1 c capillary involvement) and AHR 2 (arterial fibrinoid necrosis).

2 eritis, 28% with endarteritis, and 100% with fibrinoid necrosis.

3 within the wall of an arteriole at a site of fibrinoid necrosis.

4 ealed leukocytoclastic vasculitis with focal fibrinoid necrosis.

5 us, specific arterial lesions (endarteritis, fibrinoid necrosis, activated endothelial cells, mononuc

6 trophy and became fibrotic; some also showed fibrinoid necrosis and a mixed inflammatory cell infiltr

7 ity of CAA-associated vasculopathic changes (fibrinoid necrosis and concentric splitting of the wall)

8 nucleated giant cells (MGCs), MGC death, and fibrinoid necrosis and fibrosis.

9 nuated renal injury (albuminuria, glomerular fibrinoid necrosis, and crescent formation), but mAbs to

10 o endothelial cells, endothelial activation, fibrinoid necrosis, foam cells, and intimal fibrosis.

11 5% versus 9%; severe ATI, 75% versus 9%; and fibrinoid necrosis in glomeruli, 20% versus 0%, or arter

12 arcts, microhaemorrhage, larger haemorrhage, fibrinoid necrosis, microaneurysms, perivascular space d

13 s versus 40% (2 of 5) for those who also had fibrinoid necrosis of arteries.

14 leads to increased vascular permeability and fibrinoid necrosis of blood vessel walls.

15                       (3) Type III: arterial fibrinoid necrosis or transmural inflammation with or wi

16 ograft, intimal edema, matrix deposition and fibrinoid necrosis were specifically presented in the xe