Abstract: FR-PO0915
Acute Kidney Failure and Nephrotic Syndrome Secondary to Collapsing Focal Segmental Glomerulonephritis Associated with Parvovirus B19 in a Pediatric Patient
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
- Kliebhan, Margaret, Rush University Children's Hospital, Chicago, Illinois, United States
- Silverman, Hannah C, Rush University Children's Hospital, Chicago, Illinois, United States
- Bartlett, Deirdre, Ann and Robert H Lurie Children's Hospital of Chicago Foundation, Chicago, Illinois, United States
Introduction
Collapsing FSGS associated with Parvovirus B19 (PVB19) has rarely been reported in pediatrics.
Case Description
A 13 year old male presenting with 4 days of nausea, vomiting, progressive lower abdominal pain, intermittent lower extremity rash, and fatigue in the setting of recent URI symptoms and chronic intermittent ibuprofen use was found to have acute renal failure, azotemia, hypertension, hypoalbuminemia, normal complements, nephrotic range proteinuria, microscopic hematuria and anemia. Biopsy demonstrated collapsing FSGS, severe ATN, and mild AIN, Patient was treated with high dose corticosteroids, required 3 days of hemodialysis and was discharged home on corticosteroids with renal recovery. Collapsing FSGS has been associated with infectious causes such as PVB19 and EBV, and genetic etiologies such as APOL1, which will be tested outpatient. This patient had elevated PVB19 DNA PCR, positive IgM and IgG, with IgM>IgG suggestive of acute infection. EBV DNA PCR was also elevated, with positive IgG but negative IgM suggestive of prior infection.
Discussion
To our knowledge, this is the first report of collapsing FSGS associated with PVB19 infection in a pediatric patient. PVB19 was first associated with glomerulonephritis in patients with sickle cell disease and aplastic crisis and further associated with collapsing FSGS based on a higher prevalence of PVB19 DNA in renal biopsies and peripheral blood of collapsing FSGS patients as opposed to patients with HIVAN, other FSGS, and controls. Pathophysiology is yet undetermined, although reactivation of a latent virus during renal stress is a potential mechanism. Collapsing FSGS is also predominantly seen among people of African American origin and has been associated with patients carrying two APOL1 risk alleles. From this case, our team learned to consider viral infections as a rare but potential cause of FSGS in pediatrics.
Jones stain (right) and PAS stain (left) of glomeruli sampled on renal biopsy.