The aim of this study was to investigate the role of antiphospholipid antibodies (aPLs) in patients with proliferative and membranous lupus nephritis (LN). Patients hospitalized with LN from July 2014 to December 2017 were selected. Levels of serum IgG, IgA, and IgM anticardiolipin (aCL) antibodies, anti-β2-glycoprotein I (anti-β2-GPI) antibodies, and lupus anticoagulant (LAC) were measured. Other clinical and pathological data were obtained at the time of hospitalization for diagnosis. Overall, 75 patients with proliferative LN and 31 patients with membranous LN were analyzed. Significant differences were found between the two groups in the detection rates of aCL antibodies (45.3% vs 22.7%, p = 0.029) and IgG-aCL antibodies (40% vs 12.9%, p = 0.007). The aCL antibody–positive proliferative LN patients (n = 34) had lower serum complement C3 and C4 levels (p = 0.010 and p = 0.021, respectively) and higher intensity of complement C1q deposition in kidney tissue than the aCL antibody–negative proliferative LN patients (n = 41) (p = 0.003). Our work suggests that aCL antibodies, especially IgG-aCL antibodies, may play a role in the damage caused by proliferative LN, and this process may involve the classical pathway of complement activation.
• Classes III + V and IV + V LN, which have both proliferative and membranous LN features, were excluded.
• The proliferative LN group had significantly higher detection rates of aCL and IgG-aCL than the membranous LN group.
• aCL antibodies, especially IgG-aCL antibodies, may play a role in the damage caused by proliferative LN, and this process may involve the classical pathway of complement activation.
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This study was supported by Zhejiang Provincial Natural Science Foundation (No. LY15H050008).
This study was approved by the Wenzhou Medical University Research Ethics Committee. All patients provided verbal consent to participate in the study.
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Ding, X., Chen, C., Zhang, J. et al. Antiphospholipid antibodies in patients with proliferative and membranous lupus nephritis. Clin Rheumatol (2020). https://doi.org/10.1007/s10067-019-04917-3
- Anti-aCL antibodies
- Complement activation
- Lupus nephritis