How should kidney function be monitored during Imatinib therapy?

Serum phosphate and electrolytes; Weight/edema assessment at visits; Urinalysis for glucosuria/proteinuria if tubular dysfunction suspected; Serum creatinine and eGFR during long-term therapy.

How can kidney injury from Imatinib be prevented?

Phosphate and electrolyte repletion as needed Manage edema with dose adjustment and supportive care; TLS precautions in bulky disease

Who is at higher risk of kidney injury from Imatinib?

Prolonged therapy; Older age and lower baseline eGFR; Pre-existing renal impairment; Concurrent nephrotoxins; high tumor burden (urate risk).

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Printable monograph

BCR-ABL TKI

Imatinib

Gleevec · IMA

BCR-ABL TKI · approved 2001 · 9 citations

Recent· through 2024

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 21y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2024
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.

The pioneering BCR-ABL TKI, with fluid retention, a slow eGFR drift, and uncommon proximal tubular (Fanconi-type) injury.

MildBCR-ABL tyrosine kinase inhibitor

Chronic myeloid leukemiaPhiladelphia-positive acute lymphoblastic leukemiaGastrointestinal stromal tumor

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

Periorbital/peripheral edema and fluid retention are common. Clinically meaningful renal injury is uncommon: long-term front-line imatinib is associated with a modest, measurable decline in eGFR over years, while proximal tubular dysfunction (hypophosphatemia, aminoaciduria, rare Fanconi syndrome) and AKI (including rare urate nephropathy from disease cytoreduction) are described at the case level.Source: Molica et al., Ann Hematol 2018 (front-line TKI eGFR cohort)

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Tubular dysfunction and eGFR decline develop over months to years (edema is early).

Distilled from: “Edema early; tubular dysfunction and eGFR decline develop over months to years.”

§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.

Electrolyte Disturbance#1 · Signaturequalitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Acute Tubular NecrosisRare4%PMID 26217876 (opens PubMed in a new tab)
TKI-associated AKI in ~4% of a CML cohort, incidence highest with imatinib vs dasatinib/nilotinib
Fanconi SyndromeRareno population incidence denominator
Case-level: partial Fanconi syndrome with urinary phosphate loss / hypophosphatemia reported on long-term imatinib PMID 18215707 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence9 citations

Nephron map

Proximal Tubule

Distal Tubule / Collecting DuctFine-tuning of Na, K, Mg, acid & water

Electrolyte Disturbance

Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

§03

Kidney injury

Mechanism of kidney injury

Proximal tubular injury is the main renal-specific mechanism: experimental and clinical data implicate mitochondrial impairment and oxidative stress in proximal tubular cells, manifesting as phosphate wasting, aminoaciduria, low-molecular-weight proteinuria, and occasionally a full Fanconi pattern. Off-target inhibition of PDGFR and c-KIT contributes to fluid retention and to the slow eGFR change. Rare AKI can be prerenal/obstructive from urate nephropathy when bulky disease is rapidly debulked.

Clinical presentation

Edema and weight gain; hypophosphatemia and hypokalemia; normoglycemic glucosuria, aminoaciduria, and LMW proteinuria in Fanconi-type cases; gradual creatinine rise and eGFR decline over years; rarely anuric AKI with urate crystals.

Management

Replete phosphate/electrolytes and give supportive care for edema; reduce or interrupt the dose for significant AKI or tubular dysfunction. Tubular abnormalities and eGFR decline are generally mild and often improve with dose modification. Treat urate nephropathy with hydration and rasburicase.Lesion-level management framework

Risk factors

Prolonged therapy
Older age and lower baseline eGFR
Pre-existing renal impairment
Concurrent nephrotoxins; high tumor burden (urate risk)

Prevention

Phosphate and electrolyte repletion as needed
Manage edema with dose adjustment and supportive care; TLS precautions in bulky disease

Anticancer mechanism· how it treats cancer

First-generation tyrosine kinase inhibitor that occupies the ATP-binding pocket of BCR-ABL1 (and c-KIT and PDGFR), blocking constitutive kinase signaling that drives leukemic and stromal-tumor proliferation. Used in chronic myeloid leukemia, Ph+ ALL, and GIST.

Note · Fanconi syndrome and AKI are rare and case-level; the everyday issues are fluid retention, hypophosphatemia, and a slow eGFR decline on long-term therapy.

§04

Clinical depth

Renal dose adjustment

Decrease the starting dose by ~50% for moderate renal impairment (CrCl 20-39 mL/min; doses >400 mg not recommended), with further reduction (e.g. 100 mg) and added caution in severe impairment (CrCl <20 mL/min); mild impairment (CrCl 40-59) tolerates up to standard/600 mg. Adjust for tolerability rather than by a strict eGFR algorithm.

Dialyzability & ESKD dosing

Imatinib is highly protein-bound (~95%) with a large volume of distribution and is not appreciably removed by hemodialysis; supplemental post-dialysis dosing is not required.

Differential diagnosis

Distinguish the slow imatinib eGFR drift and Fanconi pattern from prerenal azotemia (edema can coexist with intravascular depletion), from other causes of hypophosphatemia, and from disease-related urate nephropathy. A proximal tubular signature (glucosuria with normoglycemia, phosphaturia, aminoaciduria) is the tell for direct tubular toxicity.

