http://dx.doi.org/10.1002/ehf2.12327 |
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author | Linhart, Christoph Ulrich, Christof Greinert, Daniel Dambeck, Stefanie Wienke, Andreas Girndt, Matthias Pliquett, Rainer U. |
author_facet | Linhart, Christoph Ulrich, Christof Greinert, Daniel Dambeck, Stefanie Wienke, Andreas Girndt, Matthias Pliquett, Rainer U. |
author_sort | Linhart, Christoph |
collection | PubMed |
description | AIMS: Acute cardiorenal syndrome (CRS) with and without consideration of the volume state was assessed with regard to inflammatory parameters. METHODS AND RESULTS: Blood samples from patients with acute CRS (Ronco type 1 or 3, Group 1, n = 15), end‐stage renal disease (Group 2, n = 12), hypertension (Group 3, n = 15), and, in a second cohort, with acute CRS and hypervolemia (Group 4, n = 9) and hypertension (Group 5, n = 10) were analysed with regard to lipopolysaccharide‐binding protein (LBP), interleukins (ILs), and monocyte function (flow cytometry) both on admission (all groups) and on discharge (Groups 1 and 4). By discharge, one Group 1 patient died. LBP (ANOVA for Groups 1–3: P = 0.001) and IL‐6 (Kruskal–Wallis for Groups 1–3: P < 0.0001) were higher in Group 1 (LBP: 11.7 ± 2.0 μg/mL; IL‐6: 15.0 ± 6.1 pg/mL) and in Group 2 (LBP: 10.4 ± 1.4 μg/mL; IL‐6: 14.6 ± 3.8 pg/mL) than in Group 3 (LBP: 5.8 ± 0.4 μg/mL; IL‐6: 1.8 ± 0.4 pg/mL). In a direct comparison, the proportion of activated monocytes (CD14 and CD16 positive) was higher in Group 1 (6.9% ± 0.7%) vs. Group 3 (5.1% ± 0.6%; P = 0.018). Group 4 patients had higher IL‐6 plasma levels (34.2 ± 10.1 pg/mL) than Group 1 patients (15.0 ± 6.1 pg/mL; P = 0.03). All other findings obtained in CRS groups (Groups 1 and 4) were comparable. CONCLUSIONS: In acute CRS, a state of systemic inflammation was found, which is comparable with the end‐stage renal disease situation. In comparison with hypertensive controls, a monocytic activation was found in acute CRS regardless of volume state. |
format | Online Article Text |
id | pubmed-6165938 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-61659382018-10-04 Systemic inflammation in acute cardiorenal syndrome: an observational pilot study Linhart, Christoph Ulrich, Christof Greinert, Daniel Dambeck, Stefanie Wienke, Andreas Girndt, Matthias Pliquett, Rainer U. ESC Heart Fail Original Research Articles AIMS: Acute cardiorenal syndrome (CRS) with and without consideration of the volume state was assessed with regard to inflammatory parameters. METHODS AND RESULTS: Blood samples from patients with acute CRS (Ronco type 1 or 3, Group 1, n = 15), end‐stage renal disease (Group 2, n = 12), hypertension (Group 3, n = 15), and, in a second cohort, with acute CRS and hypervolemia (Group 4, n = 9) and hypertension (Group 5, n = 10) were analysed with regard to lipopolysaccharide‐binding protein (LBP), interleukins (ILs), and monocyte function (flow cytometry) both on admission (all groups) and on discharge (Groups 1 and 4). By discharge, one Group 1 patient died. LBP (ANOVA for Groups 1–3: P = 0.001) and IL‐6 (Kruskal–Wallis for Groups 1–3: P < 0.0001) were higher in Group 1 (LBP: 11.7 ± 2.0 μg/mL; IL‐6: 15.0 ± 6.1 pg/mL) and in Group 2 (LBP: 10.4 ± 1.4 μg/mL; IL‐6: 14.6 ± 3.8 pg/mL) than in Group 3 (LBP: 5.8 ± 0.4 μg/mL; IL‐6: 1.8 ± 0.4 pg/mL). In a direct comparison, the proportion of activated monocytes (CD14 and CD16 positive) was higher in Group 1 (6.9% ± 0.7%) vs. Group 3 (5.1% ± 0.6%; P = 0.018). Group 4 patients had higher IL‐6 plasma levels (34.2 ± 10.1 pg/mL) than Group 1 patients (15.0 ± 6.1 pg/mL; P = 0.03). All other findings obtained in CRS groups (Groups 1 and 4) were comparable. CONCLUSIONS: In acute CRS, a state of systemic inflammation was found, which is comparable with the end‐stage renal disease situation. In comparison with hypertensive controls, a monocytic activation was found in acute CRS regardless of volume state. John Wiley and Sons Inc. 2018-07-17 /pmc/articles/PMC6165938/ /pubmed/30015388 http://dx.doi.org/10.1002/ehf2.12327 Text en © 2018 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Research Articles Linhart, Christoph Ulrich, Christof Greinert, Daniel Dambeck, Stefanie Wienke, Andreas Girndt, Matthias Pliquett, Rainer U. Systemic inflammation in acute cardiorenal syndrome: an observational pilot study |
title | Systemic inflammation in acute cardiorenal syndrome: an observational pilot study |
title_full | Systemic inflammation in acute cardiorenal syndrome: an observational pilot study |
title_fullStr | Systemic inflammation in acute cardiorenal syndrome: an observational pilot study |
title_full_unstemmed | Systemic inflammation in acute cardiorenal syndrome: an observational pilot study |
title_short | Systemic inflammation in acute cardiorenal syndrome: an observational pilot study |
title_sort | systemic inflammation in acute cardiorenal syndrome: an observational pilot study |
topic | Original Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6165938/ https://www.ncbi.nlm.nih.gov/pubmed/30015388 http://dx.doi.org/10.1002/ehf2.12327 |
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