COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Anais da Academia Brasileira de Ciências (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652022000700712 |
Resumo: | Abstract COVID-19 is a pandemic disease caused by the SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) responsible for millions of deaths worldwide. Although the respiratory system is the main target of COVID-19, the disease can affect other organs, including the kidneys. Acute Kidney Injury (AKI), commonly seen in patients infected with COVID-19, has a multifactorial cause. Several studies associate this injury with the direct involvement of the virus in renal cells and the indirect damage stimulated by the infection. The direct cytopathic effects of SARS-CoV-2 are due to the entry and replication of the virus in renal cells, changing several regulatory pathways, especially the renin-angiotensin-aldosterone system (RAAS), with repercussions on the kallikrein-kinin system (KKS). Furthermore, the virus can deregulate the immune system, leading to an exaggerated response of inflammatory cells, characterizing the state of hypercytokinemia. The such exaggerated inflammatory response is commonly associated with hemodynamic changes, reduced renal perfusion, tissue hypoxia, generation of reactive oxygen species (ROS), endothelial damage, and coagulopathies, which can result in severe damage to the renal parenchyma. Thereby, understanding the molecular mechanisms and pathophysiology of kidney injuries induced by SARS-COV-2 is of fundamental importance to obtaining new therapeutic insights for the prevention and management of AKI. |
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COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion DevelopmentAcute kidney injuryangiotensincoronavirusinflammationSARS-CoV-2Abstract COVID-19 is a pandemic disease caused by the SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) responsible for millions of deaths worldwide. Although the respiratory system is the main target of COVID-19, the disease can affect other organs, including the kidneys. Acute Kidney Injury (AKI), commonly seen in patients infected with COVID-19, has a multifactorial cause. Several studies associate this injury with the direct involvement of the virus in renal cells and the indirect damage stimulated by the infection. The direct cytopathic effects of SARS-CoV-2 are due to the entry and replication of the virus in renal cells, changing several regulatory pathways, especially the renin-angiotensin-aldosterone system (RAAS), with repercussions on the kallikrein-kinin system (KKS). Furthermore, the virus can deregulate the immune system, leading to an exaggerated response of inflammatory cells, characterizing the state of hypercytokinemia. The such exaggerated inflammatory response is commonly associated with hemodynamic changes, reduced renal perfusion, tissue hypoxia, generation of reactive oxygen species (ROS), endothelial damage, and coagulopathies, which can result in severe damage to the renal parenchyma. Thereby, understanding the molecular mechanisms and pathophysiology of kidney injuries induced by SARS-COV-2 is of fundamental importance to obtaining new therapeutic insights for the prevention and management of AKI.Academia Brasileira de Ciências2022-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652022000700712Anais da Academia Brasileira de Ciências v.94 suppl.3 2022reponame:Anais da Academia Brasileira de Ciências (Online)instname:Academia Brasileira de Ciências (ABC)instacron:ABC10.1590/0001-3765202220211501info:eu-repo/semantics/openAccessSILVA,ANTÔNIO V.B. DACAMPANATI,JOÃO DE A.G.BARCELOS,ISADORA DE S.SANTOS,ALBERTO C.L.DEUS,UILDSON P. DESOARES,TELMA DE J.AMARAL,LILIANY S. DE B.eng2022-12-02T00:00:00Zoai:scielo:S0001-37652022000700712Revistahttp://www.scielo.br/aabchttps://old.scielo.br/oai/scielo-oai.php||aabc@abc.org.br1678-26900001-3765opendoar:2022-12-02T00:00Anais da Academia Brasileira de Ciências (Online) - Academia Brasileira de Ciências (ABC)false |
dc.title.none.fl_str_mv |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development |
title |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development |
spellingShingle |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development SILVA,ANTÔNIO V.B. DA Acute kidney injury angiotensin coronavirus inflammation SARS-CoV-2 |
title_short |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development |
title_full |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development |
title_fullStr |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development |
title_full_unstemmed |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development |
title_sort |
COVID-19 and Acute Kidney Injury ― Direct and Indirect Pathophysiological Mechanisms Underlying Lesion Development |
author |
SILVA,ANTÔNIO V.B. DA |
author_facet |
SILVA,ANTÔNIO V.B. DA CAMPANATI,JOÃO DE A.G. BARCELOS,ISADORA DE S. SANTOS,ALBERTO C.L. DEUS,UILDSON P. DE SOARES,TELMA DE J. AMARAL,LILIANY S. DE B. |
author_role |
author |
author2 |
CAMPANATI,JOÃO DE A.G. BARCELOS,ISADORA DE S. SANTOS,ALBERTO C.L. DEUS,UILDSON P. DE SOARES,TELMA DE J. AMARAL,LILIANY S. DE B. |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
SILVA,ANTÔNIO V.B. DA CAMPANATI,JOÃO DE A.G. BARCELOS,ISADORA DE S. SANTOS,ALBERTO C.L. DEUS,UILDSON P. DE SOARES,TELMA DE J. AMARAL,LILIANY S. DE B. |
dc.subject.por.fl_str_mv |
Acute kidney injury angiotensin coronavirus inflammation SARS-CoV-2 |
topic |
Acute kidney injury angiotensin coronavirus inflammation SARS-CoV-2 |
description |
Abstract COVID-19 is a pandemic disease caused by the SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) responsible for millions of deaths worldwide. Although the respiratory system is the main target of COVID-19, the disease can affect other organs, including the kidneys. Acute Kidney Injury (AKI), commonly seen in patients infected with COVID-19, has a multifactorial cause. Several studies associate this injury with the direct involvement of the virus in renal cells and the indirect damage stimulated by the infection. The direct cytopathic effects of SARS-CoV-2 are due to the entry and replication of the virus in renal cells, changing several regulatory pathways, especially the renin-angiotensin-aldosterone system (RAAS), with repercussions on the kallikrein-kinin system (KKS). Furthermore, the virus can deregulate the immune system, leading to an exaggerated response of inflammatory cells, characterizing the state of hypercytokinemia. The such exaggerated inflammatory response is commonly associated with hemodynamic changes, reduced renal perfusion, tissue hypoxia, generation of reactive oxygen species (ROS), endothelial damage, and coagulopathies, which can result in severe damage to the renal parenchyma. Thereby, understanding the molecular mechanisms and pathophysiology of kidney injuries induced by SARS-COV-2 is of fundamental importance to obtaining new therapeutic insights for the prevention and management of AKI. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-01-01 |
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=S0001-37652022000700712 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652022000700712 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/0001-3765202220211501 |
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 |
Academia Brasileira de Ciências |
publisher.none.fl_str_mv |
Academia Brasileira de Ciências |
dc.source.none.fl_str_mv |
Anais da Academia Brasileira de Ciências v.94 suppl.3 2022 reponame:Anais da Academia Brasileira de Ciências (Online) instname:Academia Brasileira de Ciências (ABC) instacron:ABC |
instname_str |
Academia Brasileira de Ciências (ABC) |
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ABC |
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ABC |
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Anais da Academia Brasileira de Ciências (Online) |
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Anais da Academia Brasileira de Ciências (Online) |
repository.name.fl_str_mv |
Anais da Academia Brasileira de Ciências (Online) - Academia Brasileira de Ciências (ABC) |
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||aabc@abc.org.br |
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