What kind of kidney injury does Midostaurin 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 Midostaurin therapy?

TLS labs (uric acid, phosphate, potassium, calcium, creatinine) at induction; Potassium and magnesium with ECG/QTc monitoring; Volume status, weight and signs of edema.

How can kidney injury from Midostaurin be prevented?

TLS prophylaxis at induction: hydration plus allopurinol or rasburicase by risk Antiemetics and aggressive supportive hydration; manage mucositis Correct potassium/magnesium and monitor QTc Avoid additive nephrotoxins; manage mast-cell mediator release in mastocytosis

Who is at higher risk of kidney injury from Midostaurin?

High blast burden at induction (tumor-lysis risk); Volume depletion from vomiting/mucositis/sepsis; Pre-existing CKD and concurrent nephrotoxins/QT-prolonging drugs; Mast-cell mediator-release events in mastocytosis.

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Printable monograph

FLT3 / multikinase inhibitor

Midostaurin

Rydapt · MID

FLT3 / multikinase inhibitor · approved 2017 · 7 citations

Recent· through 2023

Deeply sourced7/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 13y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2023
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.

First-generation FLT3/multikinase inhibitor added to induction in AML — its renal-relevant risks are treatment-related tumor lysis, edema and QT, not a direct nephrotoxicity.

MildTargeted FLT3-inhibitor era

Newly diagnosed FLT3-mutated acute myeloid leukemia (with standard induction/consolidation chemotherapy)Advanced systemic mastocytosis, systemic mastocytosis with associated hematologic neoplasm, and mast cell leukemia

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Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Given with intensive chemotherapy, the dominant toxicities are cytopenias, nausea/vomiting, mucositis, edema and QT changes; tumor lysis is a treatment-related (largely chemotherapy-driven) hazard. No characteristic or established midostaurin-specific direct nephrotoxicity is recognized apart from a single anecdotal case report of pauci-immune necrotizing glomerulonephritis, and AKI is multifactorial (volume loss, sepsis, TLS).Source: Stone et al., N Engl J Med 2017 (RATIFY); Stone et al., Blood Adv 2018

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor lysis early in induction; prerenal/electrolyte issues track intercurrent illness.

Distilled from: “Tumor lysis early in induction; prerenal/electrolyte issues track intercurrent illness; edema across treatment.”

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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

Midostaurin has no characteristic direct renal lesion. Its renal relevance in AML is indirect: (1) nausea/vomiting/mucositis and febrile neutropenia reduce intake and cause volume depletion and prerenal azotemia; (2) cytoreduction during induction produces tumor lysis with uric-acid and calcium-phosphate crystal nephropathy and ATN; (3) edema/fluid shifts and QT prolongation (worsened by electrolyte loss) add hemodynamic and metabolic stress. In mastocytosis, mediator-release events can cause hypotension and prerenal injury.

Clinical presentation

Nausea/vomiting, mucositis, edema and cytopenias during induction; a prerenal creatinine rise with poor intake or sepsis, and TLS labs (hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia) early in treatment. QT prolongation on ECG with electrolyte depletion.

Management

Treat tumor lysis with hydration, rasburicase/allopurinol and electrolyte correction (dialysis if refractory). Restore volume for prerenal AKI and treat the precipitating sepsis/GI losses. Keep electrolytes replete and monitor QTc; hold/adjust for significant prolongation. The injury is generally reversible once the precipitant is controlled.Lesion-level management framework

Risk factors

High blast burden at induction (tumor-lysis risk)
Volume depletion from vomiting/mucositis/sepsis
Pre-existing CKD and concurrent nephrotoxins/QT-prolonging drugs
Mast-cell mediator-release events in mastocytosis

Prevention

TLS prophylaxis at induction: hydration plus allopurinol or rasburicase by risk
Antiemetics and aggressive supportive hydration; manage mucositis
Correct potassium/magnesium and monitor QTc
Avoid additive nephrotoxins; manage mast-cell mediator release in mastocytosis

Anticancer mechanism· how it treats cancer

Oral multitargeted kinase inhibitor (a staurosporine derivative) that inhibits FLT3 (ITD and TKD), KIT, PDGFR, VEGFR2 and PKC. Added to 7+3 induction/consolidation it improves survival in newly diagnosed FLT3-mutated AML and is active in KIT-driven advanced systemic mastocytosis.

