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Abstract: TH-PO0182

Corticosteroid-Resistant Acute Interstitial Nephritis Following Amivantamab Treatment: A Rare Kidney-Related Adverse Event

Session Information

Category: Onconephrology

  • 1700 Onconephrology

Authors

  • Brito, Germana Alves, A C Camargo Cancer Center, São Paulo, SP, Brazil
  • De Andrade, Luis Andre Silvestre, A C Camargo Cancer Center, São Paulo, SP, Brazil
  • Cordeiro De Lima, Vladmir Claudio, A C Camargo Cancer Center, São Paulo, SP, Brazil
  • Pereira, Benedito J., A C Camargo Cancer Center, São Paulo, SP, Brazil
  • Kwon, Alvin Guyun, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
  • Schaubschlager, Taylor, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Introduction

Amivantamab is a bispecific EGFR-MET antibody approved for EGFR exon 20-mutated NSCLC after progression on platinum-based chemotherapy. To date, no renal adverse events have been reported in the FDA FAERS database. We report two biopsy-proven cases of acute interstitial nephritis (AIN) associated with amivantamab, both corticosteroid refractory.

Case Description

Case1:A 57-year-old man with metastatic NSCLC received carboplatin (4 cycles), pemetrexed (10), and amivantamab (13). Baseline serum creatinine (sCr) was 1.1 mg/dL; Acute kidney injury prompted discontinuation (peak sCr 3.0mg/dL). Urinalysis was bland; 24-hour proteinuria <0.3 gr. Autoimmune (ANA, anti-dsDNA, C3/C4, RF, ANCA) and infectious (HIV, HBV, HCV) work-up were negative. Kidney biopsy revealed glomerulomegaly, eosinophilic AIN, focal acute tubular injury, mild fibrosis and atrophy, and arteriosclerosis. Immunofluorescence was negative; EM showed rare inflammatory cells and segmental foot process effacement. Corticosteroids were ineffective. Two doses of infliximab 5m/Kg led to partial kidney recovery (sCr 2.2mg/dL), allowing amivantamab resumption.
Case2:A 54-year-old woman with metastatic NSCLC received carboplatin/pemetrexed (4 cycles), followed by amivantamab. She developed acute kidney injury (peak sCr 2.9mg/dL). Urinalysis showed trace leukocyte esterase; urine microalbumin/creatinine ratio was 35 mg/g. Viral serologies were negative. Biopsy revealed patchy mononuclear AIN with rare eosinophils, mild tubulitis, edema, and acute tubular injury, without fibrosis or atrophy. Immunofluorescence and EM were negative for deposits; 20–30% podocyte foot process effacement was noted. Corticosteroids were ineffective, and no renal improvement was observed after initiation of mycophenolate. Infliximab was withheld due to insurance and TB risk (indeterminate QuantiFERON). Amivantamab was discontinued, and the patient experienced cancer progression. Kidney function remained impaired (sCr 2.7mg/dL).

Discussion

These appear to be the first biopsy-confirmed cases of AIN associated with amivantamab. Both were steroid-resistant, with limited response to additional immunosuppression. Recognition of renal immune-related toxicity is crucial, as it may disrupt oncologic treatment and worsen outcomes.

Digital Object Identifier (DOI)