Abstract: TH-PO0521
Minimal Change Disease-IgAN Overlap Presenting as Severe Nephrotic Syndrome
Session Information
- Glomerular Diseases: IgAN, IgA Vasculitis, and More
October 22, 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
- Sonar, Nirmay, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
- Kallakury, Bhaskar, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
- Pourafshar, Negiin, MedStar Georgetown University Hospital, Washington, District of Columbia, United States
- Aron, Abraham W., MedStar Georgetown University Hospital, Washington, District of Columbia, United States
Introduction
The coexistence of two distinct glomerular diseases, or dual glomerulopathy presents significant diagnostic and management challenges. Concurrent minimal change disease and IgA nephropathy is an under-recognized entity where overlapping clinical phenotypes can obscure the underlying diagnosis, making early kidney biopsy crucial for establishing diagnosis and guiding management.
Case Description
A 63 year old woman presented with 3-weeks of severe, sudden onset lower extremity and abdominal edema. Initial creatinine was 1.4 mg/dL with a urine-protein-creatinine ratio 14.8 g/g and serum albumin 1.8 g/dL. Serologic workup was unrevealing with ANCA undetectable, C3/C4 normal, anti-PLA2R undetectable, free light chain ratio 1.2. Empiric prednisone 60 mg daily was initiated with plans to pursue an urgent biopsy. Two days following presentation the patient was hospitalization for progressive edema, dyspnea and rapidly rising creatinine to 4.5mg/dl. She was treated with IV diuretics and underwent an expedited renal biopsy that showed a minimally hypercellular glomerulus with no background inflammation, 2+ granular mesangial IgA staining on IF, diffuse foot process fusion (70–80%) without immune complex deposits on EM, consistent with MCD and concomitant IgAN (Oxford M1E0S0T0C0). The patient’s symptoms stabilized and she was discharged. At 2 week follow up, her edema resolved. Creatinine (1.2mg/dl), serum albumin (3.2g/dL) and UPCR (1.67g/g) all improved. Due to insomnia, anxiety and jitteriness tacrolimus 3 mg BID (trough 4–7 ng/mL) was added to allow for a steroid-sparing regimen with rapid taper
Discussion
MCD-IgAN dual nephropathy is rare, occurring in 1-2% of IgAN biopsies, though seen in up to 23% with nephrotic syndrome. Two distinct mechanisms drive this entity: T-cell-mediated podocyte injury in MCD, and aberrant IgA1 glycosylation triggering complement activation and mesangial deposition in IgAN. Whether IgAN represents a true co-disease or incidental finding remains unresolved. The 88% proteinuria reduction and renal recovery within 2 weeks is more typical of podocytopathy than IgAN. The 2021 KDIGO guidelines acknowledge this uncertainty and recommend treating the primary phenotype with aggressive immunosuppression. The role of newer IgAN-specific disease-modifying therapies in dual nephropathy remains undefined and warrants further investigation
Acknowledgment
We acknowledge the role of our team: NS - abstract draft, review; AA - review, editing; BK - review, pathology slides