Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis

Brandon Michael Henry, Jens Vikse, Stefanie Benoit, Emmanuel J. Favaloro, Giuseppe Lippi

Research output: Contribution to journalComment/debate

47 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)167-173
Number of pages7
JournalClinica Chimica Acta
Volume507
Early online date26 Apr 2020
DOIs
Publication statusPublished - Aug 2020

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