Abstract
A number of obvious questions that are still largely unanswered form the basis of current research in ANCA-associated vasculitis. Do ANCA have pathogenic potential in the development of the vasculitic lesion? Why are anti-Pr3-antibodies found predominantly in WG? Does this have pathogenetic significance? How is glomerular fibrinoid necrosis related to the development of extracapillary proliferation? How specific are these lesions of systemic vasculitis syndromes? And are ANCA directly involved in the development of the histopathological lesions that are typically found in ANCA-associated vasculitis? These and other questions will hopefully be answered in the near future, enabling us to offer a more specific therapy for patients with systemic vasculitis syndromes.
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