In:
Applied Immunohistochemistry & Molecular Morphology, Ovid Technologies (Wolters Kluwer Health), Vol. 28, No. 10 ( 2020-11), p. e87-e93
Abstract:
The renal injury caused by antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are characterized by few or no immune deposits in glomerulus. A growing number of AAV patients with glomerular immunoglobulin (Ig)A deposits have been reported. We retrospectively investigated all AAV patients with glomerular IgA deposits diagnosed in our center. Serum galactose-deficient IgA1 (Gd-IgA1) level and glomerular Gd-IgA1 and IgA staining were measured. Moreover, we detected complement pathway components in their sera. A total of 168 AAV patients were enrolled, including 26 patients with glomerular IgA deposition and 142 patients with pauci-immune-complex deposition. The AAV patients with IgA deposition had a tendency of lower systemic disease activity, presenting with lower erythrocyte sedimentation rate, lower myeloperoxidase-ANCA, and tendency of lower C reactive protein and Birmingham Vasculitis Activity Score. For renal injury, there were no significant differences in clinical data, pathologic parameters, or renal outcome between groups. The serum level of Gd-IgA1 and intensity of glomerular Gd-IgA1 staining in IgA deposition AAV patients were similar to IgA nephropathy patients. All patients in the IgA nephropathy group and AAV groups with or without IgA deposition had the activation of the alternative complement pathway, whereas AAV patients with IgA deposition also had the activation of the classic complement pathway. Correlation analysis showed serum C1q level correlated directly with serum globulin and IgA levels. In conclusion, AAV patients with IgA deposition had the basis of IgA nephropathy and may present lower systemic disease activity. But it differs from pauci-immune AAV or IgA nephropathy by the possible activation of the classic complement pathway.
Type of Medium:
Online Resource
ISSN:
1541-2016
DOI:
10.1097/PAI.0000000000000819
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2020
detail.hit.zdb_id:
2052398-1
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