Introduction
COVID-19, the largest pandemic of the modern world, has surpassed its
predecessors SARS and MERS by miles. What started in Wuhan, China, has
spread worldwide within four months. It has infected over three million
people and has claimed over two hundred thousand lives. COVID-19 is
characterized by fever, cough, shortness of breath, myalgia, and
headache. The disease also takes a more severe form with
life-threatening manifestations of acute respiratory distress syndrome
(ARDS), acute cardiac injury, acute kidney injury, disseminated
intravascular coagulopathy, and cytokine storm.
Risk factors that tend to make individuals susceptible to severe disease
include older age and co-morbidities such as hypertension, diabetes, and
pre-existing heart disease.1 Another aspect of the
course that has been noted is the rapid deterioration of apparently
stable individuals within a matter of hours. This observation might call
into consideration a positive feedback loop in the pathogenesis of the
disease.
It has been elucidated that like its predecessor, the SARS CoV, the SARS
CoV-2 utilizes the ACE2 receptor to enter cells.2 This
knowledge brought into speculation the effects of a dysregulated
Renin-Angiotensin system (RAS) in the pathogenesis of COVID-19. It has
been proposed that the effects of a dysregulated RAS would lead to an
inflammatory cascade and contribute to the cytokine storm that is
central to the disease.3 This paper looks at the RAS
pathway and the possibility of a positive RAS feedback loop in the
pathogenesis of COVID-19.