Abstract: TH-PO0543
IgAN: An Inside Job
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
- Johnson, Jeshanah, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Azam, Muhammad Jibran, Vanderbilt University Medical Center, Nashville, Tennessee, United States
- Gardner, Maryn, Vanderbilt University Medical Center, Nashville, Tennessee, United States
Introduction
IgA Nephropathy is the most common form of glomerulonephritis worldwide, effecting around 25 million people yearly. The disease typically presents in the 3rd or 4th decade of life with hematuria or proteinuria noted on a urinalysis. A smaller percentage of patients can present with synpharyngitic hematuria. This case explores an atypical presentation of the disease.
Case Description
We report the case of a 60-year-old male with IgA Lambda Multiple Myeloma (MM) diagnosed by bone marrow biopsy. He presented for evaluation of acute kidney injury on mild chronic kidney disease after treatment and remission of multiple myeloma with Velcade, Lenalidomide, Dexamethasone, and autologous stem cell transplant. On evaluation, urinalysis was negative for hematuria or proteinuria. Screening tests for other auto-immune and viral causes for change in eGFR (HIV, HBV, HCV, ANA, ANCA, complements, PLA2r, anti-GBM Ab, uric acid, and LDH/haptoglobin) were unremarkable. Renal ultrasound at that time was without acute abnormalities. Creatinine was 0.9-1.0 at baseline the year prior and had acutely worsened to 1.5 - 1.7. On review of medications , Bortezomib had been removed from therapy due to neuropathy and was the only significant change. MM surveillance labs revealed that IgA levels did become more elevated about six months prior to AKI, which prompted restaging of MM; however, PET CT and bone marrow biopsy were negative for recurrence of disease. After recurrent worsening of creatinine to 2.7 from a re-established baseline, the patient underwent a renal biopsy for evaluation. The biopsy was positive for changes characteristic of IgA nephropathy (M0E0S0T1-C0) and there was no evidence of clonal restriction. Most recently, he has had one episode of synpharyngitic hematuria and AKI with creatinine to 4.6 treated with pulse dose steroids and subsequent steroid taper for presumed IgA flare.
Discussion
IgA Nephropathy remains more common than light chain deposition disease; however, this was unexpected given that his IgA levels had remained stable with negative SPEP and light chains over two years of surveillance. Our case demonstrates the need for a broad differential and prompt evaluation by kidney biopsy when serological studies remain unrevealing for pathology. It also demonstrates the importance of a multidisciplinary approach among subspecialities to determine appropriate management.