Abstract: TH-PO0542
Biopsy-Proven IgAN in a Patient with Longstanding Diabetes and Progressive CKD
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
- Watwani, Siddhant G., CORE Kidney Program, UCLA Health, Los Angeles, California, United States
- Ovalekar, Simran, CORE Kidney Program, UCLA Health, Los Angeles, California, United States
- Nakahara, Jared R., CORE Kidney Program, UCLA Health, Los Angeles, California, United States
- Chowdhary, Alisha, CORE Kidney Program, UCLA Health, Los Angeles, California, United States
- Rao, Saket, CORE Kidney Program, UCLA Health, Los Angeles, California, United States
- Sim, Zachary C., CORE Kidney Program, UCLA Health, Los Angeles, California, United States
- Rastogi, Anjay, CORE Kidney Program, UCLA Health, Los Angeles, California, United States
Introduction
Anchoring on Diabetic Kidney Disease (DKD) as the default diagnosis in long-standing diabetics with progressive CKD can delay recognition of coexisting or mimicking glomerular disease. This case presents a 69-year-old male with advanced IgAN, initially diagnosed with DKD given a 20-year history of diabetes. The patient initially declined biopsy due to procedural concerns. After 5 years, worsening eGFR, proteinuria, and hematuria prompted biopsy, revealing IgAN and redirecting management.
Case Description
A patient with HTN, T2DM, glaucoma, and pulmonary sarcoidosis presented with progressive CKD (eGFR 59→24 mL/min/1.73 m^2), rising proteinuria (ACR >1300 mg/g), and persistent hematuria. Initial workup pursued a broad differential and included renal ultrasound showing cortical thinning, negative SPEP/UPEP, ACE <10, and an unremarkable urology evaluation. Biopsy was initially declined due to slow rate of decline and procedural concerns. After 5 years of worsening eGFR, proteinuria, and hematuria, biopsy was performed and showed advanced IgAN (Oxford M1 E1 S1 T1 C1, ~70% global glomerulosclerosis, 30-40% IFTA). Lisinopril (previously held for low BP) was restarted at 2.5mg daily for antiproteinuric effect; finerenone 10mg daily was added with diet and hydration counseling. At 1-year follow-up, eGFR stabilized and ACR fell from ~950 to 11 mg/g.
Discussion
This case demonstrates that non-diabetic kidney disease may coexist with or mimic diabetic nephropathy in long-standing diabetics. Anchoring on the most likely diagnosis risks missing treatable alternatives when proteinuria, hematuria, or rate of decline do not fit the expected course. The case highlights the importance of utilizing a comprehensive set of diagnostic tests that provide multiple perspectives on the patient’s condition and demonstrates how timely diagnosis can alter management, prognosis, and long-term renal outcomes.
Immunofluorescence showing mesangial IgA deposits.