Abstract: FR-PO0733
When Fifth Disease Becomes a Sixth Hit: Parvovirus B19-Associated Collapsing FSGS
Session Information
- Glomerular Diseases: Membranous Nephropathy, FSGS, and Podocytopathies
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Ramzy, Silvia, Prime Olympia Fields Hospital, Olympia Fields, Illinois, United States
- Baba, Muhammad Jaafar, Prime Olympia Fields Hospital, Olympia Fields, Illinois, United States
- Bargicho, Ahlam, Prime Olympia Fields Hospital, Olympia Fields, Illinois, United States
- Putta, Srija, Prime Olympia Fields Hospital, Olympia Fields, Illinois, United States
- Sarguroh, Tauseef A., Prime Olympia Fields Hospital, Olympia Fields, Illinois, United States
Introduction
Collapsing focal segmental glomerulosclerosis (cFSGS) is an aggressive podocytopathy characterized by glomerular tuft collapse, marked proteinuria, and rapid progression to kidney failure. While primary forms are classically linked to podocyte injury, secondary cFSGS has been associated with viral infections, medications, APOL1 risk alleles, and autoimmune disease. Parvovirus B19 has rarely been implicated, with proposed mechanisms involving direct podocyte tropism and immune-mediated injury.
Case Description
A 57-year-old man with CKD III, HTN, HLD, and T2DM presented with two weeks of progressive edema and acute kidney injury. Blood pressure was 178/107 mmHg. Labs demonstrated creatinine 4.0 mg/dL (baseline ~1.6), bicarbonate 18 mmol/L, albumin 3.2 g/dL, and urine protein-creatinine ratio 17 g/g. Urinalysis revealed trace hematuria and 4+ proteinuria. Serum free light chains were unremarkable and imaging showed no obstruction. Kidney biopsy demonstrated collapsing glomerulopathy superimposed on diabetic nephropathy (RPS class IIB) with chronic active interstitial nephritis. HIV, urine toxicology, and APOL1 testing were negative. Parvovirus B19 serologies were positive (IgG 4.3, IgM 2.6), supporting recent infection. The overall clinicopathologic picture favored secondary cFSGS associated with Parvovirus B19 on a background of diabetic kidney disease. The patient was managed with aggressive diuresis using IV bumetanide and metolazone, then transitioned to oral therapy with close outpatient follow-up.
Discussion
This case highlights a rare presentation of Parvovirus B19–associated collapsing glomerulopathy in the setting of underlying diabetic kidney disease. Although viral-associated cFSGS is most commonly linked to HIV, Parvovirus B19 has emerged as a potential trigger for podocyte injury and glomerular collapse. Absence of APOL1 risk alleles and other secondary causes strengthened the association with recent Parvovirus infection. Coexisting diabetic nephropathy may have increased susceptibility to severe podocyte injury, contributing to nephrotic-range proteinuria and accelerated renal dysfunction. This case underscores the importance of considering infectious triggers in rapidly progressive proteinuric kidney disease, particularly when biopsy reveals collapsing features.