English 
Italian Iper-infiammazione e squilibrio del sistema renina-angiotensina-aldosterone in corso di COVID-19: una nuova ipotesi per il sospetto clinico di ipercoagulabilità e immuno-trombosi microvascolare
Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis
AUTORI
1Cardiac Intensive Care Unit, The Heart Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, USA
2Clinical Immunology Unit, Stavanger University Hospital, Stavanger, Norway
3Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
4Department of Pediatrics, University of Cincinnati, College of Medicine, Cincinnati, OH, USA
5Department of Haematology, Sydney Centres for Thrombosis and Haemostasis, Institute of Clinical Pathology and Medical Research, NSW Health Pathology, Westmead Hospital, Westmead, New South Wales, Australia
6School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, New South Wales, Australia
7Section of Clinical Biochemistry, Department of Neuroscience, Biomedicine and Movement, University of Verona, Verona, Italy
ABSTRACT
Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis.
Early clinical evidence suggests that severe cases of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are frequently characterized by hyperinflammation, imbalance of renin-angiotensin-aldosterone system, and a particular form of vasculopathy, thrombotic microangiopathy, and intravascular coagulopathy. In this paper, we present an immunothrombosis model of COVID-19. We discuss the underlying pathogenesis and the interaction between multiple systems, resulting in propagation of immunothrombosis, which through investigation in the coming weeks, may lead to both an improved understanding of COVID-19 pathophysiology and identification of innovative and efficient therapeutic targets to reverse the otherwise unfavorable clinical outcome of many of these patients.