What kind of kidney injury does Gilteritinib cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Electrolyte Disturbance.

How should kidney function be monitored during Gilteritinib therapy?

Blood chemistries (potassium, phosphate, uric acid, creatinine) frequently, especially in the first cycle; Daily weight and assessment for edema/effusions (differentiation syndrome); ECG/QTc at baseline, days 8 and 15 of cycle 1, then periodically; Blood pressure and neurologic status (PRES surveillance).

How can kidney injury from Gilteritinib be prevented?

Patient/clinician vigilance for differentiation-syndrome symptoms; treat early with dexamethasone TLS prophylaxis: hydration plus allopurinol or rasburicase based on risk Blood-pressure control and prompt evaluation of neurologic symptoms (PRES)

Who is at higher risk of kidney injury from Gilteritinib?

High leukemic burden/blast count (differentiation syndrome and TLS); Pre-existing CKD and concurrent nephrotoxins; Hypertension (PRES); Rapid responders early in therapy.

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Printable monograph

FLT3 inhibitor

Gilteritinib

Xospata · GIL

FLT3 inhibitor · approved 2018 · 7 citations

Up to date· through 2026

Deeply sourced7/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 16y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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.

Potent FLT3 inhibitor whose differentiation syndrome and tumor lysis are the renal threats — plus a boxed/labeled risk of PRES.

ModerateTargeted FLT3-inhibitor era

Relapsed or refractory FLT3-mutation-positive acute myeloid leukemia

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Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Differentiation syndrome (boxed warning) occurs in roughly 3% of treated patients and can cause capillary leak, fluid overload and renal dysfunction; tumor lysis and PRES are labeled risks. Discrete AKI incidence is not separately quantified and is largely a consequence of these syndromes.Source: Perl et al., N Engl J Med 2019 (ADMIRAL); Pulte et al., Clin Cancer Res 2021 (FDA summary)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor lysis is early; differentiation syndrome runs from a few days to ~3 months.

Distilled from: “Differentiation syndrome from a few days up to ~3 months (often within the first month); TLS early; PRES variable.”

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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 DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

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Kidney injury

Mechanism of kidney injury

Gilteritinib's renal threats are syndrome-driven. (1) Differentiation syndrome: rapid myeloblast differentiation releases inflammatory cytokines, producing fever, capillary-leak edema, pleural/pericardial effusions, hypotension and acute kidney injury (a mix of prerenal hypoperfusion and intrarenal inflammatory injury). (2) Tumor lysis syndrome: cytoreduction releases uric acid, phosphate and potassium, causing urate and calcium-phosphate crystal nephropathy with intratubular obstruction and ATN. (3) Posterior reversible encephalopathy syndrome (PRES), a labeled risk, reflects endothelial dysfunction/hypertension. Volume shifts in differentiation syndrome can be both prerenal (capillary leak) and overload.

Clinical presentation

Differentiation syndrome: dyspnea, fever, weight gain/edema, effusions, hypotension and rising creatinine days-to-weeks after starting. TLS: hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia and AKI early in treatment. PRES: headache, seizures, visual change and hypertension with characteristic MRI findings.

Management

For differentiation syndrome: start corticosteroids (e.g. dexamethasone 10 mg q12h), give diuretics for fluid overload, and interrupt gilteritinib if severe; support kidney function. For TLS: aggressive IV hydration, rasburicase for hyperuricemia, correct electrolytes, and dialyze for refractory metabolic derangement. For PRES: control blood pressure, treat seizures and hold the drug; it is typically reversible.Lesion-level management framework

Risk factors

High leukemic burden/blast count (differentiation syndrome and TLS)
Pre-existing CKD and concurrent nephrotoxins
Hypertension (PRES)
Rapid responders early in therapy

Prevention

Patient/clinician vigilance for differentiation-syndrome symptoms; treat early with dexamethasone
TLS prophylaxis: hydration plus allopurinol or rasburicase based on risk
Blood-pressure control and prompt evaluation of neurologic symptoms (PRES)

Anticancer mechanism· how it treats cancer

Oral selective inhibitor of FLT3 (including ITD and TKD/D835 mutations) and AXL. By blocking constitutively active FLT3 signaling it induces remission in relapsed/refractory FLT3-mutated AML — and, by relieving the maturation block, drives myeloblast differentiation.

