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Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality
Metabolic acidosis has been proved to be a risk factor for the progression of chronic kidney disease, but its relation to acute kidney injury (AKI) has not been investigated. In general, a diagnosis of metabolic acidosis is based on arterial blood gas (ABG) analysis, but the diagnostic role of carbo...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443206/ https://www.ncbi.nlm.nih.gov/pubmed/28565850 http://dx.doi.org/10.3892/etm.2017.4292 |
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author | Hu, Jiachang Wang, Yimei Geng, Xuemei Chen, Rongyi Xu, Xialian Zhang, Xiaoyan Lin, Jing Teng, Jie Ding, Xiaoqiang |
author_facet | Hu, Jiachang Wang, Yimei Geng, Xuemei Chen, Rongyi Xu, Xialian Zhang, Xiaoyan Lin, Jing Teng, Jie Ding, Xiaoqiang |
author_sort | Hu, Jiachang |
collection | PubMed |
description | Metabolic acidosis has been proved to be a risk factor for the progression of chronic kidney disease, but its relation to acute kidney injury (AKI) has not been investigated. In general, a diagnosis of metabolic acidosis is based on arterial blood gas (ABG) analysis, but the diagnostic role of carbon dioxide combining power (CO(2)CP) in the venous blood may also be valuable to non-respiratory patients. This retrospective study included all adult non-respiratory patients admitted consecutively to our hospital between October 01, 2014 and September 30, 2015. A total of 71,089 non-respiratory patients were included, and only 4,873 patients were evaluated by ABG analysis at admission. In patients with ABG, acidosis, metabolic acidosis, decreased HCO(3)(−) and hypocapnia at admission was associated with the development of AKI, while acidosis and hypocapnia were independent predictors of hospital mortality. Among non-respiratory patients, decreased CO(2)CP at admission was an independent risk factor for AKI and hospital mortality. ROC curves indicated that CO(2)CP was a reasonable biomarker to exclude metabolic acidosis, dual and triple acid-base disturbances. The effect sizes of decreased CO(2)CP on AKI and hospital mortality varied according to age and different underlying diseases. Metabolic acidosis is an independent risk factor for the development of AKI and hospital mortality. In non-respiratory patient, decreased CO(2)CP is also an independent contributor to AKI and mortality and can be used as an indicator of metabolic acidosis. |
format | Online Article Text |
id | pubmed-5443206 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-54432062017-05-30 Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality Hu, Jiachang Wang, Yimei Geng, Xuemei Chen, Rongyi Xu, Xialian Zhang, Xiaoyan Lin, Jing Teng, Jie Ding, Xiaoqiang Exp Ther Med Articles Metabolic acidosis has been proved to be a risk factor for the progression of chronic kidney disease, but its relation to acute kidney injury (AKI) has not been investigated. In general, a diagnosis of metabolic acidosis is based on arterial blood gas (ABG) analysis, but the diagnostic role of carbon dioxide combining power (CO(2)CP) in the venous blood may also be valuable to non-respiratory patients. This retrospective study included all adult non-respiratory patients admitted consecutively to our hospital between October 01, 2014 and September 30, 2015. A total of 71,089 non-respiratory patients were included, and only 4,873 patients were evaluated by ABG analysis at admission. In patients with ABG, acidosis, metabolic acidosis, decreased HCO(3)(−) and hypocapnia at admission was associated with the development of AKI, while acidosis and hypocapnia were independent predictors of hospital mortality. Among non-respiratory patients, decreased CO(2)CP at admission was an independent risk factor for AKI and hospital mortality. ROC curves indicated that CO(2)CP was a reasonable biomarker to exclude metabolic acidosis, dual and triple acid-base disturbances. The effect sizes of decreased CO(2)CP on AKI and hospital mortality varied according to age and different underlying diseases. Metabolic acidosis is an independent risk factor for the development of AKI and hospital mortality. In non-respiratory patient, decreased CO(2)CP is also an independent contributor to AKI and mortality and can be used as an indicator of metabolic acidosis. D.A. Spandidos 2017-05 2017-03-30 /pmc/articles/PMC5443206/ /pubmed/28565850 http://dx.doi.org/10.3892/etm.2017.4292 Text en Copyright: © Hu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Hu, Jiachang Wang, Yimei Geng, Xuemei Chen, Rongyi Xu, Xialian Zhang, Xiaoyan Lin, Jing Teng, Jie Ding, Xiaoqiang Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality |
title | Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality |
title_full | Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality |
title_fullStr | Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality |
title_full_unstemmed | Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality |
title_short | Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality |
title_sort | metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5443206/ https://www.ncbi.nlm.nih.gov/pubmed/28565850 http://dx.doi.org/10.3892/etm.2017.4292 |
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