The roles of complement 1q and anti-C1q autoantibodies in pathogenesis of lupus nephritis

Abstract

To analyze the correlation of serum levels of complement 1q (C1q) and anti-C1q autoantibodies (C1qAb) with renal pathology in lupus nephritis (LN) and to explore the probable mechanism of C1q and C1qAb in the development of systemic lupus erythematosus (SLE), especially LN. The serum samples of 80 SLE patients, 40 LN patients and 40 non-LN patients, were collected to detect the level of C1q with single radial immunodiffusion and the level of C1qAb with enzyme-linked immunosorbent assay. Renal biopsy was conducted in 25 of the 32 LN patients so as to observe the deposition of apoptotic cells and apoptotic bodies in the glomeruli with TdT-mediated dUTP nick end labeling. The serum level of C1q was (130 +/- 50) mg/L in the LN patients, significantly lower than that in the non-LN patients [(170 +/- 70) mg/L, P = 0.004]. The serum level of C1qAb (P/N value) was 7 +/- 4 in the LN patients, significantly higher than that in the non-LN patients (4 +/- 3, P < 0.001). The correlation coefficient between C1qAb and C1q in the LN patients was -0.567 (P < 0.01), showing a significant negative correlation. The correlation coefficient between C1qAb and C1q in the non-LN patients was -0.509 (P = 0.001), showing a significant negative correlation. The serum C1q level of the type IV LN patients was significantly lower than that in the type I LN patients, and the serum C1qAb level of the type IV LN patients was significantly higher than that in the type I LN patients (P < 0.05). The serum C1q was significantly lower in the LN patients with renal C1q deposition (++) than in the LN patients with renal C1q deposition (+), however, the serum C1qAb was significantly higher in the LN patients with renal C1q deposition (++) than in the LN patients with renal C1q deposition (+) (both P < 0.05). The serum C1q level was significantly lower in the LN patients with positive IgG deposition than in the LN patients with negative IgG deposition and the serum C1qAb level was significantly higher in the LN patients with positive IgG deposition than in the LN patients with IgG negative deposition (both P < 0.05). The serum C1q level in the LN patients with positive C3 deposition was significantly lower than that in the LN patients with negative C3 deposition (P < 0.05). The serum C1q level in the LN patients with marked apoptotic cells and deposition of apoptotic bodies was significantly lower than that in the LN patients without marked apoptotic cells and deposition of apoptotic bodies, and the serum C1qAb level in the LN patients with obvious apoptotic cells and deposition of apoptotic bodies was significantly higher than that in the LN patients without obvious apoptotic cells and deposition of apoptotic bodies (both P < 0.05). The decrease of serum C1q level and increase of serum C1qAb were significantly positively correlated with the deposition of C1q, IgG, and C3 in the kidney, and with the appearance of apoptotic cells and deposition of apoptotic bodies in the kidney. C1q and C1qAb may be involved in the pathogenesis of SLE, especially LN. The probable mechanism may be that they promote renal deposition of circulating immune complexes combined with C1q or promote the renal deposition of apoptotic cells and apoptotic bodies.