Abstract: FR-PO1261
Delayed Interstitial Nephritis After Chimeric Antigen Receptor-T Cell Therapy for Diffuse Large B-Cell Lymphoma
Session Information
- Onconephrology: Diagnostic Dilemmas, Therapy-Related Toxicities, and Clinical Cases
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Ling, Andrew, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, United States
- Canetta, Pietro A., Columbia University Vagelos College of Physicians and Surgeons, New York, New York, United States
- Al-Awqati, Qais, Columbia University Vagelos College of Physicians and Surgeons, New York, New York, United States
Introduction
Acute kidney injury (AKI) occurs in 5%-30% of patients following chimeric antigen receptor (CAR) T-cell therapy, most commonly from cytokine release syndrome (CRS)-associated acute tubular injury. Interstitial nephritis as a potential immune-mediated complication of CAR T-cell therapy has been rarely described. Here, we present a case of delayed kidney injury following CAR T-cell therapy with biopsy-proven interstitial nephritis and clear improvement in kidney function after corticosteroid therapy.
Case Description
A 45-year-old man with HIV, CKD stage 3, and relapsed/refractory diffuse large B-cell lymphoma underwent CAR T-cell therapy complicated by CRS and immune effector cell-associated neurotoxicity syndrome during the first week post-infusion. He was readmitted on day +31 after CAR T-cell therapy with catheter-associated bacteremia treated with antibiotics and catheter removal. Serum creatinine subsequently rose to a peak of 4.3 mg/dl on day +34 from a baseline of 1-1.1 mg/dl. Urinalysis was bland without albuminuria and complements were normal. AKI was initially attributed to acute tubular necrosis related to infection and contrast exposure; however, kidney function failed to improve despite clearance of blood cultures and supportive care.
Kidney biopsy on day +41 demonstrated resolving acute tubular injury and moderate acute interstitial nephritis. Immunostaining of infiltrating lymphocytes was CD3-positive and CD19-negative, arguing against lymphomatous infiltration. Medications including antimicrobials were reviewed and all had been administered multiple times in the past without prior associated kidney injury. Given the degree of AKI without alternative explanation for interstitial nephritis, steroids were initiated with rapid improvement in kidney function.
Discussion
Biopsy-proven interstitial nephritis following CAR T-cell therapy has been rarely described and may represent an underrecognized cause of both early and delayed AKI in this population. In this case, delayed presentation unassociated with CRS, steroid responsiveness, and lack of evidence for other medication-related causes raised concern for CAR T-cell associated interstitial nephritis. Further study is needed to better characterize interstitial nephritis as a potential immune-mediated cause of kidney injury following CAR T-cell therapy.