These observations suggest that overexpression of SARS-CoV-2 N protein may mediate severe AKI under diabetic conditions by triggering the release of DAMP molecules such as HMGB1 from the necrotic tubular cells, which then may activate M1 macrophages and stimulate the production of proinflammatory cytokines to exacerbate further AKI via a Mincle-dependent mechanism. Here, HMGB1 is linked to acute kidney injury.