The suggested pathophysiology of AKI in COVID currently relies on nonspecific mechanisms (hypovolemia, nephrotoxic drugs, high PEEP, right heart failure), direct viral injury, imbalanced renin–angiotensin–aldosterone system (RAAS) activation, elevation of proinflammatory cytokines elicited by viral infection, and a profound procoagulant state [14,16]. This evidence concerns the gene REN and viral infectious disease.