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20 Anti-neutrophil cytoplasmic antibodies in lupus nephritis
  1. May Choi1,
  2. Ann E Clarke2,
  3. Alex Chin3,
  4. Michelle Jung4,
  5. Claire Barber2 and
  6. Marvin Fritzler4
  1. 1Cumming School of Medicine, University of Calgary
  2. 2Division of Rheumatology, Cumming School of Medicine, University of Calgary
  3. 3University of Calgary, Calgary Laboratory Services
  4. 4University of Calgary


Background Anti-myeloperoxidase (MPO) antibodies have been shown to predict the development of proliferative lupus nephritis (LN) suggesting anti-neutrophil cytoplasmic antibodies (ANCA) may have a pathogenic and prognostic role in LN. This study compared the type of LN, renal function, and systemic lupus erythematosus (SLE)-related and antiphospholipid autoantibodies between LN patients who were ANCA (anti-proteinase 3 (PR3) and anti-MPO antibodies) positive and negative.

Methods Patients fulfilling the ACR or SLICC Classification Criteria for SLE were enrolled in a local cohort. We retrospectively identified patients with Class 2, 3, 4, or 5 LN on renal biopsy who also had an ANCA, plasma creatinine, and urine protein creatinine ratio (UPCR) at time of biopsy. ANCA by IIF was performed on ethanol and formalin-fixed polymorphonuclear leukocytes and a HEp-2 cell biochip (EuroPattern, Euroimmun GmbH, Luebeck, Germany) while antibodies to MPO and PR3 were determined by multiplex immunoassay (Bio-Rad, Hercules, CA: BioPlex 2200, cutoff ≥2 KEU/L). Using sera collected at enrollment, SLE-related autoantibodies (dsDNA, Sm, U1RNP, Sm, Ro52/TRIM21, Ro60/SSA, SS-B/La, Scl-70, Jo-1, RiboP, PCNA, PM/Scl) were performed by laser bead immunoassay (Euroimmune), lupus anticoagulant by tissue thromboplastin inhibition test and dilute Russell viper venom time, and anti-cardiolipin IgG and anti-2 glycoprotein-1 IgG by ELISA. Comparisons were performed with Fishers exact or Mann-Whitney U.

Results 23 SLE patients with LN were included; 82.6% were female. Most patients (20/23, 87.0%) were ANCA positive by IIF while only 5/23 (21.7%) had antibodies to MPO (3/23, 13.0%) or both MPO and PR3 (2/23, 8.7%). Anti-MPO/PR3 positive patients had p-ANCA (2/5, 40%) or an atypical pattern (3/5, 60%) on ANCA IIF. When comparing anti-MPO/PR3 positive (5) to negative (18) patients, there was no difference in LN class, creatinine, UPCR, or the presence of SLE-related autoantibodies. Anti-cardiolipin IgG antibodies were more common in anti-MPO/PR3 positive patients (60.0% vs 5.6%, p=0.021), while a nuclear pattern on ANCA IIF was more common in anti-MPO/PR3 negative patients (55.6% vs. 0%, p=0.046). Of note, three of the five LN patients with cerebrovascular accidents or venous thrombosis were anti-MPO/PR3 positive.

Conclusions Positive ANCA by IIF was common in LN, however, only a fifth of LN patients had anti-MPO/PR3 antibodies which were associated with anti-cardiolipin IgG antibodies. Anti-MPO/PR3 negative patients were more likely to have a positive ANCA IIF with nuclear staining. We are currently comparing ANCA positivity between SLE patients with and without LN.

Funding Source(s): The Arthritis Society Chair in Rheumatic Diseases at the Cumming School of Medicine, University of Calgary

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