Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis
SARS-CoV-2 may impair host antiviral response, causing subsequent hyperinflammation.
•
SARS-CoV-2 likely deranges the renin angiotensin aldosterone system (RAAS).
•
Hyperinflammation and RAAS imbalance may drive acute lung injury and coagulopathy.
•
RAAS imbalance impairs fibrinolysis, which can result in relative hypofibrinolysis.
•
This can lead widespread immunothrombosis, contributing to multi-organ damage.
Abstract
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.
