Abstract: FR-PO1291
Unmasking Acute Interstitial Nephritis in Progressive AKI After Elranatamab Exposure in AL Amyloid Kidney Disease
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
- Melendez, Ricardo J., The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
- Borcheni, Mariem, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
- Tchakarov, Amanda, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
Introduction
Elranatamab is a BCMA×CD3 bispecific T-cell-engaging antibody increasingly used in plasma cell dyscrasias. While cytokine release syndrome and infections are recognized complications, acute interstitial nephritis (AIN) has not been well described with this drug class. We present a case of biopsy-confirmed AIN following elranatamab administration, resulting in dialysis-dependent AKI.
Case Description
A 61-year-old woman with stage 2 CKD, hypertension, and hypothyroidism presented with antihypertensive intolerance, progressive edema, and carpal tunnel-like neuropathy. Workup revealed hypoalbuminemia of 2.4g/dL, proteinuria of 12g/24h, low-voltage on ECG, and a monoclonal gammopathy on SPEP/UPEP, prompting hematology evaluation. Kidney biopsy was performed and demonstrated lambda-restricted AL amyloidosis with acute tubular epithelial injury and focal lambda-restricted casts concerning for early light-chain cast nephropathy. Given rapidly progressive systemic symptoms, she was admitted for urgent therapy initiation.
creatinine had risen to 1.4 mg/dL from a baseline of 1.0 mg/dL. EGD confirmed amyloid deposition in the stomach and duodenum, establishing multiorgan involvement. Elranatamab was administered with step-up dosing followed by a full treatment dose. Tocilizumab was given for elevated IL-6, though no clinical cytokine release syndrome was observed throughout hospital course. Despite initial improvement in volume status, AKI progressed with worsening oliguria and an increasingly active urine sediment notable for WBCs and RBCs
Given progressing renal injury, repeat kidney biopsy was performed, demonstrating acute tubulointerstitial nephritis with eosinophilic infiltration, acute tubular necrosis, and persistent lambda-restricted amyloidosis with approximately 20% interstitial fibrosis and tubular atrophy. Prednisone 80 mg daily was initiated. Despite corticosteroid therapy, renal function continued to decline, requiring initiation of CRRT due to hemodynamic instability, with subsequent transition to intermittent hemodialysis. The patient remained dialysis-dependent
Discussion
This case reports biopsy-proven eosinophilic AIN temporally associated with Elranatamab, distinct from the underlying amyloid nephropathy. As bispecific T-cell engagers expand in use, AIN should be considered in unexplained AKI, and early repeat biopsy is critical to distinguish drug-induced nephritis from disease progression.