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Abstract: PO1430

Anti-SOD2 Antibodies in Lupus Nephritis as Second Wave Antibodies

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Angeletti, Andrea, Istituto Giannina Gaslini, Genova, Liguria, Italy
  • Bruschi, Maurizio, Istituto Giannina Gaslini, Genova, Liguria, Italy
  • Lugani, Francesca, Istituto Giannina Gaslini, Genova, Liguria, Italy
  • Caridi, Gianluca, Istituto Giannina Gaslini, Genova, Liguria, Italy
  • Verrina, Enrico E., Istituto Giannina Gaslini, Genova, Liguria, Italy
  • Ghiggeri, Gian Marco, Istituto Giannina Gaslini, Genova, Liguria, Italy

Group or Team Name

  • ZEUS Study
Background

Superoxide dismutase-2 (SOD2) is an enzyme with antioxidant action. Anti-SOD2 antibodies (anti-SOD2 IgG2) were recently described in the serum of subjects with Membranous Nephropathy, as antigens of a possible second wave injury. The presence of anti-SOD2 IgG2 correlated with worse outcomes in terms of response to treatment [1]. The presence and role of anti-SOD2 IgG2 in Systemic Lupus Erythematosus (SLE) and Lupus Nephritis (LN), a secondary autoimmune glomerulonephritides, are to be clarified.

Methods

We measured serum levels of anti-SOD2 IgG2 (Homemade designed ELISA), every six months, in 1.052 patients (459 LN and 573 SLE) enrolled at different times from the diagnosis (i.e., 0-1 month, 2-12 m, 13-24 m, 25-48 m, 49-96 m, and >96 m). We also evaluated the main markers of the SLE activity, such as serum complement C3 and C4, ANA, ENA, anti-dsDNA and proteinuria. Of note, 91 LN and 130 SLE had a relevant follow-up of 36 months.

Results

As main characteristics, we report median age of 40 (IQR 28-54) years, the predominance of females (88%), disease activity (SLEDAI) of 4 (IQR 2-8).
At the cross-sectional analysis, serum levels of anti-SOD2 IgG2 at T0 are significantly higher in LN than in SLE (Fig 1a). Considering LN, the serum levels of anti-SOD2 IgG2 at T0 were significantly higher than the other time points (Fig 1a). No correlation with the histological class of LN is reported. In LN, the reduction of anti-SOD2 IgG2 was in accordance with proteinuria. Anti-dsDNAs did not result as a valuable marker of disease activity (Fig 1b).

Conclusion

Circulating anti-SOD2 IgG2 are elevated in active LN.
Serum levels of Anti-SOD2 IgG2, also considering the concomitant negative serum levels of anti-dsDNAs in all phases of LN, support the hypothesis of direct involvement of anti-SOD2 antibodies in LN as second wave antibodies that actively contribute to the manifestations of autoimmune glomerulonephritides.