Author:
Camargo Rafael L.,Bombassaro Bruna,Monfort-Pires Milena,Mansour Eli,Palma Andre C.,Ribeiro Luciana C.,Ulaf Raisa G.,Bernardes Ana Flavia,Nunes Thyago A.,Agrela Marcus V.,Dertkigil Rachel P.,Dertkigil Sergio S.,Araujo Eliana P.,Nadruz Wilson,Moretti Maria Luiza,Velloso Licio A.,Sposito Andrei C.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) employs angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entrance, and studies have suggested that upon viral binding, ACE2 catalytic activity could be inhibited; therefore, impacting the regulation of the renin-angiotensin-aldosterone system (RAAS). To date, only few studies have evaluated the impact of SARS-CoV-2 infection on the blood levels of the components of the RAAS. The objective of this study was to determine the blood levels of ACE, ACE2, angiotensin-II, angiotensin (1–7), and angiotensin (1–9) at hospital admission and discharge in a group of patients presenting with severe or critical evolution of coronavirus disease 2019 (COVID-19). We showed that ACE, ACE2, angiotensin (1–7), and angiotensin (1–9) were similar in patients with critical and severe COVID-19. However, at admission, angiotensin-II levels were significantly higher in patients presenting as critical, compared to patients presenting with severe COVID-19. We conclude that blood levels of angiotensin-II are increased in hospitalized patients with COVID-19 presenting the critical outcome of the disease. We propose that early measurement of Ang-II could be a useful biomarker for identifying patients at higher risk for extremely severe progression of the disease.
Funder
Fundação de Amparo à Pesquisa do Estado de São Paulo
Subject
Cardiology and Cardiovascular Medicine
Cited by
23 articles.
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