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Kidney Week

Abstract: TH-PO099

Clinicopathological Findings of IgA Nephropathy with Subepithelial Deposits

Session Information

Category: Glomerular

  • 1004 Clinical/Diagnostic Renal Pathology and Lab Medicine

Authors

  • Kitamura, Mineaki, Nagasaki University Hospital , Nagasaki, Japan
  • Obata, Yoko, Nagasaki University Hospital , Nagasaki, Japan
  • Nishino, Tomoya, Nagasaki University Hospital , Nagasaki, Japan
Background

Approximately 10% of patients with adult IgA nephropathy (IgAN) show subepithelial deposits, although their clinical significance remains unknown. A few clinical analyses performed for IgAN with subepithelial deposits (IgAN-SD) were reported long ago, but were relatively small sized. We studied a large number of IgAN patients focusing on atypical findings of IgAN to elucidate clinicopathological features of IgAN-SD.

Methods

We examined 464 cases diagnosed as IgAN at Nagasaki University Hospitals and affiliated hospitals between 1996 and 2013. Clinicopathological findings were compared between patients with IgAN-SD and IgAN with no subepithelial deposits (IgAN-NSD). Complement levels, localization of immunoglobulins, light chain staining pattern, and intramembranous deposits were evaluated, besides typical IgAN features.

Results

Patient characteristics were: age 38 ± 18 years, 214 men and 250 women. Subepithelial deposits were noted in 51 cases (11%). Compared to IgAN-NSD, mean serum protein (6.4 g/dL vs. 6.7 g/dL; P=0.020), albumin (3.7 g/dL vs. 3.9 g/dL; P=0.018) and complement (C3) (94 mg/dL vs. 103 mg/dL; P=0.020) were significantly lower in IgAN-SD patients. Diffuse mesangial proliferation (M) (65% vs. 45%; P < 0.01), endothelial hypercellularity (E) (43% vs. 28%; P=0.029), IgA staining in glomerular capillary walls (22% vs. 8.2%; P < 0.01) were higher in IgAN-SD patients. The incidence of light chain lambda predominance was lower in IgAN-SD patients (47% vs. 63%; P=0.028). Seven cases of IgAN-SD showed intramembranous deposits.

Conclusion

We found IgAN-SD showed the tendency to display atypical findings for IgAN, viz., low C3, and light chain staining pattern. Subendothelial deposits, low C3 and not light chain lambda predominance are also observed in IgA dominant-infection related nephropathy (IgA-IRGN). Therefore, some cases of IgAN-SD might in reality be IgA-IRGN, but not get diagnosed as IgA-IRGN owing to lack of clinical history of infection. Secondary IgA nephropathy, resulting from other etiology of IgAN, could be refractory and therapeutic strategy differs from that for IgAN. Secondary IgA deposition should be considered and careful history and clinical course be monitored if we find atypical findings for IgAN.