What kind of kidney injury does Nilotinib cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Is kidney injury from Nilotinib reversible?

Variable. Typical onset: Vascular events accrue over months to years of therapy..

How should kidney function be monitored during Nilotinib therapy?

Fasting glucose/HbA1c and lipid panel periodically; Blood pressure and peripheral vascular assessment; ECG/QTc (black-box) at baseline and after dose changes.

How can kidney injury from Nilotinib be prevented?

Cardiovascular risk stratification and risk-factor management before and during therapy

Who is at higher risk of kidney injury from Nilotinib?

Pre-existing cardiovascular risk factors (diabetes, hypertension, hyperlipidemia); Longer treatment duration; Older age.

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Printable monograph

BCR-ABL TKI

Nilotinib

Tasigna · NILO

BCR-ABL TKI · approved 2007 · 8 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 10y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

A second-generation BCR-ABL TKI whose vascular profile matters more to the kidney than direct nephrotoxicity.

MildBCR-ABL tyrosine kinase inhibitor

Chronic myeloid leukemia

§01

Signature kidney injury

Signature lesion

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

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Vascular events accumulate over months to years of therapy.

Distilled from: “Vascular events accrue over months to years of therapy.”

§02

Renal toxicities, ranked

This agent's defining kidney lesion — its #1 signature. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

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.

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.Lesion-level management framework

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

Anticancer mechanism· how it treats cancer

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.

Note · The renal story is vascular/perfusion-mediated; nilotinib is not a direct tubular nephrotoxin and often spares eGFR compared with imatinib.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment is required across renal-function categories (negligible renal excretion). 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

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 & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI

Beyond the kidney — non-renal toxicities· 3 organ systems

Class-level context for the major non-renal toxicities of the BCR-ABL TKI class.

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

§05

References

6 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2015–2025 · 2 since 2023

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Case reports — ranked by strength· 2

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseC · LimitedNilotinib-Induced Unilateral Renal Artery Stenosis: A Complication Prompting Treatment-Free Remission in Chronic Myeloid Leukemia.Boshkos MC et al. · Case Rep Oncol Med 2025 · PMID 40959317Case report of unilateral renal artery stenosis attributed to nilotinib, a renovascular/hemodynamic complication causing renal compromise in a CML patient.CaseC · Limited[Renal artery stenosis following nilotinib administration in a patient with chronic myelogenous leukemia].Hatsuse M et al. · Rinsho Ketsueki 2017 · PMID 28190859Case report of renal artery stenosis developing after nilotinib therapy, a hemodynamic/renovascular cause of impaired renal perfusion in a CML patient.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Aug 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: QT PROLONGATION and SUDDEN DEATHS Nilotinib capsules prolongs the QT interval. Prior to nilotinib capsules administration and periodically, monitor for hypokalemia or hypomagnesemia and correct deficiencies [see Warnings and Precautions ( 5.2 )]. Obtain ECGs to monitor the QTc at baseline, seven days after initiation, and periodically thereafter, and following any dose adjustments [see Warnings and Precautions ( 5.2 , 5.3 , 5.7 , 5.12 )] . Sudden deaths have been reported in patients receiving nilotinib capsules [see Warnings and Precautions ( 5.3 )]. Do not administer nilotinib capsules to patients with hypokalemia, hypomagnesemia, or long QT syndrome [see Contraindications ( 4 ), Warnings and Precautions ( 5.2 )]. Avoid use of concomitant drugs known to prolong the QT interval and strong CYP3A4 inhibitors [see Drug Interactions ( 7.1 , 7.2 )]. Avoid food 2 hours before and 1 hour after taking the dose [see Dosage and Administration ( 2.1 )]. WARNING: QT PROLONGATION and SUDDEN DEATHS See full prescribing information for complete boxed warning. Nilotinib c apsules prolongs the QT interval. Prior to nilotinib capsules administration and periodically, monitor for hypokalemia or hypomagnesemia and correct deficiencies. ( 5.2 ) Obtain ECGs to monitor the QTc at baseline, seven days after initiation, and periodically thereafter, and following any dose adjustments. ( 5.2 ,…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 29,318 of them for this agent. Nobody counts the patients who were fine, so none of these numbers is an incidence, a risk, or a rate: they describe what gets reported, shaped by a drug's fame, its indication, and who was watching. How these numbers work.

