What kind of kidney injury does Revumenib 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, Crystal / Obstructive Nephropathy.

How should kidney function be monitored during Revumenib therapy?

Creatinine, potassium, phosphate, calcium and uric acid frequently during initiation (TLS watch); Daily weight, oxygenation and exam for differentiation syndrome; ECG/QTc and electrolytes (correct Mg/K to protect QT); Leukocyte count trend.

How can kidney injury from Revumenib be prevented?

TLS prophylaxis: aggressive IV hydration plus rasburicase or allopurinol per risk Early corticosteroids at the first signs of differentiation syndrome ECG/QTc and electrolyte optimization

Who is at higher risk of kidney injury from Revumenib?

High leukemic burden / rapid response; Pre-existing CKD; Inadequate TLS prophylaxis; Volume depletion; Baseline electrolyte derangement.

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Printable monograph

Menin inhibitor

Revumenib

Revuforj · Revu

Menin inhibitor · approved 2024 · 6 citations

Recent· through 2024

Fairly sourced5/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 3y)
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.

A menin inhibitor for acute leukemia — differentiation syndrome and tumor lysis stress the kidney.

ModerateMenin inhibitor

KMT2A-rearranged acute leukemia (relapsed/refractory)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Differentiation syndrome and tumor lysis syndrome are on-target risks identified during development (differentiation syndrome carries a boxed warning). Resulting AKI is hemodynamic (capillary leak, fluid shifts) and/or crystal/metabolic (TLS); renal-specific incidence is not separately well quantified. QTc prolongation is an additional class effect.Source: Issa et al., Nature 2023 / AUGMENT-101 (J Clin Oncol 2024)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

During early treatment as differentiation and lysis occur — first days to weeks.

Distilled from: “During early treatment as leukemic differentiation and lysis occur (first days–weeks).”

§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 DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Crystal / Obstructive NephropathySecondaryqualitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityReversible

Evidence6 citations

Nephron map

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Tubular Lumen

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

Two mechanisms converge on the kidney. (1) Forced leukemic differentiation triggers a differentiation syndrome (cytokine-release-like): fever, weight gain, capillary leak, pulmonary infiltrates, edema and hypotension producing pre-renal azotemia. (2) Rapid lysis of a high leukemic burden causes tumor lysis syndrome — hyperuricemia, hyperphosphatemia and hyperkalemia with intratubular uric-acid and calcium-phosphate crystal precipitation plus renal vasoconstriction, causing crystalline AKI. Hypocalcemia and QTc-relevant electrolyte shifts accompany TLS. There is no direct tubular toxin.

Clinical presentation

Differentiation syndrome: dyspnea, fever, peripheral/pulmonary edema, hypotension, rising creatinine and rising leukocyte count. TLS: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia with AKI. Monitor the QTc.

Management

Differentiation syndrome: corticosteroids (e.g., dexamethasone), diuresis for fluid overload, supportive care, and drug interruption if severe. TLS: IV hydration, rasburicase for hyperuricemia, electrolyte correction (treat hyperkalemia/hyperphosphatemia, cautious calcium), and renal replacement therapy if refractory.Lesion-level management framework

Risk factors

High leukemic burden / rapid response
Pre-existing CKD
Inadequate TLS prophylaxis
Volume depletion
Baseline electrolyte derangement

Prevention

TLS prophylaxis: aggressive IV hydration plus rasburicase or allopurinol per risk
Early corticosteroids at the first signs of differentiation syndrome
ECG/QTc and electrolyte optimization

Anticancer mechanism· how it treats cancer

Oral small-molecule inhibitor of the protein–protein interaction between menin and KMT2A (MLL), disrupting the menin-dependent transcriptional complex that sustains HOX/MEIS1 leukemogenic programs in KMT2A-rearranged and NPM1-mutant acute leukemias, thereby inducing leukemic-cell differentiation. Approved for KMT2A-rearranged relapsed/refractory acute leukemia.

§04

Clinical depth

Renal dose adjustment

Dosed with a strong CYP3A4 inhibitor co-administration strategy in the label; no well-established renal dose adjustment. Manage TLS/differentiation syndrome rather than adjust for GFR; hold for severe differentiation syndrome.

Dialyzability & ESKD dosing

Small molecule, but renal dialyzability not formally characterized; clinically, renal replacement therapy is used for TLS-driven AKI/refractory hyperkalemia, not for drug removal.

Differential diagnosis

Differentiation syndrome (capillary leak, infiltrates, leukocytosis, steroid-responsive) vs sepsis vs cardiogenic edema; TLS crystalline AKI (high uric acid/phosphate) vs pre-renal vs nephrotoxin — urine uric-acid-to-creatinine ratio and the metabolic panel distinguish them.

