Pathophysiological changes in RAAS due to distressed ACE-2 levels in patients with comorbid COVID-19 tend to show undesired outcomes, such as high levels of angiotensin II, which leads to angiogenesis, vascular aging, atherosclerosis, inflammation, and fibrosis, leading to diseases like hypertension, renal failure, and cardiac fibrosis [20]. This evidence concerns the gene AGT and acute kidney injury.