Abstract: FR-PO0455
A Rare Case of Antitubular Basement Membrane Disease
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Angle, Hannah, The University of North Carolina at Chapel Hill Kidney Center, Chapel Hill, North Carolina, United States
- Derebail, Vimal K., The University of North Carolina at Chapel Hill Kidney Center, Chapel Hill, North Carolina, United States
- Moreno, Vanessa, The University of North Carolina at Chapel Hill Kidney Center, Chapel Hill, North Carolina, United States
- Albadri, Sam, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Jain, Koyal, The University of North Carolina at Chapel Hill Kidney Center, Chapel Hill, North Carolina, United States
Introduction
Anti-tubular basement membrane (anti-TBM) disease is an exceedingly rare cause of tubulointerstitial nephritis (TIN). Here we present a case of progressive kidney injury due to anti-TBM disease.
Case Description
A 69-year-old male with metastatic prostate cancer on androgen-deprivation therapy and multiple dietary supplements presented with worsening kidney function (creatinine 0.84 to 2.7 mg/dL over 20 months) and proteinuria (UPCR 2 g/g, UACR 226 mg/g). He last received chemotherapy and immunotherapy 2 years ago. He was asked to discontinue all supplements. Kidney biopsy was notable for acute on chronic tubulointerstitial nephritis with granular IgG staining along proximal tubular basement membranes. Immunofluorescence staining was absent along glomerular basement membranes (GBM) and brush borders. Immunochemistry stains for anti-LRP2/megalin were negative. He received high-dose corticosteroids and mycophenolate mofetil. Creatinine increased to 6.11mg/dL, so repeat biopsy was done with similar findings of immune-mediated tubular injury and interstitial nephritis. Rare eosinophils raised concern for possible drug-reaction. Myoglobin casts were also seen. Creatinine kinase was normal, and myositis panel was negative. He was treated with plasmapheresis and rituximab but progressed to end-stage kidney disease (ESKD).
Discussion
Anti-TBM disease is associated with autoimmune diseases, infections, malignancies, and medications. Co-existent anti-GBM disease has also been reported. In this case, autoimmune and infectious workup were negative, and no prostate cancer progression or new malignancy was noted. Anti-TBM disease secondary to drug-reaction was favored due to patient’s extensive supplement use, features of drug-induced nephritis on biopsy, and no improvement after immunosuppression. Whether remote immunotherapy may have contributed is unclear. Due to lack of an available clinical assay, anti-TBM antibody titers were not sent. This case highlights a rare disease with poor prognosis for which additional research and diagnostic testing is needed.