Bendamustine
Treanda · Alkylator
Tumor lysis-mediated AKI is the principal risk; TMA is rare.
PRETMALYTE
ModerateOpen →
BCR-ABL TKI
Nilotinib
Tasigna · NILO
A second-generation BCR-ABL TKI whose vascular profile matters more to the kidney than direct nephrotoxicity.
MildBCR-ABL tyrosine kinase inhibitor · approved 2007
Chronic myeloid leukemia
Signature kidney injury
Prerenal / Hemodynamic AKI
Nilotinib carries a recognized risk of arterial occlusive events and metabolic effects (dysglycemia, hyperlipidemia), but direct renal toxicity is limited; in comparative CML cohorts nilotinib generally did not cause significant eGFR decline relative to imatinib. Any kidney impact is largely mediated through vascular disease and perfusion rather than intrinsic nephrotoxicity.
Source: Molica et al., Ann Hematol 2018; Sonmez et al., Clin Lymphoma Myeloma Leuk 2024
Toxicity fingerprint
Tap a signature to trace where it strikes the nephron.
Incidence not quantified
SeverityMild
ReversibilityVariable
Evidence0 refs
Nephron map
Glomerulus
Vasculature / EndotheliumGlomerular & peritubular capillaries
Proximal Tubule
Prerenal / Hemodynamic AKI
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Mechanism of kidney injury
Off-target effects promote endothelial dysfunction, accelerated atherosclerosis, and peripheral arterial occlusive disease, which can reduce renal perfusion (renovascular/prerenal physiology). Treatment-emergent hyperglycemia and hyperlipidemia compound long-term vascular and renal risk. Intrinsic tubular toxicity is not a feature.
Clinical presentation
Often stable renal function; peripheral arterial disease, ischemic events, new hyperglycemia, and hyperlipidemia. Creatinine changes are usually modest and perfusion-related.
Onset
Vascular events accrue over months to years of therapy.
Reversibility
Variable
Anticancer mechanism
Second-generation BCR-ABL1 inhibitor with higher potency and selectivity than imatinib, designed to overcome many imatinib-resistant mutations (not T315I). Used in chronic myeloid leukemia.
Management
Aggressive cardiovascular risk-factor control and vascular surveillance; manage ischemic complications with cardiology/vascular input. Renal function is generally preserved, so kidney management centers on protecting perfusion and treating vascular disease.
Risk factors
- Pre-existing cardiovascular risk factors (diabetes, hypertension, hyperlipidemia)
- Longer treatment duration
- Older age
Prevention
- Cardiovascular risk stratification and risk-factor management before and during therapy
- Monitor glucose, lipids, and blood pressure
- Periodic renal function monitoring
Note · The renal story is vascular/perfusion-mediated; nilotinib is not a direct tubular nephrotoxin and often spares eGFR compared with imatinib.
Clinical depth
Renal dose adjustment
No renal dose adjustment is required (negligible renal excretion); nilotinib is given without change across renal-function categories. Note the QT-prolongation black-box warning and the need to take it on an empty stomach.
Dialyzability & ESKD dosing
Highly protein-bound and hepatically cleared; not dialyzable and no supplemental dosing needed in ESKD.
Differential diagnosis
Attribute creatinine change to perfusion/vascular disease (renovascular, prerenal) rather than intrinsic nilotinib toxicity; exclude prerenal azotemia and contrast/atheroembolic injury after vascular interventions.
Monitoring
- Fasting glucose/HbA1c and lipid panel periodically
- Blood pressure and peripheral vascular assessment
- ECG/QTc (black-box) at baseline and after dose changes
- Serum creatinine periodically
Key trials & series
- Molica et al. front-line TKI eGFR cohort (Ann Hematol 2018)
- Sonmez et al. TKI eGFR cohort (2024)
Clinical pearls
- Nilotinib often spares eGFR compared with imatinib - the renal story is vascular, not tubular.
- Its cardiometabolic toxicity (hyperglycemia, dyslipidemia, arterial occlusion) is the indirect threat to the kidney.
Where it strikes
Nephron segments
Vasculature / Endothelium
Glomerular & peritubular capillaries
Injury signatures
Prerenal / Hemodynamic AKIHypertensionPseudo-AKI
Beyond the kidney
Class-level context for the major non-renal toxicities of bcr-abl tkis.
Vascular
Hypertension, VTE/ATE, bleeding, aneurysm
- Vascular occlusion (ponatinib), fluid retention
Pulmonary
Pneumonitis, ILD, effusions, hypertension
- Pleural effusions (dasatinib), PAH
Cardiac
Cardiomyopathy, QT, ischemia, myocarditis
- QT, heart failure
Evidence
6 peer-reviewed references. Citation metadata via PubMed / NLM.
LandmarkChanges in estimated glomerular filtration rate in chronic myeloid leukemia patients treated front line with available TKIs and correlation with cardiovascular events.Molica M et al. · Ann Hematol 2018 · PMID 29806063Nilotinib did not significantly lower eGFR over time compared with imatinib in CML.PMIDTyrosine Kinase Inhibitor-Associated Cardiovascular Toxicity in Chronic Myeloid Leukemia.Moslehi JJ et al. · J Clin Oncol 2015 · PMID 26371140Reviews nilotinib vascular/cardiometabolic toxicity underlying perfusion-related renal risk.PMIDEffect of Tyrosine Kinase Inhibitor Therapy on Estimated Glomerular Filtration Rate in Patients with Chronic Myeloid Leukemia.Sonmez O et al. · Clin Lymphoma Myeloma Leuk 2024 · PMID 38281820No significant kidney-function deterioration with second-generation TKIs including nilotinib.PMIDCardiovascular toxic effects of targeted cancer therapy.Tajiri K et al. · Jpn J Clin Oncol 2017 · PMID 28531278Describes vascular/ischemic events and metabolic effects with nilotinib and ponatinib.PMIDNew drug toxicities in the onco-nephrology world.Perazella MA et al. · Kidney Int 2015 · PMID 25671763Onco-nephrology class context for TKI renal/vascular effects.PMIDPharmacological nephrotoxicity profile in a comprehensive cancer center: What changed in two decades and predictors for the need for haemodialysis and mortality.Ferreira A et al. · Nefrologia (Engl Ed) 2025 · PMID 40783302Two-decade cancer-center AKI series documenting the rising contribution of TKIs to drug-induced AKI.
Related agents
Other agents sharing the same signature kidney injury.