What kind of kidney injury does Dasatinib cause?

Glomerular Injury / Proteinuria — Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

How should kidney function be monitored during Dasatinib therapy?

Urine albumin-creatinine ratio (UACR) at baseline and periodically; Serum albumin and edema assessment if proteinuria develops; Blood pressure; chest imaging/echocardiography if dyspnea (effusion/PAH).

How can kidney injury from Dasatinib be prevented?

Consider dose reduction or switching TKI if proteinuria develops Optimize blood pressure and consider RAAS blockade for persistent proteinuria

Who is at higher risk of kidney injury from Dasatinib?

Higher steady-state dasatinib plasma concentrations; Longer treatment duration; Pre-existing glomerular disease or proteinuria; Concurrent pleural effusion / pulmonary hypertension (shared endothelial toxicity).

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Printable monograph

BCR-ABL TKI

Dasatinib

Sprycel · DASA

BCR-ABL TKI · approved 2006 · 9 citations · FAERS AKI reporting ROR 1.84 (95% CI 1.54–2.20, 121 AKI reports)

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 12y)
Not met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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 with a distinctive signal of proteinuria and nephrotic-range glomerular injury.

ModerateBCR-ABL tyrosine kinase inhibitor

Chronic myeloid leukemiaPhiladelphia-positive acute lymphoblastic leukemia

§01

Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Representative incidence10%

Dasatinib causes significantly more albuminuria than other TKIs. In a pharmacokinetic cohort, dasatinib users had higher urine albumin-creatinine ratios and about 10% showed severely increased albuminuria (UACR >300 mg/g) versus none on other TKIs, with the degree of proteinuria correlating with plasma exposure. Nephrotic-range proteinuria with biopsy-proven glomerular injury (FSGS, podocyte foot-process effacement, endothelial injury) is reported in cases.Source: Adegbite et al., Clin J Am Soc Nephrol 2023

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Proteinuria appears within weeks to months and increases with treatment duration and exposure.

Distilled from: “Proteinuria can appear within weeks to months and increases with treatment duration and exposure.”

§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.

Glomerular Injury / Proteinuria#1 · Signaturequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

§03

Kidney injury

Mechanism of kidney injury

Off-target inhibition of SRC-family and VEGF/VEGFR-related pro-survival signaling injures the glomerular filtration barrier - the same SRC-pathway and endothelial mechanisms implicated in dasatinib pulmonary arterial hypertension also damage glomerular endothelium and podocytes, producing foot-process effacement, FSGS-pattern lesions, and proteinuria. Plasma dasatinib concentration correlates with the degree of albuminuria, supporting a dose/exposure-dependent podocyte/endothelial effect.

Clinical presentation

Proteinuria ranging from moderate albuminuria to nephrotic-range with edema and hypoalbuminemia; biopsies show foot-process effacement, FSGS, or diffuse glomerular/endothelial injury. Pleural effusions and pulmonary arterial hypertension are characteristic, mechanistically related non-renal effects.

Management

Quantify proteinuria (UACR or UPCR); reduce dose or switch to an alternative TKI (e.g., nilotinib or imatinib) for significant or nephrotic-range proteinuria, and start an ACE inhibitor/ARB for proteinuria reduction. Proteinuria and glomerular injury commonly improve or resolve after dasatinib withdrawal.Lesion-level management framework

Risk factors

Higher steady-state dasatinib plasma concentrations
Longer treatment duration
Pre-existing glomerular disease or proteinuria
Concurrent pleural effusion / pulmonary hypertension (shared endothelial toxicity)

Prevention

Consider dose reduction or switching TKI if proteinuria develops
Optimize blood pressure and consider RAAS blockade for persistent proteinuria

Anticancer mechanism· how it treats cancer

Potent second-generation inhibitor of BCR-ABL1 and SRC-family kinases (LCK, FYN, YES, SRC), with broader kinase coverage than imatinib and activity against most non-T315I resistance mutations. Used in chronic myeloid leukemia and Ph+ ALL.

Note · Proteinuria/glomerular injury is the signature and a genuinely distinguishing TKI-class signal - monitor urine protein during therapy.

§04

Clinical depth

Renal dose adjustment

No formal renal dose adjustment is specified (dasatinib is extensively hepatically metabolized with <4% renal excretion); however, the practical 'renal' adjustment is dose reduction or drug switch when treatment-emergent proteinuria appears.

Dialyzability & ESKD dosing

Dasatinib is highly protein-bound and extensively metabolized; it is not appreciably dialyzed and needs no supplemental post-dialysis dose. Standard dosing applies in ESKD with clinical monitoring.

