Volume 60, Issue 5, Pages (November 2001)

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Volume 60, Issue 5, Pages 2025-2030 (November 2001) Colocalization of ANCA-antigens and fibrinoid necrosis in ANCA-associated vasculitis Ingeborg M. Bajema, E. Christiaan Hagen, Emile De Heer, Fokko J. Van Der Woude, Jan A. Bruijn Kidney International Volume 60, Issue 5, Pages 2025-2030 (November 2001) DOI: 10.1046/j.1523-1755.2001.00019.x Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 1 Theoretical pathogenic scenario leading to antineutrophil cytoplasmic antibody (ANCA)-induced vasculitis. (A) Circulating quiescent neutrophils contain ANCA antigens not accessible to interaction with ANCA. (B) Priming of neutrophils by cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF), resulting in the expression of ANCA antigens at the cell surface. (C) ANCA bind to target antigens at the cell surface. (D) Neutrophils release toxic oxygen metabolites. (E) Neutrophils adhere to endothelial cells via adhesion molecules and ligands. (F) Vessel wall injury leading to fibrinoid necrosis. (reproduced with kind permission of J.C. Jennette and R.J. Falk) Kidney International 2001 60, 2025-2030DOI: (10.1046/j.1523-1755.2001.00019.x) Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 2 (A) Glomerular fibrinoid necrosis in trichrome Gomori staining, and (B) consecutive section in the modified Mallory staining. (C) Modified Mallory staining preceded by a peroxidase/DAB procedure, and (D) modified Mallory staining on the consecutive section showing that the specificity for fibrinoid necrosis is unaltered (all magnifications ×40). The publication of the color illustrations was financially supported by the Dutch Arthritis Association and by the Dutch Friedrich Wegener Foundation (http://www.vasculitis.nl). Kidney International 2001 60, 2025-2030DOI: (10.1046/j.1523-1755.2001.00019.x) Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 3 (A) Glomerulus without fibrinoid necrosis, proteinase-3 (Pr3) present in the interstitium. (B) Glomerulus without fibrinoid necrosis, Pr3 present in the glomerulus. (C) Fibrinoid necrosis in a glomerulus (carmine red, big arrow) with Pr3 in its near vicinity (brown DAB staining, small arrows). (D) Pr3 present inside the fibrinoid necrotic lesion: necrosis stains carmine red, and brown DAB blots indicated by small arrows (all magnifications, ×40). The publication of the color illustrations was financially supported by the Dutch Arthritis Association and by the Dutch Friedrich Wegener Foundation (http://www.vasculitis.nl). Kidney International 2001 60, 2025-2030DOI: (10.1046/j.1523-1755.2001.00019.x) Copyright © 2001 International Society of Nephrology Terms and Conditions

Figure 4 Co-localization patterns of four ANCA antigens. Antigens were stained individually. For each staining, the total number of glomeruli is divided into: those without fibrinoid necrosis (FN) with the antigen either present or absent in the glomerulus; and those with fibrinoid necrosis with the antigen present inside the lesion or in its direct vicinity, or with the antigen absent. The number of sclerosed glomeruli is indicated separately. (A) Proteinase 3 staining. (B) Elastase staining. (C) Myeloperoxidase staining. (D) Lactoferrin staining. Kidney International 2001 60, 2025-2030DOI: (10.1046/j.1523-1755.2001.00019.x) Copyright © 2001 International Society of Nephrology Terms and Conditions