| Texto completo | |
| Autor(es): |
Cruz, Nayara Azinheira Nobrega
[1]
;
Oliveira, Lilian Caroline Goncalves de
[1]
;
Silva Junior, Helio Tedesco
[1]
;
Pestana, Jose Osmar Medina
[1]
;
Casarini, Dulce Elena
[1]
Número total de Autores: 5
|
| Afiliação do(s) autor(es): | [1] Univ Fed Sao Paulo, Escola Paulista Med, Dept Med, Div Nephrol, Sao Paulo - Brazil
Número total de Afiliações: 1
|
| Tipo de documento: | Artigo de Revisão |
| Fonte: | FRONTIERS IN PHYSIOLOGY; v. 12, AUG 23 2021. |
| Citações Web of Science: | 0 |
| Resumo | |
Coronavirus disease 2019 (COVID-19) was first reported in late December 2019 in Wuhan, China. The etiological agent of this disease is severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the high transmissibility of the virus led to its rapid global spread and a major pandemic (ongoing at the time of writing this review). The clinical manifestations of COVID-19 can vary widely from non-evident or minor symptoms to severe acute respiratory syndrome and multi-organ damage, causing death. Acute kidney injury (AKI) has been recognized as a common complication of COVID-19 and in many cases, kidney replacement therapy (KRT) is required. The presence of kidney abnormalities on hospital admission and the development of AKI are related to a more severe presentation of COVID-19 with higher mortality rate. The high transmissibility and the broad spectrum of clinical manifestations of COVID-19 are in part due to the high affinity of SARS-CoV-2 for its receptor, angiotensin (Ang)-converting enzyme 2 (ACE2), which is widely expressed in human organs and is especially abundant in the kidneys. A debate on the role of ACE2 in the infectivity and pathogenesis of COVID-19 has emerged: Does the high expression of ACE2 promotes higher infectivity and more severe clinical manifestations or does the interaction of SARS-CoV-2 with ACE2 reduce the bioavailability of the enzyme, depleting its biological activity, which is closely related to two important physiological systems, the renin-angiotensin system (RAS) and the kallikrein-kinin system (KKS), thereby further contributing to pathogenesis. In this review, we discuss the dual role of ACE2 in the infectivity and pathogenesis of COVID-19, highlighting the effects of COVID-19-induced ACE2 depletion in the renal physiology and how it may lead to kidney injury. The ACE2 downstream regulation of KKS, that usually receives less attention, is discussed. Also, a detailed discussion on how the triad of symptoms (respiratory, inflammatory, and coagulation symptoms) of COVID-19 can indirectly promote renal injury is primary aborded.</p> (AU) | |
| Processo FAPESP: | 17/17027-0 - Sistemas hormonais nas doenças renais e cardiovasculares: da biologia celular a novos paradigmas fisiológicos com avanços para a terapêutica |
| Beneficiário: | Dulce Elena Casarini |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |
| Processo FAPESP: | 18/16653-7 - Análise de alterações nos sistemas renina-angiotensina e cininas-calicreínas na Obesidade infantojuvenil e sua contribuição para complicações associadas à Obesidade |
| Beneficiário: | Nayara Azinheira Nobrega Cruz |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado Direto |
| Processo FAPESP: | 18/23953-7 - Exposômica aplicada ao perfil de metabólitos e compostos obesogênicos na urina de pré-púberes não saudáveis |
| Beneficiário: | Lilian Caroline Gonçalves de Oliveira |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |