How should kidney function be monitored during Bosutinib therapy?

Serum creatinine and eGFR at baseline (sets the CrCl-banded starting dose) and periodically on therapy; a significant decline prompts dose modification; Blood pressure at visits (hypertension is a listed risk factor and a contributing factor to manage); Volume status and stool frequency (diarrhea); Liver enzymes (hepatotoxicity).

How can kidney injury from Bosutinib be prevented?

Aggressive antidiarrheal management and hydration; address concurrent nephrotoxins

Who is at higher risk of kidney injury from Bosutinib?

Lower baseline eGFR; Older age and hypertension; Longer duration / later-line therapy; Significant diarrhea with volume loss.

Back to explorer

Printable monograph

BCR-ABL TKI

Bosutinib

Bosulif · BOSU

BCR-ABL TKI · approved 2012 · 9 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 9 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 SRC/ABL TKI associated with a reversible, imatinib-like decline in eGFR over long-term therapy.

MildBCR-ABL tyrosine kinase inhibitor

Chronic myeloid leukemia

§01

Signature kidney injury

Signature lesion

Pseudo-AKI

Representative incidence11%

9–13% range across studies

Long-term bosutinib is associated with a gradual, generally reversible decline in eGFR. In a long-term analysis, renal adverse events occurred in 9% on first-line and 13% on second-line-or-later bosutinib (the 6% in that analysis is the imatinib comparator arm), and a notable fraction reached grade 3b or worse eGFR (<45 mL/min/1.73 m2), with many recovering on follow-up; the pattern resembles the eGFR decline seen with imatinib.Source: Cortes et al., Clin Lymphoma Myeloma Leuk 2017

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Renal decline develops over months of therapy, with the shortest time to grade 3b eGFR in later-line use.

Distilled from: “Develops over months of therapy; time to grade 3b eGFR is shortest with later-line use.”

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Pseudo-AKI#1 · Signature10%PMID 28807791 (opens PubMed in a new tab)
Reversible eGFR decline; grade >=3b eGFR (<45) in ~10% first-line and ~24% second-line-or-later bosutinib; ~53-58% recovered to >=45
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

11%incidence

SeverityMild

ReversibilityReversible

Evidence9 citations

Nephron map

Vasculature / Endothelium

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

Pseudo-AKI

The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.

§03

Kidney injury

Mechanism of kidney injury

The eGFR decline appears largely functional/hemodynamic rather than from overt structural injury; it parallels imatinib, is frequently reversible, and may reflect an effect on glomerular filtration/perfusion or on tubular creatinine handling rather than progressive nephron loss. Significant GI toxicity (diarrhea) can also contribute prerenal volume depletion.

Clinical presentation

Gradual rise in creatinine and fall in eGFR over months to years, often asymptomatic and detected on routine monitoring; frequently improves after dose modification or discontinuation. Diarrhea-related volume depletion can produce superimposed prerenal AKI.

Management

Monitor renal function and adjust dose for significant eGFR decline; the decline is usually reversible, and many patients recover renal function with dose modification. Manage contributing factors such as hypertension, dehydration, and diarrhea.Lesion-level management framework

Risk factors

Lower baseline eGFR
Older age and hypertension
Longer duration / later-line therapy
Significant diarrhea with volume loss

Prevention

Aggressive antidiarrheal management and hydration; address concurrent nephrotoxins

Anticancer mechanism· how it treats cancer

Dual SRC/ABL kinase inhibitor of BCR-ABL1 with minimal c-KIT/PDGFR activity, which limits the fluid retention and edema seen with imatinib. Used in chronic, accelerated, or blast-phase CML resistant to or intolerant of prior therapy.

Note · Reversible eGFR decline mirroring imatinib; not a structural nephrotoxin in the usual case.

§04

Clinical depth

Renal dose adjustment

Per labeling, reduce the starting dose in baseline renal impairment: CrCl 30-50 mL/min use a reduced starting dose (e.g., 400 mg in the resistant/intolerant setting), and CrCl <30 mL/min use a further-reduced dose (e.g., 300 mg). Titrate per response and tolerability.

Dialyzability & ESKD dosing

Highly protein-bound and hepatically metabolized; not expected to be appreciably dialyzed and no supplemental post-dialysis dosing is established. Use clinical judgment in ESKD.

Differential diagnosis

Separate the reversible bosutinib eGFR drift (parallels imatinib, recovers with dose change) from diarrhea-driven prerenal AKI and from intrinsic structural injury (uncommon). Reversibility on dose modification supports a hemodynamic mechanism.

