Abstract: FR-PO0900
A Rare Case of Lupus Nephritis in a Patient with Ulcerative Colitis
Session Information
- Glomerular Case Reports: Lupus, FSGS, Complement, and More
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Suzuki, Haruka, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Kosaka, Tatsuaki, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Yamamoto, Shinya, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Maekawa, Shohei, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Furukawa, Kodai, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Kotani, Mina, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Sugioka, Sayaka, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Kaneko, Keiichi, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
- Yanagita, Motoko, Kyoto Daigaku, Kyoto, Kyoto Prefecture, Japan
Introduction
Renal complications in ulcerative colitis (UC) typically include IgA nephropathy and tubulointerstitial nephritis (TIN), and lupus nephritis (LN) is rarely reported. Coexistence with systemic lupus erythematosus (SLE) in patients with UC is rare, with a reported prevalence of approximately 0.4%. We present a rare case of LN in a patient with UC, where kidney biopsy played a key diagnostic role.
Case Description
A 73-year-old woman with UC diagnosed 3 years prior was in stable remission with mesalazine. She developed finger joint pain 6 months ago and subsequently presented to us with bilateral leg edema. Laboratory data showed serum albumin 2.9 g/dL, proteinuria 4.4 g/gCr, serum creatinine 0.56 mg/dL, and hematuria (10–19 RBCs/high power field). Anti-Nuclear Antibody and anti-double-stranded DNA antibodies were positive, with normal complement levels. Kidney biopsy showed subepithelial spike formation with basement membrane thickening. No findings suggestive of TIN were observed. Immunofluorescence showed granular IgG, C3c, and C1q deposits along the glomerular capillary walls. Anti-Phospholipase A2 Receptor antibody was negative. IgG subclass staining showed IgG1 and IgG2 predominance, consistent with LN class V. The patient was treated with hydroxychloroquine 200 mg/day, prednisolone 30 mg/day, and tacrolimus 3 mg/day. Mesalazine was continued to maintain UC remission. Joint symptoms resolved, and the nephrotic syndrome improved, though proteinuria persists (1.7 g/gCr). Therefore, the treatment regimen was augmented with mycophenolate mofetil (200 mg/day) and belimumab (200 mg/week).
Discussion
Diagnosing concurrent LN in UC patients is challenging due to its rarity and overlapping clinical features. Moreover, in this case, despite a lack of extra-renal manifestations suggestive of SLE, a kidney biopsy finding was crucial in the diagnosis of LN. Although the possibility of mesalazine-induced LN cannot be entirely excluded, the patient's nephropathy demonstrated improvement with the continuation of mesalazine therapy alongside comprehensive immunosuppressive treatment, while UC remained stable. This case highlights the importance of considering LN in UC patients presenting with nephrotic syndrome and demonstrates that kidney biopsy is essential for accurate diagnosis and appropriate management.