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.