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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Systemic lupus erythematosus (SLE) and focal segmental glomerulosclerosis (FSGS) are distinct glomerular diseases with different pathophysiologic mechanisms. Their coexistence is rare and poses diagnostic and therapeutic challenges. We present a unique case highlighting individualized management strategies addressing overlapping immune and podocytopathic pathways to optimize renal recovery and clinical outcomes.
A 23-year-old woman, diagnosed with systemic lupus erythematosus (SLE) at 18 years old, initially presented with bilateral leg edema, recurrent oral ulcers, and an erythematous pruritic malar rash. Laboratory evaluation revealed nephrotic-range proteinuria of 3.269 g/24 h and a creatinine clearance of 1.2 mL/min. Serologic testing showed low C3 (24.5 mg/dL; normal 82–160 mg/dL), strongly positive ANA (34.5; positive >1), and markedly elevated anti–double-stranded DNA (>400 IU/mL), confirming active lupus nephritis.
She received monthly intravenous cyclophosphamide for induction, then quarterly maintenance. Over several years, she achieved partial remission, with improved edema and reduced proteinuria. By late 2024, she was maintained on mycophenolate mofetil (MMF) 2 g/day, prednisone 5 mg/day, hydroxychloroquine 200 mg/day, losartan 100 mg/day, atorvastatin 40 mg/day, and fenofibrate 200 mg nightly. Her last cyclophosphamide dose was in November 2024.
In April 2025, she consulted the nephrology service for rising proteinuria despite stable renal function. UPCR increased from 1.37 to 2.79 g/day, and lipid profile showed elevated triglycerides and very-low-density lipoproteins. Given the discordance between preserved renal function and worsening proteinuria, a kidney biopsy was performed in May 2025.
Biopsy findings demonstrated FSGS lesions. Immunofluorescence revealed trace IgM and C1q mesangial staining, negative to trace IgG and IgA, and no C3 or fibrinogen deposition, indicating a podocytopathy pattern rather than active lupus nephritis.
MMF was discontinued and replaced with cyclosporine, while low-dose prednisone and hydroxychloroquine were continued, resulting in gradual proteinuria reduction and clinical stabilization.
Following cyclosporine initiation in July 2025, the patient exhibited a significant and sustained decline in proteinuria. The UPCR decreased from 2.79 g/day in April 2025 to 0.64 g/day shortly after therapy began, then progressively declined to 0.42 g/day in August, 0.32 g/day in September, and 0.23 g/day in October 2025. Urine protein fell from 677.9 mg/dL to 32 mg/dL, with stable renal function throughout. Clinically, her blood pressure stabilized at an average of 130/90 mmHg, and peripheral edema resolved completely.
The UPCR trend demonstrated a rapid decline followed by sustained remission, reflecting favorable response to cyclosporine together with hydroxychloroquine, low-dose prednisone, and losartan in achieving proteinuria control and clinical stability in systemic lupus erythematosus with coexisting focal segmental glomerulosclerosis. The case underscores the diagnostic and therapeutic complexity of overlapping SLE and FSGS, highlighting the need for individualized management strategies guided by biopsy and evolving disease phenotype.
