Kidney Week

Abstract: PUB356

A Case of Secondary Membranous Nephropathy Caused by Rheumatoid Arthritis Accompanied by Double Positive for Anti-GBM Antibodies and Proteinase 3 (PR3)-ANCA

Session Information

• Publication Only

Category: Glomerular Diseases

• 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

• Kawamori, Saki, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Saki Kawamori

• Suzuki, Hitoshi, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Hitoshi Suzuki, MD, PhD

• Lee, Mingfeng, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Mingfeng Lee

• Umezawa, Yukako, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Yukako Umezawa, MD

• Sasatsuki, Yuya, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Yuya Sasatsuki

• Muto, Masahiro, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Masahiro Muto, MD, PhD

• Takahara, Hisatsugu, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Hisatsugu Takahara, DrMed

• Tomita, Shigeki, Juntendo Daigaku Igakubu Fuzoku Urayasu Byoin, Urayasu, Chiba, Japan

Shigeki Tomita, MD, PhD

• Suzuki, Yusuke, Juntendo Daigaku Igakubu Daigakuin Igaku Kenkyuka, Bunkyo-ku, Tokyo, Japan

Yusuke Suzuki, MD, PhD

Introduction

The underlying mechanism of double positive for ANCA and anti-GBM antibody is unclear. Up to a third of patients with anti-GBM disease are positive for ANCA, mainly with specificity to myeloperoxidase. It is postulated that GBM damage from ANCA-associated vasculitis exposes the antigens which leads to the production of GBM autoantibodies. However, there are no literature that describe the association between membranous nephropathy and dual positive for ANCA and anti-GBM antibody.

Case Description

71-year-old man was diagnosed with rheumatoid arthritis (RA) due to the appearance of polyarthral pain, synovitis, and a positive anti-CCP antibody at two months ago. Disease modifying anti-rheumatic drugs (DMARDs) and low dose steroid were initiated. Recently, he was referred to our hospital by pointing out of proteinuria. Laboratory data was as follows: eGFR, 29 mL/min/1.73 m², anti-GBM antibodies, 143 U/mL, PR3-ANCA, 4.2 U/mL and C-reactive protein, 2.4 mg/dL. Examination of anti-nuclear antibody and anti-double stranded DNA IgG antibody were negative. Urinalysis showed mild proteinuria (0.7 g/gCr) and no microscopic hematuria. No pulmonary lesions were observed. Antiglomerular basement membrane nephritis or ANCA-associated nephritis were suspected, however, pathological analysis of kidney biopsy specimens indicated no crescentic formation and peritubular capillaritis. Meanwhile, spike formation was observed in the glomerular basement membrane by PAM staining, and the fluorescent analysis showed the deposition of granular IgG (IgG1 dominant) and complement 3 on the basement membrane. Electron microscopy showed a wide range of subepithelial electron dense deposits. Glomerular PLA2R1 and THSD7A were negative. Thus, he was diagnosed as secondary membranous nephropathy caused by RA. Intensified treatment of RA resulted in remission of proteinuria.

Discussion

This is the first case of membranous nephropathy with double positive for anti-GBM antibody and PR3-ANCA in patients with RA. Several reports indicated that membranous nephropathy complicated by anti-GBM antibody or PR3-ANCA often progresses renal dysfunction rapidly. Careful observation is necessary for the appearance of vasculitis and pulmonary lesions.