How should kidney function be monitored during Quizartinib therapy?

Frequent electrolytes — K, Mg, phosphate, uric acid (TLS and QT safety); ECG/QTc at baseline and during therapy (correct K/Mg before/with dosing); Creatinine and volume status through neutropenic period.

How can kidney injury from Quizartinib be prevented?

Tumor-lysis prophylaxis (IV hydration, allopurinol/rasburicase) at induction Vigilant electrolyte monitoring/repletion (especially potassium and magnesium, also for QT safety) Prompt management of neutropenic sepsis and source control

Who is at higher risk of kidney injury from Quizartinib?

High leukemic burden at induction (TLS risk); Febrile neutropenia/sepsis; Electrolyte derangements compounding QT risk; Concurrent nephrotoxins (antimicrobials, azoles, contrast).

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Printable monograph

FLT3 inhibitor

Quizartinib

Vanflyta · QUIZ

FLT3 inhibitor · approved 2023 · 6 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
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 type II FLT3 inhibitor for AML whose renal risk centers on tumor lysis and electrolyte shifts at induction.

MildFLT3 inhibitor

FLT3-ITD-positive acute myeloid leukemia

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Representative grade ≥3 incidence12%

No established intrinsic nephrotoxicity. In QuANTUM-First the dominant grade 3-4 events were febrile neutropenia, hypokalemia and pneumonia; QT prolongation is a hallmark. Renal injury is indirect — tumor-lysis at induction, sepsis/cytopenia-related prerenal/ischemic AKI, and electrolyte derangements. AKI is common in AML induction generally (KDIGO-defined rates are high in cohort studies), but a quizartinib-attributable rate is not defined. Reported rate: grade >=3 hypokalemia in 12% — Adults with relapsed or refractory FLT3-ITD-positive acute myeloid leukemia treated with single-agent quizartinib (60… (Cortes 2019, PMID 31175001).Source: Cortes et al., Lancet Oncol 2019 (QuANTUM-R)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor-lysis-driven renal risk is highest around induction.

Distilled from: “Highest around induction (tumor lysis, neutropenic sepsis); ongoing electrolyte monitoring through therapy.”

§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.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Electrolyte DisturbanceSecondaryno population incidence denominator
Hypokalemia was among the most common grade 3/4 adverse events in the phase 3 QuANTUM-First trial (with induction/consolidation chemotherapy) PMID 37116523 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

12%grade ≥3 incidence

SeverityMild

ReversibilityReversible

Evidence6 citations

Nephron map

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Prerenal / Hemodynamic AKI

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

§03

Kidney injury

Mechanism of kidney injury

No characterized direct nephron injury. AML induction with quizartinib carries tumor-lysis-type metabolic risk (hyperuricemia/hyperphosphatemia with intratubular urate/calcium-phosphate deposition) and high rates of febrile neutropenia/sepsis driving prerenal and ischemic (ATN) AKI; electrolyte wasting (hypokalemia and hypomagnesemia) is common and dangerously interacts with the drug's QT-prolonging effect.

Clinical presentation

AKI in the setting of sepsis/volume depletion or tumor lysis; hypokalemia/hypomagnesemia and other electrolyte derangements; creatinine rise tracking these processes rather than a bland primary tubulopathy.

Management

Supportive; standard tumor-lysis treatment, sepsis/source control, correction of prerenal factors and electrolytes (K and Mg, partly for arrhythmia prevention). No drug-specific renal therapy; intrinsic nephrotoxicity has not been established.Lesion-level management framework

Risk factors

High leukemic burden at induction (TLS risk)
Febrile neutropenia/sepsis
Electrolyte derangements compounding QT risk
Concurrent nephrotoxins (antimicrobials, azoles, contrast)

Prevention

Tumor-lysis prophylaxis (IV hydration, allopurinol/rasburicase) at induction
Vigilant electrolyte monitoring/repletion (especially potassium and magnesium, also for QT safety)
Prompt management of neutropenic sepsis and source control

Anticancer mechanism· how it treats cancer

Oral, highly selective type II FLT3 inhibitor (binds the inactive kinase conformation, targeting FLT3-ITD). Added to standard induction/consolidation chemotherapy and given as continuation monotherapy for FLT3-ITD-positive newly diagnosed AML.

Note · 2023 approval; no renal-specific literature. The prerenal/TLS/electrolyte framing is conservative AML-induction class reasoning, supported by the pivotal trial's toxicity profile and AML-AKI cohort data.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment is specified for mild-moderate impairment; quizartinib is hepatically (CYP3A) metabolized. Strong CYP3A inhibitors (common azole antifungals in neutropenia) raise exposure and require dose reduction, mainly for QT safety. Limited data in severe impairment/dialysis.

Dialyzability & ESKD dosing

Not characterized; highly protein-bound, hepatically cleared — not expected to be meaningfully dialyzed. No ESKD dosing guidance.