Monitoring

Creatinine, potassium, phosphate, calcium and uric acid frequently during initiation (TLS watch)
Daily weight, oxygenation and exam for differentiation syndrome
ECG/QTc and electrolytes (correct Mg/K to protect QT)
Leukocyte count trend

Key trials & series

Issa Nature 2023 first-in-human revumenib
AUGMENT-101 (Issa JCO 2024) registrational trial

Clinical pearls

Two on-target renal hits: differentiation syndrome (hemodynamic) and tumor lysis (crystalline) — anticipate both at initiation.
Differentiation syndrome carries a boxed warning — start corticosteroids early and don't wait for full-blown organ failure.
TLS prophylaxis (hydration + rasburicase/allopurinol) and frequent labs prevent most crystalline AKI.
Correct magnesium and potassium not only for the kidney but to protect against menin-inhibitor QTc prolongation.

Beyond the kidney — non-renal toxicities· 2 organ systems

Class-level context for the major non-renal toxicities of the Menin inhibitor class.

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Differentiation syndrome

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

QT prolongation

§05

References

6 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2021–2024 · 4 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.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING: DIFFERENTIATION SYNDROME, QTc PROLONGATION and TORSADES DE POINTES Differentiation syndrome, which can be fatal, has occurred with REVUFORJ. Signs and symptoms may include fever, dyspnea, hypoxia, pulmonary infiltrates, pleural or pericardial effusions, rapid weight gain or peripheral edema, hypotension, and renal dysfunction. If differentiation syndrome is suspected, immediately initiate corticosteroid therapy and hemodynamic monitoring until symptom resolution. [see Dosage and Administration (2.3 ) , Warnings and Precautions (5.1) , and Adverse Reactions (6.1) ] . QTc prolongation and Torsades de Pointes have occurred in patients receiving REVUFORJ. Correct hypokalemia and hypomagnesemia prior to and during treatment. Do not initiate REVUFORJ in patients with QTcF > 450 msec. If QTc interval prolongation occurs, interrupt, reduce, or permanently discontinue REVUFORJ. [see Dosage and Administration (2.3) , Warnings and Precautions (5.2) , and Adverse Reactions (6.1) ] WARNING: DIFFERENTIATION SYNDROME, and QTc PROLONGATION and TORSADES DE POINTES See full prescribing information for complete boxed warning. Differentiation syndrome, which can be fatal, has occurred with REVUFORJ. If differentiation syndrome is suspected, immediately initiate corticosteroid therapy and hemodynamic monitoring until symptom resolution ( 2.3 , 5.1 ) QTc prolongation and Torsades de…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 878 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· 14% of reports w/ death · 30.3% w/ hospitalization

14%

Reported with a death outcome

123 of 878 reports

30.3%

Reported with hospitalization

266 of 878 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 878 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 0.1695% CI 0.02–1.11· 1 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Platelet Count Decreased139White Blood Cell Count Decreased64Haemoglobin Decreased43Neutrophil Count Decreased37Thrombocytopenia33

Gastrointestinal

Nausea139Vomiting65Diarrhoea44Abdominal Discomfort23

General / constitutional

Fatigue86Pyrexia52Peripheral Swelling26Asthenia23

Nervous system

Headache29Taste Disorder24

Cardiac

Electrocardiogram Qt Prolonged42

Metabolic & electrolyte

Decreased Appetite32

Musculoskeletal

Arthralgia28

Respiratory

Dyspnoea24

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 Revumenib 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

Epcoritamab

Epkinly · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#1 · 86% phenotype match

Gemtuzumab ozogamicin

Mylotarg · Antibody-drug conjugate (CD33/calicheamicin)

Profile

Tumor lysis and veno-occlusive disease.

PRELYTEXTAL

Moderate#2 · 86% phenotype match

Glofitamab

Columvi · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#3 · 86% phenotype match

Inotuzumab ozogamicin

Besponsa · Antibody-drug conjugate (CD22/calicheamicin)

Profile

Tumor lysis and VOD in ALL.

PRELYTEXTAL

Moderate#4 · 86% phenotype match

Mosunetuzumab

Lunsumio · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis in lymphoma.

PRELYTEXTAL

Moderate#5 · 86% phenotype match

Afamitresgene autoleucel (Afami-cel)

Tecelra · MAGE-A4 TCR-T cell therapy

Profile

First TCR-T cell therapy for a solid tumor; CRS-associated hemodynamic AKI.

PRELYTE

Moderate#6 · 84% phenotype match

Compare Revumenib 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 targeted agents

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.