Analysis of the correlation between autoantibodies against AT1 receptors and risk of lupus nephritis
10.3760/cma.j.c141217-20200326-00123
- VernacularTitle:抗血管紧张素Ⅱ1型受体自身抗体与狼疮肾炎发病风险的分析
- Author:
Yanxiang SUN
1
;
Mingxia WANG
;
Li FENG
;
Yong YUAN
Author Information
1. 中山大学附属中山医院心血管内科 528400
- From:
Chinese Journal of Rheumatology
2020;24(10):656-659,c10-1
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the correlation between autoantibodies against AT1 receptors (AT1-AAs) and risk of lupus nephritis (LN).Methods:Thirty-six normal subjects and 32 patients with LN were selected. The AT1-AAs in sera of donors were detected by enzyme-linked immuno sorbent assay (ELISA). The level of AT1-AAs, C-reactive protein (CRP), serum creatinine, lipids and serum glucose in different groups were observed. We tested the serum cystatin c, erythrocyte sedimentation rate (ESR), complement C3, C4, antinuclear antibodies (ANA) and anti-dsDNA antibodies in LN patients. The structures of the glomeruli were stained by renal biopsy hematoxylin-eosin staining (HE) and schiff periodic acid shiff (PAS) . Statistical analysis was performed using independent sample t-test, Chi-square test, Spearman correlation analysis and multiple linear regression. Results:Serum creatinine and CRP were significantly higher in the LN group [(103±37) μmol/L, (21±8) mg/L, respectively] than in the control group [(72±22) μmol/L, (7±3) mg/L], all P<0.01. The average A value of AT1-AA was higher in LN patients (0.33±0.04) than in controls (0.25±0.06), P<0.01. Multiple linear regression analysis showed that the expression of AT1-AA was positively correlated with the amount of CRP ( Beta=0.364, P=0.037) and urine protein ( Beta=0.497, P=0.004), and was negatively correlated with the level of complement C3 ( Beta=-0.276, P=0.05). Pathological results showed that mesangial hyperplasia and capillary endothelial proliferation and glomerulosclerosis were more obvious in the AT1-AA positive group than the AT1-AA negative group. Conclusion:The expression of AT1-AA is significantly increased in patients with LN and correlated with CRP, urinary protein and complement C3, indicating that the AT1-AA may be involved in the pathogenesis and the progression of LN.
