Abstract: FR-PO0715
A Case of IgA Vasculitis with Nephritis and Co-Occurring Postinfectious Glomerulonephritis
Session Information
- Pediatric Nephrology: CKD, ESKD, and Glomerular Diseases
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Pediatric Nephrology
- 1900 Pediatric Nephrology
Authors
- Izarra Boscan, Carlos A, University of Nebraska Medical Center College of Medicine, Omaha, Nebraska, United States
- Floen, Miranda J., University of Nebraska Medical Center College of Medicine, Omaha, Nebraska, United States
- Muff-Luett, Melissa A., University of Nebraska Medical Center College of Medicine, Omaha, Nebraska, United States
- Taylor, Veronica, University of Nebraska Medical Center College of Medicine, Omaha, Nebraska, United States
Introduction
IgAVN and PIGN are among the most common causes of glomerulonephritis in pediatrics but rarely happen simultaneously. We describe an approach to evaluating and managing a patient with features of both.
Case Description
A 7-year-old female was diagnosed with IgAV by her pediatrician based on initial symptoms of bilateral lower extremity pain, palpable purpura, with normal BP. Initial urinalysis showed microscopic hematuria without proteinuria. Serum chemistry showed normal renal function. She presented a week later with worsening edema, hypertension, proteinuria, and hematuria. Other recent history includes treatment of Streptococcal pharyngitis 3 weeks prior.
On exam, she was noted to be hypertensive (118/72 mmHg; 95th percentile) and tachycardic (118 bpm). Pertinent physical exam findings included periorbital, pedal edema, and palpable purpura of the lower extremities. Her abdomen was nontender, and the rest of her exam was normal.
She was transferred to our institution for further workup. Renal function testing showed KDIGO stage 1 AKI. Urine studies were significant for nephrotic range proteinuria and dysmorphic RBC casts indicative of glomerular disease. Serology workup was remarkable for low C3 & C4, and positive ASO titers. A kidney biopsy was performed to evaluate the underlying cause of her glomerulonephritis.
Biopsy demonstrated diffuse proliferative glomerulonephritis without necrosis or crescent formation. Immunofluorescence was significant for glomerular 2-3+ C3 deposits and 1+ mesangial IgA & IgG staining. Electron microscopy showed mesangial with occasional subendothelial and subepithelial deposits.
Discussion
The biopsy, physical exam, and lab findings suggest resolving PIGN with a possible component of IgAVN vs an early C3-dominant GN.
Clinicians facing sudden changes in the course of IgAVN (rapid onset hypertension, edema, or new urinary findings) should be prompted to seek further investigation of new glomerular disease.
We saw clinical improvement in this patient with steroid therapy, including resolving AKI, improved proteinuria, and well-managed hypertension on Amlodipine.
IgA deposits (1A) and IgG deposits (1B) as seen on Immunofluorescence