A recent New England Journal of Medicine article proposed "endothelialitis" as the unifying mechanism for the widespread pathology of COVID-19. In a prior Medscape interview, Medscape contributor Andrew N. Wilner, MD, discussed this intriguing hypothesis with William Li, MD, one of the article's authors.
An alternative view suggests that virus-induced upregulation of the renin-angiotensin system (RAS) — a hormonal network that regulates blood pressure fluid, and electrolytes — accounts for the diverse systemic effects of COVID-19. Maureen Czick, MD, a proponent of this theory, is an anesthesiologist at the University of Connecticut with an academic interest in cell biology and coronavirus pathophysiology. Dr Czick was kind enough to share her insights in an email interview with Dr Wilner.
What is your medical background and experience with COVID-19? How did you come up with this concept around the RAS?
When I was in the middle of my first year of anesthesiology residency in 2003, the original SARS coronavirus struck East Asia. One of my mentors, Dr Joseph McIsaac, an expert on hospital preparedness for epidemics and mass casualties, told me then, "Pay attention to this thing, because it'll be back." So I began to follow the SARS basic science research, especially the emerging work on angiotensin-converting enzyme (ACE) 2, which helped me understand that the RAS has extensive physiologic reach, much more than just blood pressure regulation.
