Conclusion
A dysregulated RAS axis is central to the pathogenesis of COVID-19. The
rapid deterioration of patients and the existence of severe
manifestations, call into question the presence of a positive feedback
loop (or the suppression of negative feedback). The existence of such a
loop in RAS might warrant an investigation into the peptides present
higher up in the pathway such as renin and prorenin. Knowledge about the
functions of these molecules and their role in disease is still in its
infancy. This paper has tried to elucidate possible mechanisms for the
involvement of RAS in the pathogenesis of COVID-19.
Most of the studies discussed have delved into RAS as a mediator for
hypertension, cardiovascular disease, and kidney disease. We believe
that their results may be extrapolated into the acute context of RAS
disruption in COVID-19. The lack of severe activation with positive
feedback does not exist in the context of chronic diseases like
hypertension; Though the existence of renal crisis in scleroderma and
sympathetic crashing acute pulmonary edema might indicate otherwise. The
reason for this ”RAS-crisis” in the context of COVID-19 is beyond us,
but we imagine is worth considering.