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Nephron. 2019 Aug 27:1-6. doi: 10.1159/000501857. [Epub ahead of print]

Antiphospholipid Antibodies in Patients with Membranous Nephropathy.

Author information

1
Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Institute of Nephrology, Zhejiang University, Key Laboratory of Kidney Disease Prevention and Control Technology, Zhejiang Province, Hangzhou, China.
2
Division of Nephrology, Lishui Hospital of Zhejiang University, Lishui Central Hospital, Lishui, China.
3
Kidney Disease Center, the First Affiliated Hospital, College of Medicine, Zhejiang University, Institute of Nephrology, Zhejiang University, Key Laboratory of Kidney Disease Prevention and Control Technology, Zhejiang Province, Hangzhou, China, zjukidney@zju.edu.cn.

Abstract

BACKGROUND/AIM:

The aim of this study was to investigate the prevalence and significance of antiphospholipid antibodies in patients with membranous nephropathy (MN).

METHODS:

Patients hospitalized with MN during June 2015 to June 2017 were selected and patients with minimal change disease (MCD) or focal segmental glomerulosclerosis (FSGS) in the same period were selected as controls.

RESULTS:

Overall, 267 patients with MN and 131 patients with MCD/FSGS (n = 101 MCD and n = 30 FSGS) were analyzed. There was a significant difference in the detection rate of anti-β2-glycoprotein I (anti-β2-GPI) antibodies (11.9% in MN vs. 4.5% in MCD/FSGS, p = 0.018) and IgG-anti-β2-GPI antibodies (3.7% in MN vs. 0% in MCD/FSGS, p = 0.034) between the 2 groups. Anti-β2-GPI antibody-positive MN patients (n = 32) had a lower serum C4 level than anti-β2-GPI antibody-negative MN patients (n = 235; 21.6 ± 7.6 vs. 24.6 ± 7.1 mg/dL, p = 0.030). Anti-β2-GPI antibody-positive MN patients had significant improvement of serum creatinine compared to anti-β2-GPI antibody-negative patients after 24 weeks of treatment (p = 0.006).

CONCLUSIONS:

Anti-β2-GPI antibody may play a role in the progression of MN, and this process might involve classic complement activation.

KEYWORDS:

Anti-β2-glycoprotein I antibodies; Complement activation; Focal segmental glomerulosclerosis; Membranous nephropathy; Minimal change disease

PMID:
31454804
DOI:
10.1159/000501857

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