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Background: Involvement of the complement system in the pathogenesis of lupus nephritis (LN) is well accepted, but its exact role remains unclear. The aim of this study was to investigate the relationship of complement activation pathway to clinical and pathological characteristics and renal outcome in patients with LN., Material and Methods: Patients with LN were divided into two groups: those in whom the complement system was mainly activated through the classical pathway (low serum C3 and C4 levels; CP group); and those in whom the complement system was solely activated through the alternative pathway (low serum C3 with normal C4 levels; AP group). Clinical and pathological data and renal outcomes were compared between the two groups., Results: A total of 102 LN patients were enrolled in this study, 63 patients (61.8%) in the CP group and 39 patients (38.2%) in the AP group. LN patients in the CP group had significantly higher SLEDAI (p < 0.001), more anti-dsDNA (p = 0.001), higher renal activity index (p < 0.001), and more class IV LN (p = 0.008) than LN patients in the AP group. Mean length of follow-up was 50.6 ± 26.4 months. Renal outcome in the form of progression of kidney disease was significantly poorer in the CP group in the AP group (p = 0.037)., Conclusion: Our findings suggest that evaluation of the complement activation pattern may be useful for evaluating disease activity and predicting the prognosis of LN., (© 2021. Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Objectives: This study aimed to investigate the association of antiphospholipid antibodies (aPL) with clinical activity and renal pathological activity in patients with lupus nephritis (LN)., Methods: Levels of anticardiolipin () antibodies, anti-β2-glycoprotein I (anti-β2-GPI) antibodies and lupus anticoagulant (LAC) were measured, and other clinical and pathological data were also obtained during the same period before renal biopsy., Results: A total of 83 patients with LN were included in this study, 40 patients (48.2%) in the s positive group and 43 patients in the aPL negative group. LN patients with positive aPL had significantly higher SLEDAI (p = 0.012), more hematuria (p = 0.043), lower serum C3 (p = 0.003) and C4 (p = 0.014), and a higher pathological activity index (p = 0.012), more micro-thrombosis (p = 0.046) and more C3 deposits (p = 0.038) in the glomerulus than patients with negative aPL The level of IgG- was significantly correlated with SLEDAI and serum level of C3 (r = 0.44, p < 0.001; r = -0.39, p = 0.003, respectively). The level of IgM- was significantly correlated with SLEDAI, and serum levels of C3 and C4 (r = 0.27, p = 0.014; r = -0.22, p = 0.041; r = -0.23, p = 0.035, respectively)., Conclusions: Our work suggests that aPL, especially, are correlated with both clinical activity and renal pathological activity in patients with LN.

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.