Tumour necrosis factor-alpha plus interleukin-10 low producer phenotype predicts acute kidney injury and death in intensive care unit patients
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , , , , , , |
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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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 |
|
_version_ |
1802764169745793024 |