Severe #COVID19 induces an endotheliitis: a pseudo-vasculitis phenotype with a viral renal-lung syndrome and ARDS. Nephrologists report AKI without shock/renal hypoperfusion. Microvascular endotheliitis also explains cardiac manifestations & thrombosis https://www.thelancet.com/action/showPdf?pii=S0140-6736%2820%2930937-5

Whether the renovascular injury is primary or secondary to parenchymal injury is, however, unclear. The renal pathology shows more than simple endotheliitis with virus seen in renal tubules and podocytes as well as microthrombi. https://www.sciencedirect.com/science/article/pii/S0085253820303690

The view of severe #COVID19 as a pseudo-vasculitis explains why those pre-primed by vascular risk factors (DM, HT etc) are prone to lethal complications. Vascular risk factors produce endothelial dysfunction and promote microvesicular tissue factor driven thromboinflammation

We know that ANCA vasculitis induced immunothrombosis with a resultant increase in the rate of both venous and arterial thrombosis. The endotheliitis we are seeing in #COVID19 might produce a rapidly progressive virally driven version of the same thing https://www.ncbi.nlm.nih.gov/pubmed?term=29588079

As viral infiltration into cells is the driver of this pseudo-vasculitis we should be wary of thinking that immunosuppressive treatments for primary immunogenic vasculitis will help. It's catch-22. Any immunosuppressive drug eg Il-6 inhibitors may exacerbate the primary infection