Monitoring

Serum phosphate and electrolytes
Weight/edema assessment at visits
Urinalysis for glucosuria/proteinuria if tubular dysfunction suspected
Serum creatinine and eGFR during long-term therapy

Key trials & series

IRIS (long-term front-line imatinib outcomes in CML)
Molica et al. front-line TKI eGFR cohort (Ann Hematol 2018)

Clinical pearls

Everyday imatinib renal issues are fluid retention, hypophosphatemia, and a gradual eGFR decline - not dramatic AKI.
Think Fanconi when you see normoglycemic glucosuria plus phosphate wasting on imatinib.
Imatinib is not dialyzed - no supplemental dosing needed in ESKD.

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 · 2012–2024 · 1 since 2022

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 · ModerateAcute renal failure secondary to imatinib mesylate treatment in chronic myeloid leukemia.Pou M et al. · Leuk Lymphoma 2003 · PMID 12916879CML patient developed acute renal failure with biopsy-proven acute tubular necrosis temporally linked to imatinib, reversible after drug withdrawal.CaseB · ModerateAcute renal failure secondary to imatinib mesylate treatment in prostate cancer.Foringer JR et al. · Ann Pharmacother 2005 · PMID 16288076Imatinib-induced acute renal failure requiring hemodialysis with renal biopsy showing tubular vacuolization, indicating direct proximal tubular toxicity.CaseC · LimitedPartial fanconi syndrome induced by imatinib therapy: a novel cause of urinary phosphate loss.François H et al. · Am J Kidney Dis 2008 · PMID 18215707CML patient on imatinib developed partial Fanconi syndrome with proximal tubular dysfunction and urinary phosphate wasting causing hypophosphatemia, matching the electrolyte-wasting signature.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

The effect of renal impairment on the pharmacokinetics of imatinib was assessed in 59 patients with cancer and varying degrees of renal impairment at single and steady state imatinib doses ranging from 100 to 800 mg/day. The mean exposure to imatinib (dose normalized AUC) in patients with mild and moderate renal impairment increased 1.5- to 2-fold compared to patients with normal renal function. There are not sufficient data in patients with severe renal impairment [see Clinical Pharmacology ( 12.3 )] . Dose reductions are necessary for patients with moderate and severe renal impairment [ see Dosage and Administration ( 2.12 ) ]. Table 17: Renal Function Classification Renal dysfunction Renal function tests Mild CrCL = 40 to 59 mL/min Moderate CrCL = 20 to 39 mL/min Severe CrCL = less than 20 mL/min Abbreviation: CrCL, creatinine clearance.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 41,417 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· 6 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

Acute Tubular Necrosiscorroborated · ROR 2.38
Electrolyte Disturbancecorroborated · ROR 1.14 — on the terms that name the lesion (ROR 1.68)
Fanconi SyndromeNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

Hemorrhagic Cystitis

ROR 2.5695% CI 2.31–2.85· 348 reports

Acute Tubular Necrosis

ROR 2.3895% CI 1.78–3.17· 46 reports

Thrombotic Microangiopathy

ROR 2.2095% CI 1.73–2.79· 67 reports

Glomerular Injury / Proteinuria

ROR 2.0895% CI 1.74–2.49· 119 reports

Crystal / Obstructive Nephropathy

ROR 1.4695% CI 1.25–1.70· 160 reports

Electrolyte Disturbance

ROR 1.1495% CI 1.04–1.26· 431 reports

FAERS outcomes & reporting trend· 21.5% of reports w/ death · 21.7% w/ hospitalization

21.5%

Reported with a death outcome

8,910 of 41,417 reports

21.7%

Reported with hospitalization

9,004 of 41,417 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 41,417 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 0.9395% CI 0.82–1.04· 279 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Nausea2,849Diarrhoea2,510Vomiting1,795Abdominal Pain953

General / constitutional

Fatigue2,116Malaise1,378Asthenia1,182Pyrexia1,171Pain853

Musculoskeletal

Muscle Spasms1,128Arthralgia1,000Myalgia840

Respiratory

Dyspnoea1,476Pleural Effusion1,025

Nervous system

Headache1,030Dizziness815

Skin

Rash1,394

Blood & lymphatic

Anaemia1,135

Immune / infection

Pneumonia799

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 Imatinib 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

Trastuzumab deruxtecan

Enhertu · Antibody-drug conjugate (HER2/DXd)

Profile

Emerging AKI/proteinuria reports — under-published.

ATNFANCLYTE

Moderate#1 · 84% phenotype match

Streptozocin

Zanosar · Nitrosourea alkylator

Profile

Classic proximal tubular toxin → Fanconi and dose-limiting AKI.

FANCATNLYTE

Severe#2 · 78% phenotype match

Azacitidine

Vidaza · Hypomethylating agent

Profile

Proximal (type 2) RTA / Fanconi-like tubulopathy; overt AKI uncommon.

FANCATNLYTE

Moderate#3 · 72% phenotype match

Nirogacestat

Ogsiveo · Gamma-secretase inhibitor

Profile

2023 desmoid-tumor agent; phosphate/electrolyte disturbance.

LYTEFANC

Mild#4 · 70% phenotype match

Nedaplatin

Aqupla · Platinum agent

Profile

Second-gen platinum with reduced renal toxicity vs cisplatin.

ATNLYTE

Moderate#5 · 68% phenotype match

Zoledronic acid

Zometa · Bisphosphonate

Profile

Toxic ATN, infusion-rate dependent.

ATNFANC

Moderate#6 · 68% phenotype match

Compare Imatinib 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
3BosutinibPSEUDO — Pseudo-AKIMild
4Imatinib· this agentLYTE — 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 Imatinib’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 Imatinib; 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 95 clinical records among all 136 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.