AKI in COVID-19 patients could be mediated by innate immune system over-activation, cytokine release, complement activation, angiotensin II (Ang II) hyperactivity, development of a hypercoagulable state, hypovolemia secondary to excessive diuresis, and/or increased venous pressure secondary to high positive pressure at the end of expiration [45,47]. Here, AGT is linked to COVID-19.