COL4A3 and nephritis: Similarly to Streptococcus- and influenza-induced anti-GBM nephritis, the severe endothelial damage from SARS-CoV-2 could conceivably expose basement membrane antigens (e.g., Goodpasture antigen) in the respiratory tract and renal tissue; epitope similarity would then cause autoantibodies to attack glomeruli (96, 108).