Reporting odds ratio (ROR) — is kidney injury named in this agent's reports more often than in every other drug's? Above 1 means yes, disproportionately.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
Outcomes — a share of this agent's own reports, not of patients: how many were filed as involving a death or a hospitalization. Not a case-fatality rate.

FAERS reported renal phenotypes· 3 signals

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Hemorrhagic Cystitis

ROR 2.7295% CI 2.40–3.07· 261 reports

Hypertension

ROR 1.8795% CI 1.75–1.99· 990 reports

Crystal / Obstructive Nephropathy

ROR 1.4495% CI 1.20–1.73· 112 reports

FAERS outcomes & reporting trend· 19.2% of reports w/ death · 21.9% w/ hospitalization

19.2%

Reported with a death outcome

5,616 of 29,318 reports

21.9%

Reported with hospitalization

6,425 of 29,318 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 29,318 reports

Bars rank systems by summed reaction-term mentions (a report counts once per term it names) — an ordinal “more vs less reported” cue, not a tally of distinct reports. Renal & urinary first. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 0.4595% CI 0.37–0.55· 96 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

General / constitutional

Fatigue2,112Pain1,344Malaise1,139Pyrexia1,129Asthenia1,058

Gastrointestinal

Nausea1,545Diarrhoea1,215Vomiting1,058Abdominal Pain821Abdominal Pain Upper802

Respiratory

Dyspnoea1,391Pleural Effusion780Cough748

Musculoskeletal

Arthralgia1,089Pain In Extremity872Myalgia831

Skin

Rash1,653Pruritus1,132

Nervous system

Headache1,490Dizziness917

Blood & lymphatic

Platelet Count Decreased826Anaemia778

Cardiac

Myocardial Infarction894

Guidelines & consensus· 13

Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.

Where Nilotinib sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

Asparaginase

Elspar · Enzyme

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild#1 · 89% phenotype match

Belzutifan

Welireg · HIF-2α inhibitor

Profile

Anemia/hypoxia; emerging renal profile in VHL/RCC.

PRE

Mild#2 · 89% phenotype match

Dacarbazine

DTIC · Alkylator

Profile

Rare hepatic veno-occlusive disease; minimal direct renal injury.

PRE

Mild#3 · 89% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#4 · 89% phenotype match

Irinotecan

Camptosar · Topoisomerase I inhibitor

Profile

Diarrhea-driven prerenal AKI.

PRE

Mild#5 · 89% phenotype match

Mirvetuximab soravtansine

Elahere · Antibody-drug conjugate (FRα/DM4)

Profile

Ocular toxicity dominates; renal involvement indirect/case-level (GI volume loss).

PRE

Mild#6 · 89% phenotype match

Compare Nilotinib with its nearest agents

Nearest agents by kidney-injury phenotype (shared injuries, nephron target, severity, class) — a similarity approximation, not a claim of shared drug identity or mechanism.

Kidney risk across BCR-ABL inhibitors

Same-class agents ordered by their documented kidney-injury profile — atlas severity, an acute-kidney-injury FAERS signal, and how many injury types each is documented to cause. Agents nearer the top carry the lighter documented renal profile.

1Nilotinib· this agentPRE — Prerenal / Hemodynamic AKIMild
2AsciminibHTN — HypertensionMild
3BosutinibPSEUDO — Pseudo-AKIMild
4ImatinibLYTE — Electrolyte DisturbanceMild
5OlverembatinibGLOM — Glomerular Injury / ProteinuriaMild
6PonatinibHTN — HypertensionModerate
7DasatinibGLOM — Glomerular Injury / ProteinuriaFAERS AKIModerate

A comparison of documented kidney-injury data within one drug class — not a substitution recommendation. Efficacy, indication, and non-renal toxicity differ between these agents and are out of scope here. Educational only, not medical advice.

Who studies this

The leading contributors to Nilotinib’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Nilotinib; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 23 clinical records among all 37 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.