A small vessel vasculitis is defined as infiltration of the vessel wall (transmural) by leukocytes (mononuclear or polymorphonuclear leukocytes), endothelial damage, segmental or circumferential eosinophilic “fibrinoid” necrosis of the wall with neutrophils, fragmented nuclei, and elastic membrane disruption, features similar to those seen in small vessel vasculitides. There is no inflammation seen in the vessel wall in this case.
The image illustrates a lupus vasculopathy, descriptively termed a noninflammatory necrotizing vasculopathy. The term describes the most important features for a diagnosis: lack of vessel wall inflammation as seen in a true vasculitis and the presence of necrotizing changes secondary to the presence of both fibrin tactoids and immune complex deposits (seen by immunofluorescence and electron microscopy).
As with Choice A, whether seen in the setting of lupus or ANCA, a small vessel vasculitis is defined as infiltration of the vessel wall (transmural) by leukocytes (mononuclear or polymorphonuclear leukocytes), endothelial damage, segmental or circumferential eosinophilic “fibrinoid” necrosis of the wall with neutrophils, fragmented nuclei, and elastic membrane disruption, features similar to those seen in small vessel vasculitides. There is no inflammation seen in the vessel wall in this case.
In hypertension, there are no immune deposits or fibrin tactoids present in the vessel walls on immunofluorescence and electron microscopy studies.
Amyloidosis is characterized by the presence of fibrillar deposits that are Congo red positive. There is no deposition of fibrin tactoids or immune deposits.