Differential diagnosis

Dasatinib glomerulopathy (exposure-dependent, reversible on withdrawal, with foot-process effacement) versus primary FSGS, diabetic or hypertensive glomerulosclerosis, and paraprotein-related glomerular disease. The temporal link to dasatinib, exposure correlation, and resolution after switching distinguish it.

Monitoring

Urine albumin-creatinine ratio (UACR) at baseline and periodically
Serum albumin and edema assessment if proteinuria develops
Blood pressure; chest imaging/echocardiography if dyspnea (effusion/PAH)

Key trials & series

Adegbite et al. patient-specific PK and dasatinib nephrotoxicity cohort (CJASN 2023)

Clinical pearls

Dasatinib is the TKI that causes glomerular proteinuria - check a UACR before and during therapy; it is a genuinely distinguishing class signal.
The proteinuria is exposure-dependent and usually reverses on dose reduction or switch to another TKI.
Pleural effusion/PAH and glomerular injury share a SRC/endothelial mechanism - their co-occurrence is a clue.

Where it strikes· nephron segments & injury signatures

Nephron segments

Glomerulus

Filtration barrier (podocytes + endothelium)

Injury signatures

Glomerular Injury / Proteinuria

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

7 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

7 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· 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.

CaseB · ModerateDasatinib-induced renal (or chronic) thrombotic microangiopathy in a patient with chronic myeloid leukemia: A case report.Sabour R et al. · SAGE Open Med Case Rep 2025 · PMID 39967609Biopsy-confirmed renal-limited (chronic) thrombotic microangiopathy attributed to dasatinib in a CML patient, progressing to dialysis despite drug withdrawal — a distinct vascular lesion beyond the classic dasatinib proteinuria.CaseC · LimitedDasatinib-induced nephrotic-range proteinuria.Wallace E et al. · Am J Kidney Dis 2013 · PMID 23540262CML patient who developed nephrotic-range proteinuria after starting dasatinib that resolved on switching to imatinib, with proposed VEGF-inhibition glomerular mechanism.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 9,103 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· 5 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

Glomerular Injury / Proteinuriacorroborated · ROR 5.02 — on the terms that name the lesion (ROR 9.02)

Glomerular Injury / Proteinuria

ROR 5.0295% CI 3.92–6.44· 63 reports

Thrombotic Microangiopathy

ROR 4.0395% CI 2.76–5.88· 27 reports

Acute Tubular Necrosis

ROR 2.1195% CI 1.10–4.06· 9 reports

Electrolyte Disturbance

ROR 1.7595% CI 1.48–2.06· 144 reports

SIADH / Hyponatremia

ROR 1.7295% CI 1.33–2.22· 60 reports

FAERS outcomes & reporting trend· 14.7% of reports w/ death · 30.6% w/ hospitalization

14.7%

Reported with a death outcome

1,338 of 9,103 reports

30.6%

Reported with hospitalization

2,784 of 9,103 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 9,103 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 1.8495% CI 1.54–2.20· 121 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Respiratory

Pleural Effusion1,186Dyspnoea409Pulmonary Hypertension180

Blood & lymphatic

Thrombocytopenia425Anaemia326Neutropenia285Febrile Neutropenia231Pancytopenia194

Gastrointestinal

Diarrhoea438Nausea368Vomiting257Abdominal Pain197

General / constitutional

Fatigue375Pyrexia366

Hepatobiliary

Hepatotoxicity328

Skin

Rash323

Nervous system

Headache305

Immune / infection

Pneumonia284

Cardiac

Pericardial Effusion188

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 Dasatinib 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

Belantamab mafodotin

Blenrep · Antibody-drug conjugate (BCMA/MMAF)

Profile

Myeloma ADC; renal data emerging.

GLOM

Mild#1 · 84% phenotype match

Pamidronate

Aredia · Bisphosphonate

Profile

Collapsing FSGS — first drug ever linked.

GLOM

Severe#2 · 84% phenotype match

Interferon-α

Intron A · Cytokine

Profile

Collapsing FSGS in APOL1 carriers.

GLOMTMA

Severe#3 · 60% phenotype match

Fruquintinib

Fruzaqla · VEGFR TKI

Profile

2023 colorectal VEGFR-TKI; hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#4 · 54% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#5 · 54% phenotype match

Cabozantinib

Cabometyx · VEGFR/MET TKI

Profile

Hypertension and proteinuria; nephrotic case reports.

HTNGLOM

Moderate#6 · 54% phenotype match

Compare Dasatinib 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
4ImatinibLYTE — Electrolyte DisturbanceMild
5OlverembatinibGLOM — Glomerular Injury / ProteinuriaMild
6PonatinibHTN — HypertensionModerate
7Dasatinib· this agentGLOM — 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 Dasatinib’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 Dasatinib; 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 47 clinical records among all 64 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.