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.