Abstract: SA-PO703
Endothelial Cell Injury Can Be Significant in Cases of Membranoproliferative Glomerulonephritis with Monoclonal IgG Deposition
Session Information
- Pathology and Lab Medicine: Clinical
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pathology and Lab Medicine
- 1602 Pathology and Lab Medicine: Clinical
Authors
- Sawada, Anri, Nippon Medical School, Tokyo, Japan
- Kawanishi, Kunio, University of Tsukuba, Tsukuba, Japan
- Taneda, Sekiko, Tokyo Women's Medical University, Tokyo, Japan
- Fuchinoue, Shohei, Tokyo Women's Medical University, Tokyo, Japan
- Tanabe, Kazunari, Tokyo Women's Medical University, Tokyo, Japan
- Koike, Junki, St. Marianna University, Kawasaki, Japan
- Honda, Kazuho, Showa University School of Medicine, Tokyo, Japan
- Shimizu, Akira, Nippon Medical School, Tokyo, Japan
- Nitta, Kosaku, Tokyo Women's Medical University, Tokyo, Japan
- Nagashima, Yoji, Tokyo Women's Medical University, Tokyo, Japan
Background
Pathological and clinical features of proliferative glomerulonephritis with monoclonal IgG deposition (PGNMID) are not fully revealed. This study focused on glomerular endothelial alterations characterized by plasmalemmal vesicle associated protein-1 (PV-1) and Weibel–Palade body. PV-1 is a component of caveolae and considered an indicator of endothelial injury and Weibel–Palade body.
Methods
A total of 23 cases of PGNMID were compared with cases of lupus nephritis (n = 52), primary membranoproliferative glomerulonephritis (MPGN) (n = 7), and IgA nephropathy (n = 25). Informed consent from the patients and ethical approval from Tokyo Women’s Medical University was obtained. PV-1 expression in the glomerular endothelium was evaluated using PAL-e antibody to verify endothelial changes in both PGNMID and control groups. Further, we compared monoclonal IgG patterns and complement deposition. We also examined histological types of MPGN and endothelial alterations as Weibel–Palade body using electron microscopy.
Results
Histological analysis in PGNMID group revealed MPGN type I (n = 10), MPGN type III (n = 8), membranous nephropathy (n = 3), endocapillary proliferative glomerulonephritis, and minor glomerular abnormality (n = 1). Deposit patterns were identified as IgG1 (IgG1κ, n = 6), IgG2 (IgG2λ, n = 1), and IgG3 (IgG3κ, n = 13; IgG3λ, n = 3). Further, 16 cases showed C1q deposition, and 21 cases showed C3 deposition. Electron dense deposits were located in subepithelial (n = 11), intramembranous (n = 16), subendothelial (n = 21), and mesangial (n = 19) sites. The percentage of PAL-e antibody-positive patients was significantly higher in PGNMID group (69.6%, n = 23) than in control groups (19.0%, n = 84). Weibel–Palade body density and caveolae were considerably elevated in PGNMID groups.
Conclusion
These results suggest that PGNMID-related damage is characterized by glomerular endothelium alterations; further studies are required to investigate whether such endothelial alterations are associated with clinical prognosis.