tetano
Editor, Senior Moderator
Nat Rev Nephrol
. 2020 Oct 19.
doi: 10.1038/s41581-020-00357-4. Online ahead of print.
Immunity, endothelial injury and complement-induced coagulopathy in COVID-19
Luca Perico[SUP] 1 [/SUP], Ariela Benigni[SUP] 1 [/SUP], Federica Casiraghi[SUP] 1 [/SUP], Lisa F P Ng[SUP] 2 3 4 [/SUP], Laurent Renia[SUP] 2 3 [/SUP], Giuseppe Remuzzi[SUP] 5 6 [/SUP]
Affiliations
Abstract
In December 2019, a novel coronavirus was isolated from the respiratory epithelium of patients with unexplained pneumonia in Wuhan, China. This pathogen, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causes a pathogenic condition that has been termed coronavirus disease 2019 (COVID-19) and has reached pandemic proportions. As of 17 September 2020, more than 30 million confirmed SARS-CoV-2 infections have been reported in 204 different countries, claiming more than 1 million lives worldwide. Accumulating evidence suggests that SARS-CoV-2 infection can lead to a variety of clinical conditions, ranging from asymptomatic to life-threatening cases. In the early stages of the disease, most patients experience mild clinical symptoms, including a high fever and dry cough. However, 20% of patients rapidly progress to severe illness characterized by atypical interstitial bilateral pneumonia, acute respiratory distress syndrome and multiorgan dysfunction. Almost 10% of these critically ill patients subsequently die. Insights into the pathogenic mechanisms underlying SARS-CoV-2 infection and COVID-19 progression are emerging and highlight the critical role of the immunological hyper-response - characterized by widespread endothelial damage, complement-induced blood clotting and systemic microangiopathy - in disease exacerbation. These insights may aid the identification of new or existing therapeutic interventions to limit the progression of early disease and treat severe cases.
. 2020 Oct 19.
doi: 10.1038/s41581-020-00357-4. Online ahead of print.
Immunity, endothelial injury and complement-induced coagulopathy in COVID-19
Luca Perico[SUP] 1 [/SUP], Ariela Benigni[SUP] 1 [/SUP], Federica Casiraghi[SUP] 1 [/SUP], Lisa F P Ng[SUP] 2 3 4 [/SUP], Laurent Renia[SUP] 2 3 [/SUP], Giuseppe Remuzzi[SUP] 5 6 [/SUP]
Affiliations
- PMID: 33077917
- DOI: 10.1038/s41581-020-00357-4
Abstract
In December 2019, a novel coronavirus was isolated from the respiratory epithelium of patients with unexplained pneumonia in Wuhan, China. This pathogen, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causes a pathogenic condition that has been termed coronavirus disease 2019 (COVID-19) and has reached pandemic proportions. As of 17 September 2020, more than 30 million confirmed SARS-CoV-2 infections have been reported in 204 different countries, claiming more than 1 million lives worldwide. Accumulating evidence suggests that SARS-CoV-2 infection can lead to a variety of clinical conditions, ranging from asymptomatic to life-threatening cases. In the early stages of the disease, most patients experience mild clinical symptoms, including a high fever and dry cough. However, 20% of patients rapidly progress to severe illness characterized by atypical interstitial bilateral pneumonia, acute respiratory distress syndrome and multiorgan dysfunction. Almost 10% of these critically ill patients subsequently die. Insights into the pathogenic mechanisms underlying SARS-CoV-2 infection and COVID-19 progression are emerging and highlight the critical role of the immunological hyper-response - characterized by widespread endothelial damage, complement-induced blood clotting and systemic microangiopathy - in disease exacerbation. These insights may aid the identification of new or existing therapeutic interventions to limit the progression of early disease and treat severe cases.