Abstract: SA-PO0345
Sequential Drug Sensitization Leading to Drug-Induced Hypersensitivity Syndrome/Toxic Epidermal Necrolysis Triggered by Valacyclovir-Induced AKI and Oxypurinol Accumulation
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 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
Author
- Miyata, Hitomi, Kyoto Katsura Byoin, Kyoto, Kyoto Prefecture, Japan
Introduction
Drug reaction with eosinophilia and systemic symptoms (DRESS), also known as drug-induced hypersensitivity syndrome (DIHS), is characterized by multiorgan involvement and viral reactivation. Sequential drug sensitization triggered by acute kidney injury (AKI) is rarely documented. We report a case in which valacyclovir-associated AKI and continued allopurinol therapy facilitated delayed T-cell sensitization to oxypurinol, culminating in DIHS with toxic epidermal necrolysis (TEN).
Case Description
A woman in her 60s developed labial herpes on Day-12 and was prescribed valacyclovir 500 mg twice daily. On Day -8, she developed purpura; skin biopsy showed leukocytoclastic vasculitis without IgA deposition. On Day -7, she was found to have worsening renal function (Cr 1.7 mg/dL) and was treated as IgA vasculitis with prednisolone 45 mg, which she discontinued after one day before later resuming due to worsening symptoms. She continued allopurinol 100 mg daily throughout this period despite progressive renal dysfunction. On Day 0 (admission), she received intravenous acyclovir 250 mg, after which her creatinine acutely increased to 3.3 mg/dL, consistent with early valacyclovir-associated AKI. Initial DLST was positive only for valacyclovir (230%). Although her skin lesions transiently improved with steroid pulse therapy, they rapidly worsened after switching to oral steroids on Day +4, progressing to painful blistering and epidermal detachment requiring ICU care. Laboratory findings included eosinophilia (25%), hypogammaglobulinemia, nephrotic-range proteinuria, and HHV-6 reactivation on Day +14. On Day +90, DLST became newly positive for oxypurinol, indicating delayed T-cell sensitization likely facilitated by oxypurinol accumulation due to impaired renal clearance. These findings support a sequential drug-sensitization mechanism leading to DIHS/TEN.
Discussion
This case demonstrates a rare biphasic course in which valacyclovir-induced AKI and continued allopurinol therapy promoted oxypurinol accumulation and subsequent delayed hypersensitivity, resulting in DRESS/DIHS with TEN. Careful review and adjustment of renally cleared medications during AKI may prevent secondary sensitization and severe drug reactions.
Acknowledgment
We would like to express our sincere gratitude to Dr. Makiko Ishikawa, dermatologist, for her expert advice, and to the physicians at Kyoto University Hospital for providing intensive care management.