Classic microscopic features of<unk>  include inflammation of blood vessels associated with poorly formed granulomas, necrosis, and many giant cells. Bacterial colonization with Staphylococcus aureus has been hypothesized as an initiating factor of the autoimmunity seen in people with<unk> . Several genes involved in the immune system including PTPN22, CTLA4, and human leukocyte antigen genes may influence the risk of developing<unk> . It is now widely presumed that the anti-neutrophil cytoplasmic antibodies (ANCAs) are responsible for the inflammation in<unk> . The typical ANCAs in<unk>  are those that react with proteinase 3, an enzyme prevalent in neutrophil granulocytes. In vitro studies have found that ANCAs can activate neutrophils, increase their adherence to endothelium, and induce their degranulation that can damage endothelial cells. In theory, this phenomenon could cause extensive damage to the vessel wall, in particular of arterioles.
Granulomatosis with polyangiitis
Microscopic polyangiitis
Polyarteritis nodosa
Thromboangiitis obliterans
Eosinophilic granulomatosis with polyangiitis
Lupus vasculitis
Nephrogenic systemic fibrosis
Transplant glomerulopathy