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Shunichiro Hanai, Yoshiaki Kobayashi, Moe Watanabe, Kojiro Ikeda, Soichiro Kubota, Daiki Nakagomi, Improvement of proteinuria by upadacitinib in a patient with refractory lupus membranous nephropathy, Rheumatology, Volume 64, Issue 3, March 2025, Pages 1548–1549, https://doi.org/10.1093/rheumatology/keae552
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Dear Editor, LN is a major organ involvement of SLE. Lupus membranous nephropathy (LMN) is observed in 10–15% of patients with LN [1]. LMN can present with nephrotic-range proteinuria that can be prolonged despite treatment, leading to the impairment of kidney function [2]. Glucocorticoids and intravenous cyclophosphamide or mycophenolate with or without combination with belimumab or calcineurin inhibitors are recommended for LN, but optimal treatment strategies for LMN have not yet been established [3]. Janus kinase (JAK) inhibitors appear promising as pharmacotherapy for SLE, but the efficacy confirmed in clinical trials has been limited to cutaneous and articular involvements [4]. Although some reports have shown the efficacy of JAK inhibitors such as baricitinib and filgotinib for LMN [2, 5], no reports appear to have shown the efficacy of upadacitinib for LMN. We present the case of a Japanese woman with LMN who was successfully treated using upadacitinib.
A 69-year-old woman had been diagnosed with SLE and LMN at 36 years old, based on erythema, pancytopenia, proteinuria and positive results for anti-double-stranded DNA antibodies. High-dose glucocorticoid therapy improved the proteinuria, and urine protein/creatinine ratio (UPCR) was maintained at around 0.1–0.5 g/gCr under oral prednisolone at 2 mg/day and hydroxychloroquine at 200 mg/day. At 66 years old, she developed nephrotic-range proteinuria after withdrawal of prednisolone. Kidney biopsy revealed LMN. Prednisolone at 30 mg/day combined with mycophenolate improved proteinuria, but mycophenolate mofetil had to be discontinued due to cytopenia as an adverse event. Weekly subcutaneous injection of belimumab was therefore initiated. Proteinuria persisted with a UPCR of 1.0–2.0 g/gCr, and reduction of the prednisolone dose to below 10 mg/day proved difficult because of mild proteinuria, polyarthritis and thrombocytopenia. Belimumab was switched to intravenous anifrolumab and tapering of prednisolone was again attempted. UPCR increased with a prednisolone dose of 6 mg/day (UPCR: 3.0–8.7 g/gCr) and arthritis recurred. Although rituximab was a therapeutic option for LMN, JAK inhibitors were considered for their effects on articular involvements based on clinical trials [4], and our patient preferred oral medications. Anifrolumab was then switched to upadacitinib at 15 mg/day (Fig. 1). Laboratory findings before starting upadacitinib administration were as follows: haemoglobin, 12.5 g/dl; white blood cell count, 7380/µl; and platelets, 89 000/µl. No liver dysfunction was identified. The serum creatinine level was 0.91 mg/dl. No hypocomplementemia was observed and results for anti-double-stranded DNA antibody were negative (1.2 U/ml). Upadacitinib rapidly improved both proteinuria (UPCR: 1.0–2.0 g/gCr) and arthritis without any increase in prednisolone dosage, and prednisolone was subsequently tapered to 2 mg/day without any exacerbation of proteinuria (Fig. 1).
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