Diagnostic pitfall: NSAID-induced membranous nephropathy with PLA2R positivity, IgG1-predominant deposits, C1q positivity, and concurrent acute interstitial nephritis-A case report.

Authors

Jingzhen Li, Qianqian Zhang, Zhengyue Chen, Yingyin Qiu, Yuanping Liu

Published in

Clinica chimica acta; international journal of clinical chemistry. Pages 121249. Jul 26, 2026. Epub Jul 26, 2026.

Abstract

Serum anti-phospholipase A2 receptor (PLA2R) antibody is widely used to diagnose primary membranous nephropathy (MN), but PLA2R positivity also occurs in secondary MN, especially nonsteroidal anti-inflammatory drug (NSAID)-induced MN, leading to a common diagnostic pitfall. We report a 71-year-old female with long-term unsupervised NSAID administration for polymyalgia rheumatica, presenting with recurrent nephrotic syndrome and acute kidney injury. Initial laboratory tests revealed severe hypoalbuminemia (15.7 g/L), elevated serum creatinine (3.98 mg/dL), massive proteinuria (10.24 g/24 h), and positive anti-PLA2R antibody (39.69 U/mL). The etiology of her first nephrotic episode remained unclear, and renal biopsy during disease relapse finally confirmed NSAID-induced secondary MN. Pathological examination demonstrated PLA2R-positive MN with immunoglobulin G1 (IgG1)-predominant immune deposits, moderate (2+) glomerular complement component 1q (C1q) deposition, and concomitant severe acute interstitial nephritis. The patient achieved clinical remission after NSAID discontinuation and treatment with intravenous methylprednisolone combined with rituximab, but disease relapse occurred after inadvertent NSAID re-exposure. This case highlights that PLA2R positivity does not exclude drug-induced secondary MN. IgG subclass profiling and C1q staining are critical complementary biomarkers for precise differential diagnosis and can effectively prevent the common diagnostic pitfall of attributing PLA2R positivity exclusively to primary MN. Permanent NSAID discontinuation remains the cornerstone of disease management.

PMID:
42503368
Bibliographic data and abstract were imported from PubMed on 27 Jul 2026.

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