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Abstract: TH-PO148

Tocilizumab-Induced Immune Complex Glomerulonephritis in a Patient with Rheumatoid Arthritis

Session Information

Category: Trainee Case Report

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Hibino, Shinya, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Hara, Satoshi, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Yamano, Takahiro, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Kawahara, Hiroyuki, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Zoshima, Takeshi, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Nishioka, Ryo, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Ito, Kiyoaki, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Mizushima, Ichiro, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Fujii, Hiroshi, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
  • Hirata, Masayoshi, Takaoka City Hospital, Takaoka, Japan
  • Kawano, Mitsuhiro, Division of Rheumatology, Department of Internal Medicine, Kanazawa University Graduate School of Medicine, Kanazawa, Kanazawa, Japan
Introduction

Anti-TNF-α inhibitors used in the treatment of rheumatoid arthritis (RA) often cause immune complex glomerulonephritis (IC-GN) as part of biologics-induced autoimmune renal disorder. However, similar effects due to anti-IL-6 receptor inhibitors are very rare. Here, we report a case of tocilizumab (TCZ)-induced IC-GN in a patient with RA.

Case Description

A 70-year-old Japanese man was admitted to our hospital due to acute nephritic syndrome. He was diagnosed with RA 14 years previously and had received methotrexate (MTX) and biologics. Three years ago, the biologic was switched from adalimumab to TCZ. RA had been in remission, and his serum creatinine (Cr) was 0.8 mg/dL. One month ago, after showing flu-like symptoms, he developed bilateral lower leg edema, renal dysfunction (Cr 1.3 mg/dL), hematuria, and proteinuria, indicating acute nephritic syndrome. On admission, renal dysfunction (Cr 1.77 mg/dL, eGFR 30.7 ml/min/1.73 m2), urinary protein 0.75 g/gCr, urinary red blood cells 50–99/high power field, and hypocomplementemia (C3, 24 mg/dL; C4, 1 mg/dL; CH50, 0 IU/L) were found. Anti-nuclear antibody, anti-dsDNA antibody, parvoviral B19DNA, and anti-streptolysin O were negative, whereas cryoglobulin was weakly positive. Renal biopsy revealed mesangial cell proliferation and endocapillary hypercellularity with partial crescent formation. Immunofluorescence analysis indicated IgG, IgA, IgM, C3, and C1q deposition in the mesangium, so a diagnosis of IC-GN was made. After discontinuing TCZ and MTX, intravenous methylprednisolone was administered at a dose of 500 mg/day for three days and then prednisolone (PSL) was initiated at 60 mg/day. His renal function and urinary abnormalities improved, and serum complement levels increased. After 5 months of treatment, his renal function has been maintained using PSL 10 mg/day.

Discussion

The anti-IL-6 receptor antibody, TCZ, may lead to the development of IC-GN, similar to anti-TNFα inhibitor. The mechanism remains unknown because only one case of TCZ-induced IC-GN has been reported to date. Rheumatologists and nephrologists should be aware of this lesion and similar cases should be collected in future.