Abstract: SA-PO0791
Full House Without Lupus: Diagnostic and Therapeutic Challenges in a Seronegative Patient
Session Information
- Glomerular Diseases: Lupus Nephritis, Monoclonal Gammopathy-Related Disease, and Transplantation
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Hussain, Syed Sadam, Westchester Medical Center, Valhalla, New York, United States
- Kumar, Daneet, New York City Health and Hospitals Metropolitan, New York, New York, United States
- Ali, Wajid, The University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States
- Masaud, Faryal, Hayatabad Medical Complex, Peshawar, K.P.K, Pakistan
- Salam, Latif, Westchester Medical Center, Valhalla, New York, United States
Introduction
A "full-house" immunofluorescence pattern co-deposition of IgG, IgA, IgM, C3 & C1q is the hallmark of LN but rarely occurs without SLE. Idiopathic non-lupus full-house nephropathy (iFH-N) has a poor prognosis, with up to 80% progressing to ESKD.
Case Description
A 26 Y old female with hypothyroidism & CKD 3B presented in Dec 2024 with nephrotic-range proteinuria. Serologic workup—ANA, anti-dsDNA, anti-PLA2R, complements, ANCA & viral serologies—was unremarkable. Kidney biopsy showed membranous nephropathy with IgG & C3 deposition, including mesangial & subendothelial deposits, without evidence of systemic disease. She was started on steroids but presented with overt nephrotic syndrome. Repeat biopsy showed a full-house pattern of IgG, IgA (1+), IgM, C3 (2–3+), C1q (1+), kappa (2–3+) without clinical or serologic SLE features. She received rituximab (RTX) 1g x 2. Despite complete B-cell depletion (CD19=0), creatinine increased from 2.2 to 3.2 mg/dL with ongoing heavy proteinuria. She was transitioned to MMF with a prednisone taper.
Discussion
This case highlights the challenges of diagnosing and managing iFH-N. Several features against membranous nephropathy are mesangial & subendothelial deposits, absent IgG4 predominance & negative PLA2R serology. The full-house pattern raised concern for latent lupus, though Rijnink et al. found no iFH-N patients developed SLE over 20 yrs & identified membranous-pattern iFH-N as an independent ESRD risk factor (HR 5.31). RTX failure despite peripheral B-cell depletion may reflect urinary drug losses, anti-RTX Ab, or persistent tissue-resident autoreactive cells. Obinutuzumab showed higher remission rates than RTX retreatment in refractory MN (54.6% vs 9.1%) & represents the best rescue therapy. In conclusion, iFH-N needs early diagnosis, prompt treatment, clinicopathologic correlation, and long-term follow-up.