Abstract: FR-PO0469
AKI in the Setting of Immune Checkpoint Inhibitor Use with Possible ALECT2 Amyloidosis
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
- Jaison, Joshua A., University of California Irvine School of Medicine, Irvine, California, United States
- Gee, Caroline A., University of California Irvine School of Medicine, Irvine, California, United States
- Hanna, Ramy Magdy, University of California Irvine School of Medicine, Irvine, California, United States
Introduction
Immune checkpoint inhibitors (ICIs) are increasingly used in the treatment of advanced malignancies, including hepatocellular carcinoma (HCC), but are associated with immune-related adverse events, including kidney injury. Acute interstitial nephritis (AIN) is the most commonly reported renal manifestation; however, a range of alternative and overlapping pathologies may occur, making diagnosis challenging.
Case Description
We report the case of a 77-year-old Hispanic male with unresectable HCC treated with combination ICI therapy (durvalumab and tremelimumab) who developed progressive acute kidney injury (AKI). His creatinine rose from a baseline of 1.5–1.8 mg/dL to a peak of 8.1 mg/dL over approximately six months, with initial onset occurring within three months of ICI initiation. His HCC remained radiographically stable on combination ICI therapy. Given concern for ICI-associated nephritis, immunotherapy was held and high-dose corticosteroids were initiated without improvement. Renal biopsy demonstrated diffuse ALECT2 amyloidosis with predominantly interstitial involvement, acute tubular injury, mild IgA nephropathy, and moderate chronic changes. Notably, there was no evidence of interstitial nephritis. In the context of stable oncologic disease and limited alternative treatment options, ICI-mediated nephritis was considered less likely and immunotherapy was subsequently resumed. The patient’s renal function progressively declined to end-stage renal disease over the following months, requiring initiation of hemodialysis, while continuing ICI therapy.
Discussion
This case demonstrates a clinicopathologic discordance in suspected ICI-associated AKI, in which biopsy revealed acute tubular injury rather than immune-mediated nephritis. The absence of steroid responsiveness further supports a non–immune-mediated mechanism. Although ICIs have been associated with a range of renal pathologies, there is currently no established association between ICI therapy and ALECT2 amyloidosis. The patient’s renal failure was most consistent with multifactorial injury, including acute tubular injury in the setting of underlying chronic kidney disease and cirrhosis.