Abstract: TH-PO0205
Outcome of Imatinib-Induced Interstitial Nephritis: A Case Report
Session Information
- Onconephrology: Anticancer Therapies, PTLD, Paraneoplastic Diseases, and More
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Jaryal, Ajay, All India Institute of Medical Sciences Bilaspur, Bilaspur, HP, India
- Dhiman, Pravesh, All India Institute of Medical Sciences Bilaspur, Bilaspur, HP, India
- Vikrant, Sanjay, All India Institute of Medical Sciences Bilaspur, Bilaspur, HP, India
- Garg, Garima, Dr Lal PathLabs Limited, Gurugram, HR, India
Introduction
Long term use of Imatinib can rarely lead to renal dysfuntion. We present a case of acute on chronic interstitial nephritis (ACIN) due to prolonged use of imatinib. Treatment with steroids and change to nilotinib led to improvement.
Case Description
A 53-year-old male on a tyrosine kinase inhibitor (TKI) imatinib 400 mg/day for 11 years for chronic myeloid leukemia (CML), with disease in complete remission (undetectable BCR ABL), was evaluated for insidiously rising serum creatinine (Scr) for last 1.5 years. Investigations revealed: hemoglobin 7.7 gm/dl, urea 112 mg/dl, Scr 4.2 mg/dl, urine protein 1+, RBC 2-3/HPF, WBC 8-10/HPF, sterile urine culture & 24-hour urine protein 480 mg. So, a kidney biopsy was done which on light microscopy showed: 17 glomeruli, 11 globally sclerosed, interstitial fibrosis tubular atrophy 30-35%, acute tubular injury & multifocal chronic interstitial inflammation with plenty of eosinophils (Image 1). In view of ongoing eosinophilic interstitial inflammation consistent with ACIN patient was treated with IV methylprednisolone 250 mg/day for 3 days & tapering course of oral steroids over 4 weeks. After oncology review, imatinib was stopped in view of longstanding complete remission of CML. It led to improvement in GFR. But, after 3 months of stopping imatinib patient had elevation of BCR ABL, so nilotinib was started. Treatment with steroids and stoppage of culprit drug causing ACIN led to sustained (> 12 months) improvement in GFR, anemia & metabolic bone disease (Table 1).
Discussion
Establishing a cause of renal dysfunction in drug induced nephrotoxicity has therapeutic benefit. The case highlights that nephrotoxicity of one TKI can be ameliorated by changing to another TKI with dual benefits of salvaging kidney and treating CML.
Trend of eGFR and hemoglobin over 1 year
| Baseline | Month 1 | Month 6 | Month 12 | |
| eGFR (2021-CKD EPI creatinine) (ml/min/1.73m2) | 16 | 19 | 21 | 25 |
| Hemoglobin (gm/dl) | 7.7 | - | 11 | 10.8 |
Renal biopsy showing eosinophil rich lymphoplasmacytic interstitial inflammation (H&Ex400)