Abstract: FR-PO0945
Clinicopathologic Discordance in Pediatric Patients with Systemic Lupus Erythematosus: Why Early Kidney Biopsy Matters
Session Information
- Pediatric Nephrology: Genetic Diseases, Development, Neonatal Nephrology, Glomerular Diseases, and More
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pediatric Nephrology
- 1800 Pediatric Nephrology
Authors
- Suresh, Ananthakrishnan, University of Miami Department of Pediatrics, Miami, Florida, United States
- Gavcovich, Tara Bree, University of Miami Division of Pediatric Nephrology, Miami, Florida, United States
- Seeherunvong, Wacharee, University of Miami Division of Pediatric Nephrology, Miami, Florida, United States
- Zuo, Yiqin, University of Miami Health System, Miami, Florida, United States
- Ibanez, Daniel, University of Miami Health System, Miami, Florida, United States
- Ajjegowda, Ashwini, University of Miami Department of Pediatrics, Miami, Florida, United States
- Yahya, Majd Hilmi, University of Miami Division of Pediatric Nephrology, Miami, Florida, United States
Group or Team Name
- University of Miami, department of pediatrics
Introduction
Lupus nephritis (LN) is the most common major organ manifestation of systemic lupus erythematosus (SLE). The 2024 ACR guidelines lowered the renal biopsy proteinuria threshold from >1 to 0.5 g/24h. This case highlights a clinical–pathologic mismatch in pediatric LN and the role of early biopsy for risk stratification.
Case Description
A 14-year-old female presented with fatigue, abdominal pain, and weight loss. Workup revealed anemia and mild acute kidney injury (AKI), while elevated ANA and anti-dsDNA, low C3, and positive anti-SSA and anti-chromatin antibodies confirmed SLE. She had mild, sub-nephrotic proteinuria without hematuria (Figure 1a). Despite these mild findings, renal biopsy revealed mixed class III+V LN (ISN/RPS) with a cellular crescent, full-house immune complex deposition, and numerous subepithelial/intramembranous deposits (activity index 3/24, chronicity index 3/12) (Figure 2). She was treated with methylprednisolone, mycophenolate mofetil, and hydroxychloroquine. Three months later, she developed a lupus flare with recurrent AKI. Repeat biopsy showed histologic progression with activity index increasing to 6/24 and new subendothelial deposits. Therapy was escalated to cyclophosphamide with improvement (Figure 1b).
Discussion
This clinical–pathologic mismatch underscores that urine studies alone may not reflect LN severity, supporting the 2024 ACR lower biopsy threshold. Although initial treatment likely would not have changed, the first biopsy established a histologic baseline enabling quantification of progression and timely escalation to cyclophosphamide.