Monitoring

Serum creatinine and eGFR at baseline (sets the CrCl-banded starting dose) and periodically on therapy; a significant decline prompts dose modification
Blood pressure at visits (hypertension is a listed risk factor and a contributing factor to manage)
Volume status and stool frequency (diarrhea)
Liver enzymes (hepatotoxicity)

Key trials & series

Cortes et al. long-term bosutinib renal-function analysis (2017)
Sonmez et al. TKI eGFR cohort (2024)

Clinical pearls

Bosutinib’s eGFR decline mirrors imatinib and is usually reversible - monitor, don’t panic.
Diarrhea is a frequent bosutinib toxicity and a common prerenal contributor; hydrate and treat it.

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 · 3 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· 3

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.

CaseB · ModerateEffects of SLC22A2 808G>T polymorphism and bosutinib concentrations on serum creatinine in patients with chronic myeloid leukemia receiving bosutinib therapy.Abumiya M et al. · Sci Rep 2021 · PMID 33737618Small study (28 patients) linking bosutinib trough concentration and the SLC22A2/OCT2 808G/G genotype to reversible serum creatinine elevation, the mechanism underlying bosutinib pseudo-AKI.CaseB · ModerateStopping bosutinib reverses bosutinib-induced elevation of serum creatinine in patients with chronic myeloid leukemia.Abumiya M et al. · Int J Hematol 2025 · PMID 40000571Small series (11 CML patients) showing bosutinib raises serum creatinine via OCT2 inhibition and that discontinuation reverses it, i.e. a pseudo-AKI laboratory abnormality rather than true CKD.CaseC · LimitedClinical Spectrum of Bosutinib Related Side Effects in a Patient of CML: A Case Report and Review of Literature.Sharma V et al. · Int J Hematol Oncol Stem Cell Res 2025 · PMID 41281789Single CML case report in which bosutinib was identified as the cause of renal impairment, prompting drug discontinuation.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Reduce the BOSULIF starting dose in patients with moderate (creatinine clearance [CL cr ] 30 to 50 mL/min, estimated by Cockcroft-Gault (C-G)) and severe (CL cr less than 30 mL/min, C-G) renal impairment at baseline. For patients who have declining renal function while on BOSULIF who cannot tolerate the starting dose, follow dose adjustment recommendations for toxicity [see Dosage and Administration (2.3 , 2.5) and Clinical Pharmacology (12.3) ] . BOSULIF has not been studied in patients undergoing hemodialysis.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 8,931 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.
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 outcomes & reporting trend· 8.8% of reports w/ death · 21.5% w/ hospitalization

8.8%

Reported with a death outcome

782 of 8,931 reports

21.5%

Reported with hospitalization

1,918 of 8,931 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 8,931 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 1.2495% CI 0.99–1.54· 80 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Diarrhoea2,071Nausea1,015Vomiting542Abdominal Pain266Abdominal Pain Upper246

General / constitutional

Fatigue726Malaise298Asthenia248Pain220Weight Decreased219

Respiratory

Pleural Effusion455Dyspnoea364

Skin

Rash491Pruritus176

Nervous system

Headache337Dizziness184

Musculoskeletal

Arthralgia255

Immune / infection

Pneumonia206

Metabolic & electrolyte

Decreased Appetite199

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 Bosutinib 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

Alectinib

Alecensa · ALK TKI

Profile

Creatinine rise via reduced tubular secretion.

PSEUDOPRE

Mild#1 · 89% phenotype match

Ceritinib

Zykadia · ALK TKI

Profile

GI-driven prerenal AKI.

PREPSEUDO

Mild#2 · 89% phenotype match

Momelotinib

Ojjaara · JAK/ACVR1 inhibitor

Profile

2023 myelofibrosis JAK inhibitor.

PSEUDOPRE

Mild#3 · 86% phenotype match

Vimseltinib

Romvimza · CSF1R tyrosine kinase inhibitor

Profile

A clean-kidney targeted TKI — watch the CPK, not the nephron.

PSEUDOPRE

Mild#4 · 86% phenotype match

Abemaciclib

Verzenio · CDK4/6 inhibitor

Profile

Benign creatinine rise via tubular secretion block.

PSEUDOPRE

Mild#5 · 78% phenotype match

Capmatinib

Tabrecta · MET inhibitor

Profile

Reversible creatinine rise and edema.

PSEUDOPRE

Mild#6 · 78% phenotype match

Compare Bosutinib 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.

1NilotinibPRE — Prerenal / Hemodynamic AKIMild
2AsciminibHTN — HypertensionMild
3Bosutinib· this agentPSEUDO — 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 Bosutinib’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 Bosutinib; 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 13 clinical records among all 16 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.