Schematic diagram depicting interplay between SARS-CoV-2 and pneumocyte. SARS-CoV-2 gains entry into the pneumocyte using angiotensin-converting enzyme 2 (ACE2) as a receptor. ACE2 is upregulated with the prior use of angiotensin-converting enzyme inhibitors (ACEi)/angiotensin-receptor blockers (ARBs). Following entry into the pneumocyte, the virus replicates and ACE2 gets downregulated. As a result, there is reduced degradation of angiotensin-II which in turn leads to increased secretion of aldosterone and subsequent renal potassium wasting.