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Acute kidney injury after cardiac arrest

INTRODUCTION: The aim of this study was to evaluate the incidence and determinants of AKI in a large cohort of cardiac arrest patients. METHODS: We reviewed all patients admitted, for at least 48 hours, to our Dept. of Intensive Care after CA between January 2008 and October 2012. AKI was defined as...

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Autores principales: Tujjar, Omar, Mineo, Giulia, Dell’Anna, Antonio, Poyatos-Robles, Belen, Donadello, Katia, Scolletta, Sabino, Vincent, Jean-Louis, Taccone, Fabio Silvio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4416259/
https://www.ncbi.nlm.nih.gov/pubmed/25887258
http://dx.doi.org/10.1186/s13054-015-0900-2
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author Tujjar, Omar
Mineo, Giulia
Dell’Anna, Antonio
Poyatos-Robles, Belen
Donadello, Katia
Scolletta, Sabino
Vincent, Jean-Louis
Taccone, Fabio Silvio
author_facet Tujjar, Omar
Mineo, Giulia
Dell’Anna, Antonio
Poyatos-Robles, Belen
Donadello, Katia
Scolletta, Sabino
Vincent, Jean-Louis
Taccone, Fabio Silvio
author_sort Tujjar, Omar
collection PubMed
description INTRODUCTION: The aim of this study was to evaluate the incidence and determinants of AKI in a large cohort of cardiac arrest patients. METHODS: We reviewed all patients admitted, for at least 48 hours, to our Dept. of Intensive Care after CA between January 2008 and October 2012. AKI was defined as oligo-anuria (daily urine output <0.5 ml/kg/h) and/or an increase in serum creatinine (≥0.3 mg/dl from admission value within 48 hours or a 1.5 time from baseline level). Demographics, comorbidities, CA details, and ICU interventions were recorded. Neurological outcome was assessed at 3 months using the Cerebral Performance Category scale (CPC 1–2 = favorable outcome; 3–5 = poor outcome). RESULTS: A total of 199 patients were included, 85 (43%) of whom developed AKI during the ICU stay. Independent predictors of AKI development were older age, chronic renal disease, higher dose of epinephrine, in-hospital CA, presence of shock during the ICU stay, a low creatinine clearance (CrCl) on admission and a high cumulative fluid balance at 48 hours. Patients with AKI had higher hospital mortality (55/85 vs. 57/114, p = 0.04), but AKI was not an independent predictor of poor 3-month neurological outcome. CONCLUSIONS: AKI occurred in more than 40% of patients after CA. These patients had more severe hemodynamic impairment and needed more aggressive ICU therapy; however the development of AKI did not influence neurological recovery.
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spelling pubmed-44162592015-05-02 Acute kidney injury after cardiac arrest Tujjar, Omar Mineo, Giulia Dell’Anna, Antonio Poyatos-Robles, Belen Donadello, Katia Scolletta, Sabino Vincent, Jean-Louis Taccone, Fabio Silvio Crit Care Research INTRODUCTION: The aim of this study was to evaluate the incidence and determinants of AKI in a large cohort of cardiac arrest patients. METHODS: We reviewed all patients admitted, for at least 48 hours, to our Dept. of Intensive Care after CA between January 2008 and October 2012. AKI was defined as oligo-anuria (daily urine output <0.5 ml/kg/h) and/or an increase in serum creatinine (≥0.3 mg/dl from admission value within 48 hours or a 1.5 time from baseline level). Demographics, comorbidities, CA details, and ICU interventions were recorded. Neurological outcome was assessed at 3 months using the Cerebral Performance Category scale (CPC 1–2 = favorable outcome; 3–5 = poor outcome). RESULTS: A total of 199 patients were included, 85 (43%) of whom developed AKI during the ICU stay. Independent predictors of AKI development were older age, chronic renal disease, higher dose of epinephrine, in-hospital CA, presence of shock during the ICU stay, a low creatinine clearance (CrCl) on admission and a high cumulative fluid balance at 48 hours. Patients with AKI had higher hospital mortality (55/85 vs. 57/114, p = 0.04), but AKI was not an independent predictor of poor 3-month neurological outcome. CONCLUSIONS: AKI occurred in more than 40% of patients after CA. These patients had more severe hemodynamic impairment and needed more aggressive ICU therapy; however the development of AKI did not influence neurological recovery. BioMed Central 2015-04-17 2015 /pmc/articles/PMC4416259/ /pubmed/25887258 http://dx.doi.org/10.1186/s13054-015-0900-2 Text en © Tujjar et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Tujjar, Omar
Mineo, Giulia
Dell’Anna, Antonio
Poyatos-Robles, Belen
Donadello, Katia
Scolletta, Sabino
Vincent, Jean-Louis
Taccone, Fabio Silvio
Acute kidney injury after cardiac arrest
title Acute kidney injury after cardiac arrest
title_full Acute kidney injury after cardiac arrest
title_fullStr Acute kidney injury after cardiac arrest
title_full_unstemmed Acute kidney injury after cardiac arrest
title_short Acute kidney injury after cardiac arrest
title_sort acute kidney injury after cardiac arrest
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4416259/
https://www.ncbi.nlm.nih.gov/pubmed/25887258
http://dx.doi.org/10.1186/s13054-015-0900-2
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