Abstract: SA-PO1246
Neurotoxicity Is Associated with AKI After Chimeric Antigen Receptor-T Cell Therapy Independent of Cytokine Release Syndrome
Session Information
- Onconephrology: Epidemiological Trends, Risk Stratification, and Clinical Outcomes
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Del Castillo Rix, Daniel Sebastian, University of Miami Department of Medicine, Miami, Florida, United States
- De Alencar Salazar Primo, Guilherme, University of Miami Department of Medicine, Miami, Florida, United States
- Duque, Nicolas, University of Miami Department of Medicine, Miami, Florida, United States
- Dejman, Adriana, University of Miami Department of Medicine, Miami, Florida, United States
- Sosa, Marie Anne, University of Miami Department of Medicine, Miami, Florida, United States
- Duque, Juan, University of Miami Department of Medicine, Miami, Florida, United States
Background
Cytokine release syndrome (CRS) is widely considered the primary driver of organ toxicity following chimeric antigen receptor T-cell (CAR-T) therapy. However, the mechanisms underlying acute kidney injury (AKI) in this setting remain poorly understood, and the contribution of immune effector cell-associated neurotoxicity syndrome (ICANS) to AKI has not been systematically evaluated.
Methods
We conducted a retrospective cohort study of adults undergoing CAR-T therapy at a large academic center between 2017 and 2025. AKI occurring within 7 days of infusion was defined using KDIGO serum creatinine criteria. Associations between AKI and CAR-T–related toxicities, including CRS and neurotoxicity, were evaluated. Multivariable logistic regression was performed, adjusting for CRS, age, sex, baseline eGFR, and Karnofsky performance score.
Results
Among 305 patients receiving CAR-T therapy, 43 (14.1%) developed AKI. CRS incidence was similar between patients with and without AKI (79.1% vs 80.5%, p=0.823), with no significant differences in CRS severity, tocilizumab use, or corticosteroid exposure. In contrast, neurotoxicity occurred more frequently among patients with AKI (58.1% vs 40.1%, p=0.026). In multivariable logistic regression, neurotoxicity remained independently associated with AKI (OR 2.37, 95% CI 1.15–4.86, p=0.019), whereas CRS was not independently associated with AKI (OR 0.60, 95% CI 0.25–1.43, p=0.245) (Table 1). Among patients with AKI, median neurotoxicity onset occurred 6 days after infusion (IQR 5–9), similar to AKI onset (median 5 days, IQR 4–7).
Conclusion
In this retrospective cohort, neurotoxicity was associated with AKI following CAR-T therapy, while CRS and CRS-directed treatment were not significantly associated with AKI. The relationship between neurotoxicity and AKI remains incompletely understood and should be considered hypothesis-generating. Future prospective studies should evaluate whether the clinical or biologic factors predisposing to neurotoxicity also increase AKI risk.
Table 1. Multivariable predictors of AKI following CAR-T therapy
| Variable | Adjusted OR | 95% CI | p-value |
| Neurotoxicity | 2.37 | 1.15–4.86 | 0.019 |
| CRS | 0.60 | 0.25–1.43 | 0.245 |
| Age | 0.99 | 0.96–1.02 | 0.461 |
| Male sex | 1.18 | 0.58–2.39 | 0.649 |
| Baseline eGFR | 1.00 | 0.98–1.03 | 0.874 |
| Karnofsky score | 0.98 | 0.95–1.01 | 0.247 |