Abstract: TH-PO0808
The Great Masquerader: Phospholipase A2 Receptor-Negative Membranous Nephropathy Secondary to Sarcoidosis
Session Information
- Glomerular Case Reports: Membranous, PGN, GBM, and More
November 06, 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
- Killen, John P., Macquarie University, Sydney, New South Wales, Australia
- Wang, Rosy, Northern Beaches Hospital, Frenchs Forest, New South Wales, Australia
- Teh, Tobias T K, Macquarie University, Sydney, New South Wales, Australia
- Yun, James, Northern Beaches Hospital, Frenchs Forest, New South Wales, Australia
Introduction
Sarcoidosis is a multisystem granulomatous disease that causes renal impairment in under 10% of cases. While this typically manifests as tubulointerstitial disease, membranous nephropathy (MN) is the predominant glomerular form.
Case Description
A 62-year-old female with hypercholesterolaemia and Crohn’s disease in remission, presented with subacute myalgia and generalised oedema. She was normotensive with preserved renal function, raised creatine kinase (CK) 9000 U/L and features of nephrotic syndrome: serum albumin 23 g/L, urine albumin/creatinine ratio (UACR) 369 mg/mmol. Glomerulonephritis screen was unremarkable including negative phospholipid A2 receptor (PLA2R) antibody. Kidney biopsy confirmed MN. Muscle biopsy demonstrated non-caseating granulomas and resolving statin-induced rhabdomyolysis. A subsequent positron emission tomography scan revealed mediastinal lymphadenopathy, with polyclonal lymphoid cells on fine needle aspirate. Acid-fast bacilli cultures were negative on both muscle and lymph node tissue. Following these extensive investigations, the patient was diagnosed with sarcoidosis.
In the absence of high-risk features for disease progression, the patient received optimal supportive care with diuretics, valsartan, dapagliflozin and therapeutic apixaban. CK resolved with statin cessation. Six-month follow-up chest imaging showed resolution of mediastinal lymphadenopathy without parenchymal fibrosis. One year after initial diagnosis, the patient remains stable on conservative management with UACR 354 mg/mmol, serum albumin 33 g/L and normal renal function (creatinine 50 umol/L, eGFR > 90 mL/min/1.73m2).
Discussion
Membranous nephropathy is an exceedingly rare manifestation of sarcoidosis, and we highlight a unique presentation of nephrotic syndrome synchronously with statin-induced myopathy. While hypoalbuminaemia may have potentiated free drug levels and statin toxicity, non-caseating granulomas on muscle biopsy point towards sarcoidosis as the unifying diagnosis. The antigen profile in sarcoidosis-associated MN mimics that of primary MN with PLA2R and neural epidermal growth factor-like 1 being the most common. The causative antigen in our patient remains unknown, although we will send any future kidney biopsy tissue for mass spectrometry to characterise the culprit antigen.