Note · The renal link is indirect — treatment-related tumor lysis, dehydration/edema and QT-relevant electrolyte shifts rather than a direct midostaurin nephrotoxicity. AKI in this setting is multifactorial.

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Clinical depth

Renal dose adjustment

No specific renal dose adjustment for mild-moderate impairment; severe impairment/ESKD not well characterized (extensive hepatic CYP3A4 metabolism, highly protein-bound). Modifications driven by hematologic/GI toxicity and QT.

Dialyzability & ESKD dosing

Highly protein-bound; not expected to be dialyzable. Dialysis is used for TLS metabolic complications, not drug clearance.

Differential diagnosis

Separate tumor-lysis crystalline nephropathy (early, hyperuricemia/hyperphosphatemia) from prerenal azotemia (volume-responsive), sepsis-associated ATN and chemotherapy co-toxicity. In mastocytosis, consider mediator-release hypotension.

Monitoring

TLS labs (uric acid, phosphate, potassium, calcium, creatinine) at induction
Potassium and magnesium with ECG/QTc monitoring
Volume status, weight and signs of edema

Key trials & series

RATIFY/CALGB 10603 (Stone, NEJM 2017) — registrational trial adding midostaurin to induction
Stone et al. (Blood Adv 2018) — discovery-to-approval review including AML and mastocytosis safety

Clinical pearls

Midostaurin's renal risk is essentially the AML-induction context — tumor lysis and dehydration, not a drug-specific nephropathy.
It is given with cytotoxic chemotherapy, so attribute AKI multifactorially.
Keep magnesium and potassium replete to protect both the kidneys' milieu and the QT interval.
In mastocytosis, mediator-release events can produce transient hypotensive prerenal injury.

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 · 2010–2023 · 1 since 2021

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 · ModerateUnique case of ANCA-negative pauci-immune necrotizing glomerulonephritis with diffuse alveolar hemorrhage, potentially associated with midostaurin.Pankow JD et al. · CEN Case Rep 2020 · PMID 31955389A man with FLT3-mutated AML on midostaurin developed acute kidney injury requiring hemodialysis with biopsy-proven ANCA-negative pauci-immune necrotizing glomerulonephritis attributed to the drug.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,943 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· 23.9% of reports w/ death · 25.8% w/ hospitalization

23.9%

Reported with a death outcome

465 of 1,943 reports

25.8%

Reported with hospitalization

502 of 1,943 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 5 systems · 1,943 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 1.0695% CI 0.64–1.77· 15 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Pancytopenia93Febrile Neutropenia78Bone Marrow Failure76Platelet Count Decreased57Myelosuppression48

Gastrointestinal

Nausea166Vomiting105Diarrhoea90

General / constitutional

Pyrexia91Malaise46Fatigue39

Immune / infection

Pneumonia53Sepsis44Infection40

Skin

Skin Toxicity57Rash35

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 Midostaurin 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

Gilteritinib

Xospata · FLT3 inhibitor

Profile

Differentiation syndrome, tumor lysis and PRES in AML.

PRELYTE

Moderate#1 · 94% phenotype match

Mogamulizumab

Poteligeo · Anti-CCR4 antibody

Profile

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

PRELYTE

Mild#2 · 89% phenotype match

Tafasitamab

Monjuvi · Anti-CD19 antibody

Profile

Tumor lysis and infusion reactions in lymphoma.

PRELYTE

Mild#3 · 89% phenotype match

Tazemetostat

Tazverik · EZH2 inhibitor

Profile

Tumor lysis; generally low direct renal toxicity.

PRELYTE

Mild#4 · 89% phenotype match

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#5 · 88% phenotype match

Quizartinib

Vanflyta · FLT3 inhibitor

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild#6 · 88% phenotype match

Compare Midostaurin 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.