Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Jornal Brasileiro de Nefrologia |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000200105 |
Resumo: | ABSTRACT Introduction: Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4. Methods: We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium. Results: Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W. Conclusions: TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4. |
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Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal modelkidney diseasescardio-renal syndrometissue microarray, cardiac biomarkersABSTRACT Introduction: Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4. Methods: We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium. Results: Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W. Conclusions: TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4.Sociedade Brasileira de Nefrologia2018-06-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000200105Brazilian Journal of Nephrology v.40 n.2 2018reponame:Jornal Brasileiro de Nefrologiainstname:Sociedade Brasileira de Nefrologia (SBN)instacron:SBN10.1590/2175-8239-jbn-3878info:eu-repo/semantics/openAccessDionísio,Laura MattanaLuvizoto,Mateus JustiGribner,CarolineCarneiro,DanielleCarvalho,VivianeRobes,FrancieleSheidemantel,MarcosRego,FabianeNoronha,Lúcia dePecoits-Filho,RobertoHauser,Aline Borsatoeng2018-07-24T00:00:00Zoai:scielo:S0101-28002018000200105Revistahttp://www.bjn.org.br/ONGhttps://old.scielo.br/oai/scielo-oai.php||jbn@sbn.org.br2175-82390101-2800opendoar:2018-07-24T00:00Jornal Brasileiro de Nefrologia - Sociedade Brasileira de Nefrologia (SBN)false |
dc.title.none.fl_str_mv |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
title |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
spellingShingle |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model Dionísio,Laura Mattana kidney diseases cardio-renal syndrome tissue microarray, cardiac biomarkers |
title_short |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
title_full |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
title_fullStr |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
title_full_unstemmed |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
title_sort |
Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
author |
Dionísio,Laura Mattana |
author_facet |
Dionísio,Laura Mattana Luvizoto,Mateus Justi Gribner,Caroline Carneiro,Danielle Carvalho,Viviane Robes,Franciele Sheidemantel,Marcos Rego,Fabiane Noronha,Lúcia de Pecoits-Filho,Roberto Hauser,Aline Borsato |
author_role |
author |
author2 |
Luvizoto,Mateus Justi Gribner,Caroline Carneiro,Danielle Carvalho,Viviane Robes,Franciele Sheidemantel,Marcos Rego,Fabiane Noronha,Lúcia de Pecoits-Filho,Roberto Hauser,Aline Borsato |
author2_role |
author author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Dionísio,Laura Mattana Luvizoto,Mateus Justi Gribner,Caroline Carneiro,Danielle Carvalho,Viviane Robes,Franciele Sheidemantel,Marcos Rego,Fabiane Noronha,Lúcia de Pecoits-Filho,Roberto Hauser,Aline Borsato |
dc.subject.por.fl_str_mv |
kidney diseases cardio-renal syndrome tissue microarray, cardiac biomarkers |
topic |
kidney diseases cardio-renal syndrome tissue microarray, cardiac biomarkers |
description |
ABSTRACT Introduction: Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4. Methods: We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium. Results: Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W. Conclusions: TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-06-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000200105 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002018000200105 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/2175-8239-jbn-3878 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Nefrologia |
publisher.none.fl_str_mv |
Sociedade Brasileira de Nefrologia |
dc.source.none.fl_str_mv |
Brazilian Journal of Nephrology v.40 n.2 2018 reponame:Jornal Brasileiro de Nefrologia instname:Sociedade Brasileira de Nefrologia (SBN) instacron:SBN |
instname_str |
Sociedade Brasileira de Nefrologia (SBN) |
instacron_str |
SBN |
institution |
SBN |
reponame_str |
Jornal Brasileiro de Nefrologia |
collection |
Jornal Brasileiro de Nefrologia |
repository.name.fl_str_mv |
Jornal Brasileiro de Nefrologia - Sociedade Brasileira de Nefrologia (SBN) |
repository.mail.fl_str_mv |
||jbn@sbn.org.br |
_version_ |
1752122064741859328 |