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Classification and Pathogenicity of ANCA-Associated Vasculitis 195

[98] Donald, K. J., Edwards, R. L., McEvoy, J. D. An ultrastructural study of the
pathogenesis of tissue injury in limited Wegener's granulomatosis. Pathology 1976; 8:
161-169.

[99] Monach, P. A., Kumpers, P., Lukasz, A., et al. Circulating angiopoietin-2 as a
biomarker in ANCA-associated vasculitis. PLoS One 2012; 7:e30197.

[100] Monach, P. A., Tomasson, G., Specks, U., et al. Circulating markers of vascular injury
and angiogenesis in antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis
Rheum. 2011; 63:3988-3997.

[101] Kumpers, P., Hellpap, J., David, S., et al. Circulating angiopoietin-2 is a marker and
potential mediator of endothelial cell detachment in ANCA-associated vasculitis with
renal involvement. Nephrol. Dial. Transplant. 2009; 24:1845-1850.

[102] Erdbruegger, U., Grossheim, M., Hertel, B., et al. Diagnostic role of endothelial
microparticles in vasculitis. Rheumatology 2008; 47:1820-1825.

[103] De Groot, K., Goldberg, C., Bahlmann, F. H., et al. Vascular endothelial damage and
repair in antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Rheum.
2007; 56:3847-3853.

[104] Zavada, J., Kideryova, L., et al. Reduced number of endothelial progenitor cells is
predictive of early relapse in anti-neutrophil cytoplasmic antibody-associated vasculitis.
Rheumatology 2009; 48:1197-1201.

[105] Zavada, J., Kideryova, L., Pytlik, R., et al. Circulating endothelial progenitor cells in
patients with ANCA-associated vasculitis. Kidney Blood Press. Res. 2008; 31:247-254.

[106] Radford, D. J., Luu, N. T., Hewins, P., et al. Antineutrophil cytoplasmic antibodies
stabilize adhesion and promote migration of flowing neutrophils on endothelial cells.
Arthritis Rheum. 2001; 44:2851-2861.

[107] Calderwood, J. W., Williams, J. M., Morgan, M. D., et al. ANCA induces {beta}2
integrin and CXC chemokine-dependent neutrophil-endothelial cell interactions that
mimic those of highly cytokine-activated endothelium. J. Leukoc. Biol. 2005; 77:33-43.

[108] Mayet, W. J., Meyer zum Buschenfelde, K. H. Antibodies to proteinase 3 increase
adhesion of neutrophils to human endothelial cells. Clin. Exp. Immunol. 1993; 94:440-
6.

[109] Tse, W., Nash, G., Savage, C., et al. ANCA-induced neutrophil F-actin polymerization:
implications for microvascular inflammation. Kidney Int. 2005; 67: 130-139.

[110] Savage, C. O., Pottinger, B. E., Gaskin, G., et al. Autoantibodies developing to
myeloperoxidase and proteinase 3 in systemic vasculitis stimulate neutrophil
cytotoxicity toward cultured endothelial cells. Am. J. Pathol. 1992; 141:335-342.

[111] Hu, N., Westra, J., Rutgers, A., et al. Decreased CXCR1 and CXCR2 expression on
neutrophils in anti-neutrophil cytoplasmic autoantibody-associated vasculitides
potentially increases neutrophil adhesion and impairs migration. Arthritis Res. Ther. 13:
R201.

[112] Harper, L., Ren, Y., Savill, J., et al. Antineutrophil cytoplasmic antibodies induce
reactive oxygen-dependent dysregulation of primed neutrophil apoptosis and clearance
by macrophages. Am. J. Pathol. 2000; 157:211-220.

[113] Harper, L., Cockwell, P., Adu, D., et al. Neutrophil priming and apoptosis in anti-
neutrophil cytoplasmic autoantibody-associated vasculitis. Kidney Int. 2001; 59:1729-
1738.

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