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The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study

BACKGROUND: The aim was to investigate whether the use of N-acetylcysteine and ascorbic acid reduce contrast-induced nephropathy incidence in critical care patients. METHODS: This was a one-center, two-arm, prospective, randomized, open-label, controlled trial in the Intensive Care Unit of the Unive...

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Autores principales: Palli, Eleni, Makris, Demosthenes, Papanikolaou, John, Garoufalis, Grigorios, Tsilioni, Irini, Zygoulis, Paris, Zakynthinos, Epaminondas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664844/
https://www.ncbi.nlm.nih.gov/pubmed/29089038
http://dx.doi.org/10.1186/s13054-017-1862-3
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author Palli, Eleni
Makris, Demosthenes
Papanikolaou, John
Garoufalis, Grigorios
Tsilioni, Irini
Zygoulis, Paris
Zakynthinos, Epaminondas
author_facet Palli, Eleni
Makris, Demosthenes
Papanikolaou, John
Garoufalis, Grigorios
Tsilioni, Irini
Zygoulis, Paris
Zakynthinos, Epaminondas
author_sort Palli, Eleni
collection PubMed
description BACKGROUND: The aim was to investigate whether the use of N-acetylcysteine and ascorbic acid reduce contrast-induced nephropathy incidence in critical care patients. METHODS: This was a one-center, two-arm, prospective, randomized, open-label, controlled trial in the Intensive Care Unit of the University Hospital of Larissa, Greece. Patients with stable renal function, who underwent non urgent contrast-enhanced computed tomography for diagnostic purposes, were included in the study. Patients in the treatment group (NacA, n = 60) received intravenously N-acetylcysteine (1200 mg) and ascorbic acid (2 g) dissolved separately in 100 ml of normal saline 2 hours before, and at 10 hours and 18 hours following the infusion of contrast agent, while control group patients (CG, n = 64) received only normal saline. All patients received additional hydration. Contrast-induced nephropathy was defined as relative increase by 25% of the baseline values of serum creatinine. RESULTS: Contrast-induced nephropathy in NacA and CG were 18.33% and 15.6%, respectively (p = 0.81). The percentage change median (interquartile range (IR)) of serum cystatin-C (mg/L) from baseline in patients who underwent contrast-induced tomography, were 37.23% (28.53) and 93.20% (46.90) in NacA and in CG, respectively (p = 0.03). The 8-isoprostane serum levels in NacA were significantly lower compared to CG at 2 hours (p = 0.012) and 24 hours (p = 0.006) following radiocontrast infusion. Multivariate analysis revealed that contrast-induced nephropathy was independently associated with a higher baseline ratio of serum urea/creatinine (odds ratio, 1.02; 95 CI%, 1.00–1.05) and with the use of nephrotoxic medications (odds ratio, 0.24; 95 CI%, 0.06–0.94). CONCLUSION: Intravenous administration of N-acetylcysteine and ascorbic acid failed to reduce contrast-induced nephropathy in critically ill patients who underwent contrast-enhanced computed tomography, despite a significant reduction of 8-isoprostane levels in treated patients. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01017796. Registered on 20 November 2009. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13054-017-1862-3) contains supplementary material, which is available to authorized users.
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spelling pubmed-56648442017-11-08 The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study Palli, Eleni Makris, Demosthenes Papanikolaou, John Garoufalis, Grigorios Tsilioni, Irini Zygoulis, Paris Zakynthinos, Epaminondas Crit Care Research BACKGROUND: The aim was to investigate whether the use of N-acetylcysteine and ascorbic acid reduce contrast-induced nephropathy incidence in critical care patients. METHODS: This was a one-center, two-arm, prospective, randomized, open-label, controlled trial in the Intensive Care Unit of the University Hospital of Larissa, Greece. Patients with stable renal function, who underwent non urgent contrast-enhanced computed tomography for diagnostic purposes, were included in the study. Patients in the treatment group (NacA, n = 60) received intravenously N-acetylcysteine (1200 mg) and ascorbic acid (2 g) dissolved separately in 100 ml of normal saline 2 hours before, and at 10 hours and 18 hours following the infusion of contrast agent, while control group patients (CG, n = 64) received only normal saline. All patients received additional hydration. Contrast-induced nephropathy was defined as relative increase by 25% of the baseline values of serum creatinine. RESULTS: Contrast-induced nephropathy in NacA and CG were 18.33% and 15.6%, respectively (p = 0.81). The percentage change median (interquartile range (IR)) of serum cystatin-C (mg/L) from baseline in patients who underwent contrast-induced tomography, were 37.23% (28.53) and 93.20% (46.90) in NacA and in CG, respectively (p = 0.03). The 8-isoprostane serum levels in NacA were significantly lower compared to CG at 2 hours (p = 0.012) and 24 hours (p = 0.006) following radiocontrast infusion. Multivariate analysis revealed that contrast-induced nephropathy was independently associated with a higher baseline ratio of serum urea/creatinine (odds ratio, 1.02; 95 CI%, 1.00–1.05) and with the use of nephrotoxic medications (odds ratio, 0.24; 95 CI%, 0.06–0.94). CONCLUSION: Intravenous administration of N-acetylcysteine and ascorbic acid failed to reduce contrast-induced nephropathy in critically ill patients who underwent contrast-enhanced computed tomography, despite a significant reduction of 8-isoprostane levels in treated patients. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01017796. Registered on 20 November 2009. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13054-017-1862-3) contains supplementary material, which is available to authorized users. BioMed Central 2017-10-31 /pmc/articles/PMC5664844/ /pubmed/29089038 http://dx.doi.org/10.1186/s13054-017-1862-3 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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
Palli, Eleni
Makris, Demosthenes
Papanikolaou, John
Garoufalis, Grigorios
Tsilioni, Irini
Zygoulis, Paris
Zakynthinos, Epaminondas
The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study
title The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study
title_full The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study
title_fullStr The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study
title_full_unstemmed The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study
title_short The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study
title_sort impact of n-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664844/
https://www.ncbi.nlm.nih.gov/pubmed/29089038
http://dx.doi.org/10.1186/s13054-017-1862-3
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