Abstract: FR-PO0934
When Lupus Nephritis Takes a Rare Turn: A Case of Lupus Podocytopathy with Collapsing FSGS Variant
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
- Moore, Kareen, Yale University, New Haven, Connecticut, United States
- Alsmaan, Hafez, Berkshire Medical Center, Pittsfield, Massachusetts, United States
- Albert, David A., Berkshire Medical Center, Pittsfield, Massachusetts, United States
- Quiusky, Kevin, Berkshire Medical Center, Pittsfield, Massachusetts, United States
Introduction
Lupus podocytopathy is an uncommon histologic pattern in lupus nephritis (LN), subclassified as minimal change disease or focal segmental glomerulosclerosis on biopsy, and accounts for ~1% of LN cases. A subset of collapsing FSGS (cFSGS) is even more rare, and associated with poor outcomes.
Case Description
A 29-year-old African American female with type 2 diabetes, presented with worsening fatigue, dyspnea, and bilateral leg swelling. Outpatient labs showed elevated creatinine, prompting emergency evaluation. On arrival, blood pressure was 170/110 mmHg and physical exam revealed anasarca. Labs showed creatinine 5.8 mg/dL (baseline 1.0), potassium 5.6 mEq/L, serum albumin 1.2 g/dL, hemoglobin 8.8 g/dL, urinalysis with 4+ protein and >50 RBCs, urine protein-to-creatinine ratio 12.9 gm. Chest X-ray revealed pulmonary edema. Doppler ultrasound of the legs was negative for DVT, and renal ultrasound showed bilateral cortical echogenicity. Autoimmune workup revealed ANA 1:2560 (homogenous pattern), positive anti-dsDNA antibody, C3 65 mg/dL, and undetectable C4. Viral and vasculitis panels were negative. Kidney biopsy demonstrated 100% effacement of podocyte foot processes, global glomerular basement membrane collapse, class III LN with diffuse mesangial and focal segmental endocapillary proliferative glomerulonephritis, tubular atrophy, and moderate interstitial fibrosis. She was treated with pulse-dose steroids, mycophenolate mofetil, hydroxychloroquine, and warfarin. Due to refractory hyperkalemia and volume overload, she required hemodialysis for several weeks, after which Losartan was also added to the regimen. At 24-month follow-up, she remains dialysis-free with creatinine of 1.4 mg/dL, improved proteinuria, and normalized complement levels.
Discussion
Lupus nephritis is a type III hypersensitivity reaction involving immune complex deposition in glomerular structures, triggering inflammation and complement pathway activation. Viral triggers and APOL1 gene variants have been proposed as contributing factors for cFSGS, while only a limited number of cases were seen in LN. cFSGS may represent a severe form of lupus podocytopathy and is associated with progression to end-stage kidney disease in over 50% of cases. Enhancing treatment guidelines for this subset of LN is of essence as early recognition and intervention can improve overall outcomes.