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Abstract: SA-PO695

The Clinicopathologic Characteristics and Complement Activation of Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitides with Glomerular IgA Deposition

Session Information

Category: Pathology and Lab Medicine

  • 1602 Pathology and Lab Medicine: Clinical

Authors

  • Ma, Yanhong, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, ZheJiang, China
  • Han, Fei, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, ZheJiang, China
Background

The renal injury caused by anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are characterized by few or no immune deposits in glomerulus. A growing number of AAV patients with glomerular IgA deposits have been reported.

Methods

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.

Results

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 ESR, lower MPO-ANCA, tendency of lower CRP and BVAS. For renal injury, there were no significant differences in clinical data, renal pathological 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 with IgA nephropathy patients. All patients in IgA nephropathy group, AAV groups with or without IgA deposition had the activation of alternative complement pathway, while AAV patients with IgA deposition also had the activation of classical complement pathway. Correlation analysis showed serum C1q level correlated directly with serum globulin and IgA levels.

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 classical complement pathway.