Note · The renal link is indirect but important: AKI arises from differentiation syndrome (capillary leak/inflammation), tumor lysis (crystalline nephropathy) and the labeled PRES, rather than a primary tubular drug toxicity.

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Clinical depth

Renal dose adjustment

No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied (predominantly hepatic CYP3A4 metabolism). Manage interruptions for differentiation syndrome/TLS/PRES rather than by GFR.

Dialyzability & ESKD dosing

Highly protein-bound; not appreciably dialyzable. Dialysis is used for TLS metabolic complications, not drug removal.

Differential diagnosis

Distinguish differentiation-syndrome AKI (capillary leak, effusions, responds to steroids) from sepsis/ATN, TLS crystalline nephropathy (early hyperuricemia/hyperphosphatemia), and prerenal azotemia. PRES is identified by neurologic features and MRI, separating it from metabolic encephalopathy.

Monitoring

Blood chemistries (potassium, phosphate, uric acid, creatinine) frequently, especially in the first cycle
Daily weight and assessment for edema/effusions (differentiation syndrome)
ECG/QTc at baseline, days 8 and 15 of cycle 1, then periodically
Blood pressure and neurologic status (PRES surveillance)

Key trials & series

ADMIRAL (Perl, NEJM 2019) — registrational RCT establishing survival benefit and the differentiation-syndrome/PRES safety profile
FDA approval summary (Pulte, Clin Cancer Res 2021) — codifies boxed differentiation-syndrome warning and PRES/QT/pancreatitis warnings

Clinical pearls

Differentiation syndrome is the boxed warning — start dexamethasone early and don't wait for full-blown organ failure.
Gilteritinib carries a distinct labeled PRES risk; new headache/seizure/visual change with hypertension is PRES until proven otherwise.
Tumor lysis is an early-treatment renal hazard — risk-stratify and pre-treat with hydration +/- rasburicase.
Frequent electrolyte and ECG monitoring is mandated by the label.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Tubular Lumen

The urine flow path

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

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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 · 2010–2021 · 5 since 2019

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 · ModeratePost-transplantation gilteritinib maintenance therapy and therapeutic drug monitoring in pediatric acute myeloid leukemia with FLT3-internal tandem duplication.Yanagimachi M et al. · Cancer Chemother Pharmacol 2026 · PMID 41554949Pediatric case series in which a child developed renal dysfunction (with thrombocytopenia) at an elevated gilteritinib trough concentration, reversible with dose reduction.

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 Gilteritinib 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

Midostaurin

Rydapt · FLT3 / multikinase inhibitor

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild#1 · 94% phenotype match

Olutasidenib

Rezlidhi · IDH1 inhibitor

Profile

Differentiation syndrome and tumor lysis in AML.

PRELYTE

Moderate#2 · 89% phenotype match

Obecabtagene autoleucel (Obe-cel)

Aucatzyl · CD19 CAR-T cell therapy

Profile

CD19 CAR-T for adult B-ALL; CRS- and tumor-lysis-associated AKI, with notably lower high-grade CRS.

PRELYTE

Moderate#3 · 89% phenotype match

Mogamulizumab

Poteligeo · Anti-CCR4 antibody

Profile

Tumor lysis and rare AKI; cutaneous T-cell lymphoma.

PRELYTE

Mild#4 · 84% phenotype match

Tafasitamab

Monjuvi · Anti-CD19 antibody

Profile

Tumor lysis and infusion reactions in lymphoma.

PRELYTE

Mild#5 · 83% phenotype match

Tazemetostat

Tazverik · EZH2 inhibitor

Profile

Tumor lysis; generally low direct renal toxicity.

PRELYTE

Mild#6 · 83% phenotype match

Compare Gilteritinib 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.