Kidney Week

Abstract: FR-PO1271

Nilotinib-Induced Proteinuria

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

• Hasan, Sara, NYU Langone Health, New York, New York, United States

Sara Hasan, DO

• Cohen, Eric P., NYU Langone Health, New York, New York, United States

Eric P. Cohen, MD

Introduction

Nilotinib is a second-generation tyrosine kinase inhibitor (TKI) used as first-line treatment for chronic myeloid leukemia (CML) against BCR-ABL. Renal adverse effects remain incompletely characterized. We present a case of progressive proteinuria and acute kidney injury associated with nilotinib use.

Case Description

A 69-year-old female with chronic-phase CML was started on nilotinib due to inability to tolerate imatinib and dasatinib. Several months after initiation, she developed intermittent foamy urine, weak urinary stream, and decreased frequency.
Before nilotinib initiation, serum creatinine ranged from 0.7–0.87 mg/dL with estimated glomerular filtration rate (eGFR) 80–95 mL/min/1.73 m2 and bland urinalysis. A few months later, urinalysis demonstrated trace proteinuria with urine protein-to-creatinine ratio (UPCR) of 1350 mg/g and urine albumin-to-creatinine ratio (UACR) of 120 mg/g. Serum creatinine increased to 0.95–1.53 mg/dL with eGFR decline to 37–72 mL/min/1.73 m2.
Renal biopsy demonstrated mild mesangial expansion, normal to mildly thickened capillary loops, focal tubular atrophy and interstitial fibrosis, and mild arteriolar hyalinosis. Immunofluorescence showed trace mesangial staining for IgA. Electron microscopy revealed mild segmental foot process effacement. Findings were consistent with focal global glomerulosclerosis, not fulfilling the criteria for IgA nephropathy.
Nilotinib was discontinued with marked improvement in proteinuria and foamy urine, including reduction of UPCR to 138 mg/g and UACR to 14 mg/g. Reinitiation of nilotinib resulted in worsening renal function and recurrent proteinuria, prompting transition to an alternative TKI.

Discussion

Limited literature exists regarding renal toxicity from BCR-ABL TKIs. Class adverse effects include nephrotic syndrome, renal artery stenosis, thrombotic microangiopathy, tumor lysis syndrome-related kidney injury, and acute interstitial nephritis. This case highlights proteinuria and azotemia associated with nilotinib use and underscores the need for attention to TKI-related nephrotoxicity.

Timeline