IMMUNOPATHOLOGICAL STUDIES OF POLYARTERITIS NODOSA AND WEGENERS GRANULOMATOSIS - A REPORT OF 43 PATIENTS WITH 51 RENAL BIOPSIES

Abstract

Although it is generally considered that vasculitis of the polyarteritis nodosa (PAN) group and Wegener''s granulomatosis (WG) is immune complex (IC) mediated, there are no simultaneous data on circulating IC [CIC], complement levels, and deposits of Ig and complement in the kidney. A retrospective study of 43 patients suffering from PAN and WG was performed. Ig glomerular deposits were uncommon and scanty, except in 2 patients with WG; C3 [complement component 3] deposits were detected in 12 patients, whereas fibrinogen was constantly found when lesions were recent and active. Similar data were obtained for the renal vessel walls. Contrasting with these results, rheumatoid factors and cryoglobulins, suggestive of the presence of circulating IC, were detected, respectively, in 9 of 39 and 7 of 37 patients, and IC activity assessed by the [Burkitts'' lymphoma] Raji cell assay, and the C1q binding assay was found, respectively, in 6 of 17 and 9 of 10 patients before treatment, and in none of 10 and 5 of 7 patients in remission. Hemolytic complement activity and complement components were never decreased, but the C3d breakdown product of C3 was elevated in all the 8 patients studied before treatment. Signs of persistent hepatitis B virus (HBV) infection were detected in 5 of 25 patients of the PAN group, whereas 3 of 8 patients with WG had only anti-HBV antibodies. Cytomegalovirus (CMV) could be isolated from the blood in a case of WG before the treatment was started. Persistent interferonemia was detected in 1 of 5 patients. Either renal deposition of CIC is transient, the paucity of Ig deposits being due to rapid clearance of IC by phagocytic cells; or, alternatively, vascular and glomerular lesion are not caused by CIC, as in some cases of experimental vasculitis induced by infectious agents.