Direct viral invasion of kidney cells occurs through the ACE2 receptor on endothelial cells and podocytes resulting in endothelial dysfunction and nephritis, inciting a hyperinflammatory response, hypercoagulability, and complement activation.30,31 Indirect renal consequences of COVID-19 may relate to hemodynamic instability in severe disease, organ cross-talk, activation of the renin-angiotensin-aldosterone system, rhabdomyolysis and sepsis or acute respiratory distress syndrome-associated AKI.30,31. Here, REN is linked to nephritis.