Differential diagnosis

Distinguish tumor-lysis AKI (early, urate/phosphate), neutropenic-sepsis ATN, and prerenal AKI of volume depletion; the drug is not a direct tubular toxin but its electrolyte effects amplify QT/arrhythmia risk.

Monitoring

Frequent electrolytes — K, Mg, phosphate, uric acid (TLS and QT safety)
ECG/QTc at baseline and during therapy (correct K/Mg before/with dosing)
Creatinine and volume status through neutropenic period

Key trials & series

QuANTUM-First (Erba, Lancet 2023) — registrational phase 3; febrile-neutropenia/hypokalemia/QT-dominant safety

Clinical pearls

Replete K and Mg aggressively — both for the kidney/TLS picture AND to mitigate quizartinib's QT prolongation.
Beware azole antifungal co-administration: CYP3A inhibition raises exposure and QT risk in exactly the febrile-neutropenic patients most likely to need them.
Renal injury at induction is TLS- and sepsis-driven, not a quizartinib tubulopathy.

§05

References

5 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

5 references · 2019–2025 · 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· 1

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 · ModerateNephrotic syndrome associated with tyrosine kinase inhibitors for pediatric malignancy: case series and review of the literature.Ruebner RL et al. · Pediatr Nephrol 2014 · PMID 24310825Pediatric case series of nephrotic syndrome (one patient with TMA features) during TKI therapy including quizartinib, mostly resolving after drug discontinuation.

FDA label — boxed warning & renal dosing· boxed warning · renal impairment

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

Boxed warning

WARNING: QT PROLONGATION, TORSADES DE POINTES, and CARDIAC ARREST VANFLYTA prolongs the QT interval in a dose- and concentration-related manner [see Clinical Pharmacology (12.2) ] . Prior to VANFLYTA administration and periodically, monitor for hypokalemia or hypomagnesemia, and correct deficiencies. Perform ECGs to monitor the QTc at baseline, weekly during induction and consolidation therapy, weekly for at least the first month of maintenance, and periodically thereafter [see Dosage and Administration (2.3) and Warnings and Precautions (5.1) ]. Torsades de pointes and cardiac arrest have occurred in patients receiving VANFLYTA. Do not administer VANFLYTA to patients with severe hypokalemia, severe hypomagnesemia, or long QT syndrome [see Contraindications (4) and Warnings and Precautions (5.1) ] . Do not initiate treatment with VANFLYTA or escalate the VANFLYTA dose if the QT interval corrected by Fridericia's formula (QTcF) is greater than 450 ms [see Dosage and Administration (2.3) and Warnings and Precautions (5.1) ] . Monitor ECGs more frequently if concomitant use of drugs known to prolong the QT interval is required [see Dosage and Administration (2.3) and Warnings and Precautions (5.1) ] . Reduce the VANFLYTA dose when used concomitantly with strong CYP3A inhibitors, as they may increase quizartinib exposure [see Dosage and Administration (2.4) and Warnings and…

Renal impairment — from the label

No dosage adjustment is recommended in patients with mild to moderate renal impairment (i.e., estimated creatinine clearance [CLcr] by Cockcroft-Gault equation: CLcr 30 to 89 mL/min). VANFLYTA has not been studied in patients with severe renal impairment (CLcr <30 mL/min) [see Clinical Pharmacology (12.3) ] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 634 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· 15.8% of reports w/ death · 34.2% w/ hospitalization

15.8%

Reported with a death outcome

100 of 634 reports

34.2%

Reported with hospitalization

217 of 634 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 634 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 0.2295% CI 0.03–1.53· 1 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Platelet Count Decreased42Febrile Neutropenia33White Blood Cell Count Decreased22Myelosuppression19Haemoglobin Decreased13

General / constitutional

Pyrexia39Fatigue33Asthenia17

Gastrointestinal

Nausea43Diarrhoea22Vomiting16

Immune / infection

Infection34Pneumonia27

Cardiac

Electrocardiogram Qt Prolonged33

Skin

Rash13

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 Quizartinib 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

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#1 · 100% phenotype match

Imetelstat

Rytelo · Telomerase inhibitor

Profile

2024 MDS agent; tumor lysis risk.

PRELYTE

Mild#2 · 89% phenotype match

Zanidatamab

Ziihera · HER2 bispecific antibody

Profile

2024 biliary-tract HER2 bispecific; renal data emerging.

PRELYTE

Mild#3 · 89% phenotype match

Zenocutuzumab

Bizengri · HER2×HER3 bispecific antibody

Profile

2024 NRG1-fusion bispecific; mostly grade 1-2 AEs — at most diarrhea-related prerenal risk, no CRS/TLS mechanism.

PRELYTE

Mild#4 · 89% phenotype match

Mirdametinib

Gomekli · MEK inhibitor

Profile

2025 NF1 MEK inhibitor; creatinine rise and edema.

PRELYTE

Mild#5 · 89% phenotype match

Midostaurin

Rydapt · FLT3 / multikinase inhibitor

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild#6 · 88% phenotype match

Compare Quizartinib 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 Other kinase 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.

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.