Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients

Detalhes bibliográficos
Autor(a) principal: Dalboni, Maria Aparecida [UNIFESP]
Data de Publicação: 2013
Outros Autores: Quinto, B. M. R. [UNIFESP], Grabulosa, C. C. [UNIFESP], Narciso, R. [UNIFESP], Monte, J. C. [UNIFESP], Durao, M. [UNIFESP], Rizzo, L. [UNIFESP], Cendoroglo, M. [UNIFESP], Santos, O. P. [UNIFESP], Batista, M. C. [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/36561
http://dx.doi.org/10.1111/cei.12100
Resumo: Genetic polymorphism studies of cytokines may provide an insight into the understanding of acute kidney injury (AKI) and death in intensive care unit (ICU) patients. the aim of this study was to investigate whether the genetic polymorphisms of -308 G < A tumour necrosis factor (TNF)-alpha, - 174 G > C interleukin (IL)- 6 and - 1082 G > A IL- 10 may predispose ICU patients to the development of AKI and/or death. in a prospective nested case-control study, 303 ICU patients and 244 healthy individuals were evaluated. the study group included ICU patients who developed AKI (n = 139) and 164 ICU patients without AKI. the GG genotype of TNF-alpha (low producer phenotype) was significantly lower in the with AKI than without AKI groups and healthy individuals (55 versus 62 versus 73%, respectively; P = 0.01). When genotypes were stratified into four categories of TNF-alpha/IL-10 combinations, it was observed that low TNF-a plus low IL- 10 producer phenotypes were more prevalent in patients with AKI, renal replacement therapy and death (P < 0.05). in logistic regression analysis, low TNF-alpha producer plus low IL-10 producer phenotypes remained as independent risk factors for AKI and/or death [ odds ratio (OR) = 2.37, 95% confidence interval (CI): 1.16- 4.84; P = 0.02] and for renal replacement therapy (RRT) and/or death (OR = 3.82, 95% CI: 1.19- 12.23; P = 0.02). in this study, the combination of low TNF-alpha plus low IL- 10 producer phenotypes was an independent risk factor to AKI and/or death and RRT and/or death in critically ill patients. Our results should be validated in a larger prospective study with long- term follow- up to emphasize the combination of these genotypes as potential risk factors to AKI in critically ill patients.
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spelling Dalboni, Maria Aparecida [UNIFESP]Quinto, B. M. R. [UNIFESP]Grabulosa, C. C. [UNIFESP]Narciso, R. [UNIFESP]Monte, J. C. [UNIFESP]Durao, M. [UNIFESP]Rizzo, L. [UNIFESP]Cendoroglo, M. [UNIFESP]Santos, O. P. [UNIFESP]Batista, M. C. [UNIFESP]Universidade Federal de São Paulo (UNIFESP)Tufts Univ New England Med Ctr2016-01-24T14:32:01Z2016-01-24T14:32:01Z2013-08-01Clinical and Experimental Immunology. Hoboken: Wiley-Blackwell, v. 173, n. 2, p. 242-249, 2013.0009-9104http://repositorio.unifesp.br/handle/11600/36561http://dx.doi.org/10.1111/cei.1210010.1111/cei.12100WOS:000321287500009Genetic polymorphism studies of cytokines may provide an insight into the understanding of acute kidney injury (AKI) and death in intensive care unit (ICU) patients. the aim of this study was to investigate whether the genetic polymorphisms of -308 G < A tumour necrosis factor (TNF)-alpha, - 174 G > C interleukin (IL)- 6 and - 1082 G > A IL- 10 may predispose ICU patients to the development of AKI and/or death. in a prospective nested case-control study, 303 ICU patients and 244 healthy individuals were evaluated. the study group included ICU patients who developed AKI (n = 139) and 164 ICU patients without AKI. the GG genotype of TNF-alpha (low producer phenotype) was significantly lower in the with AKI than without AKI groups and healthy individuals (55 versus 62 versus 73%, respectively; P = 0.01). When genotypes were stratified into four categories of TNF-alpha/IL-10 combinations, it was observed that low TNF-a plus low IL- 10 producer phenotypes were more prevalent in patients with AKI, renal replacement therapy and death (P < 0.05). in logistic regression analysis, low TNF-alpha producer plus low IL-10 producer phenotypes remained as independent risk factors for AKI and/or death [ odds ratio (OR) = 2.37, 95% confidence interval (CI): 1.16- 4.84; P = 0.02] and for renal replacement therapy (RRT) and/or death (OR = 3.82, 95% CI: 1.19- 12.23; P = 0.02). in this study, the combination of low TNF-alpha plus low IL- 10 producer phenotypes was an independent risk factor to AKI and/or death and RRT and/or death in critically ill patients. Our results should be validated in a larger prospective study with long- term follow- up to emphasize the combination of these genotypes as potential risk factors to AKI in critically ill patients.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo, Hosp Israelita Albert Einstein, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, BR-04039032 São Paulo, BrazilTufts Univ New England Med Ctr, Boston, MA USAUniversidade Federal de São Paulo, Hosp Israelita Albert Einstein, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, BR-04039032 São Paulo, BrazilFAPESP: 07/58363-0FAPESP: 05/59242-7Web of Science242-249engWiley-BlackwellClinical and Experimental Immunologyhttp://olabout.wiley.com/WileyCDA/Section/id-406071.htmlinfo:eu-repo/semantics/openAccesscytokinesinterleukinspolymorphismrenal immunologydiseaseTumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patientsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/365612022-09-27 11:18:56.577metadata only accessoai:repositorio.unifesp.br:11600/36561Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-09-27T14:18:56Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
title Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
spellingShingle Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
Dalboni, Maria Aparecida [UNIFESP]
cytokines
interleukins
polymorphism
renal immunology
disease
title_short Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
title_full Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
title_fullStr Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
title_full_unstemmed Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
title_sort Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
author Dalboni, Maria Aparecida [UNIFESP]
author_facet Dalboni, Maria Aparecida [UNIFESP]
Quinto, B. M. R. [UNIFESP]
Grabulosa, C. C. [UNIFESP]
Narciso, R. [UNIFESP]
Monte, J. C. [UNIFESP]
Durao, M. [UNIFESP]
Rizzo, L. [UNIFESP]
Cendoroglo, M. [UNIFESP]
Santos, O. P. [UNIFESP]
Batista, M. C. [UNIFESP]
author_role author
author2 Quinto, B. M. R. [UNIFESP]
Grabulosa, C. C. [UNIFESP]
Narciso, R. [UNIFESP]
Monte, J. C. [UNIFESP]
Durao, M. [UNIFESP]
Rizzo, L. [UNIFESP]
Cendoroglo, M. [UNIFESP]
Santos, O. P. [UNIFESP]
Batista, M. C. [UNIFESP]
author2_role author
author
author
author
author
author
author
author
author
dc.contributor.institution.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
Tufts Univ New England Med Ctr
dc.contributor.author.fl_str_mv Dalboni, Maria Aparecida [UNIFESP]
Quinto, B. M. R. [UNIFESP]
Grabulosa, C. C. [UNIFESP]
Narciso, R. [UNIFESP]
Monte, J. C. [UNIFESP]
Durao, M. [UNIFESP]
Rizzo, L. [UNIFESP]
Cendoroglo, M. [UNIFESP]
Santos, O. P. [UNIFESP]
Batista, M. C. [UNIFESP]
dc.subject.eng.fl_str_mv cytokines
interleukins
polymorphism
renal immunology
disease
topic cytokines
interleukins
polymorphism
renal immunology
disease
description Genetic polymorphism studies of cytokines may provide an insight into the understanding of acute kidney injury (AKI) and death in intensive care unit (ICU) patients. the aim of this study was to investigate whether the genetic polymorphisms of -308 G < A tumour necrosis factor (TNF)-alpha, - 174 G > C interleukin (IL)- 6 and - 1082 G > A IL- 10 may predispose ICU patients to the development of AKI and/or death. in a prospective nested case-control study, 303 ICU patients and 244 healthy individuals were evaluated. the study group included ICU patients who developed AKI (n = 139) and 164 ICU patients without AKI. the GG genotype of TNF-alpha (low producer phenotype) was significantly lower in the with AKI than without AKI groups and healthy individuals (55 versus 62 versus 73%, respectively; P = 0.01). When genotypes were stratified into four categories of TNF-alpha/IL-10 combinations, it was observed that low TNF-a plus low IL- 10 producer phenotypes were more prevalent in patients with AKI, renal replacement therapy and death (P < 0.05). in logistic regression analysis, low TNF-alpha producer plus low IL-10 producer phenotypes remained as independent risk factors for AKI and/or death [ odds ratio (OR) = 2.37, 95% confidence interval (CI): 1.16- 4.84; P = 0.02] and for renal replacement therapy (RRT) and/or death (OR = 3.82, 95% CI: 1.19- 12.23; P = 0.02). in this study, the combination of low TNF-alpha plus low IL- 10 producer phenotypes was an independent risk factor to AKI and/or death and RRT and/or death in critically ill patients. Our results should be validated in a larger prospective study with long- term follow- up to emphasize the combination of these genotypes as potential risk factors to AKI in critically ill patients.
publishDate 2013
dc.date.issued.fl_str_mv 2013-08-01
dc.date.accessioned.fl_str_mv 2016-01-24T14:32:01Z
dc.date.available.fl_str_mv 2016-01-24T14:32:01Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.citation.fl_str_mv Clinical and Experimental Immunology. Hoboken: Wiley-Blackwell, v. 173, n. 2, p. 242-249, 2013.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/36561
http://dx.doi.org/10.1111/cei.12100
dc.identifier.issn.none.fl_str_mv 0009-9104
dc.identifier.doi.none.fl_str_mv 10.1111/cei.12100
dc.identifier.wos.none.fl_str_mv WOS:000321287500009
identifier_str_mv Clinical and Experimental Immunology. Hoboken: Wiley-Blackwell, v. 173, n. 2, p. 242-249, 2013.
0009-9104
10.1111/cei.12100
WOS:000321287500009
url http://repositorio.unifesp.br/handle/11600/36561
http://dx.doi.org/10.1111/cei.12100
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Clinical and Experimental Immunology
dc.rights.driver.fl_str_mv http://olabout.wiley.com/WileyCDA/Section/id-406071.html
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://olabout.wiley.com/WileyCDA/Section/id-406071.html
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 242-249
dc.publisher.none.fl_str_mv Wiley-Blackwell
publisher.none.fl_str_mv Wiley-Blackwell
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv
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