What kind of kidney injury does Olutasidenib 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 Olutasidenib therapy?

Blood chemistries (potassium, phosphate, uric acid, creatinine) frequently, especially early; Daily weight and assessment for edema/effusions (differentiation syndrome); Liver tests and ECG/QTc periodically; Volume status and blood pressure.

How can kidney injury from Olutasidenib be prevented?

Vigilance for differentiation-syndrome symptoms; early corticosteroids and, if needed, drug interruption TLS prophylaxis: hydration plus allopurinol or rasburicase by risk Frequent blood-chemistry monitoring; correct potassium/magnesium Treat fluid overload with diuretics

Who is at higher risk of kidney injury from Olutasidenib?

High leukemic burden/blast count (differentiation syndrome and TLS); Pre-existing CKD and concurrent nephrotoxins; Rapid responders early in therapy; Concurrent QT-prolonging drugs and electrolyte depletion.

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Printable monograph

IDH1 inhibitor

Olutasidenib

Rezlidhi · OLU

IDH1 inhibitor · approved 2022 · 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: 15y)
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.

Mutant-IDH1 inhibitor for AML whose differentiation syndrome and tumor lysis are the renal threats — a maturation-driven, not tubular, kidney risk.

ModerateMutant-IDH-inhibitor era

Relapsed or refractory acute myeloid leukemia with a susceptible IDH1 (R132) mutation

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Differentiation syndrome (boxed warning) occurred in ~14% of patients (grade >=3 ~9%, with rare fatality) in the pivotal cohort; tumor lysis is a labeled risk. Discrete AKI incidence is not separately quantified and is largely consequent on these syndromes.Source: de Botton et al., Blood Adv 2023 (pivotal R/R AML cohort; ~14% differentiation syndrome — the AKI is a downstream complication, not a primary rate)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor lysis early in treatment.

Distilled from: “Differentiation syndrome within days to a few months (often early); tumor lysis early in treatment.”

§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).

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Kidney injury

Mechanism of kidney injury

Olutasidenib's renal threats are differentiation-driven, analogous to other IDH/FLT3 inhibitors. (1) Differentiation syndrome: rapid blast maturation releases inflammatory cytokines causing fever, capillary-leak edema, effusions, hypotension and acute kidney injury (mixed prerenal hypoperfusion and intrarenal inflammatory injury). (2) Tumor lysis syndrome: cytoreduction releases uric acid, phosphate and potassium, producing urate and calcium-phosphate intratubular crystal nephropathy and ATN. There is no characteristic direct tubular drug toxicity.

Clinical presentation

Differentiation syndrome: dyspnea, fever, weight gain/edema, pleural/pericardial effusions, hypotension and rising creatinine, typically within the first weeks-to-months. TLS: hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia and AKI early in treatment.

Management

For differentiation syndrome: start corticosteroids (dexamethasone) promptly, use diuretics for fluid overload, hold olutasidenib if severe, and support kidney function. For TLS: aggressive IV hydration, rasburicase for hyperuricemia, electrolyte correction and dialysis for refractory derangement. Renal injury generally reverses with timely treatment of the underlying syndrome.Lesion-level management framework

Risk factors

High leukemic burden/blast count (differentiation syndrome and TLS)
Pre-existing CKD and concurrent nephrotoxins
Rapid responders early in therapy
Concurrent QT-prolonging drugs and electrolyte depletion

Prevention

Vigilance for differentiation-syndrome symptoms; early corticosteroids and, if needed, drug interruption
TLS prophylaxis: hydration plus allopurinol or rasburicase by risk
Frequent blood-chemistry monitoring; correct potassium/magnesium
Treat fluid overload with diuretics

Anticancer mechanism· how it treats cancer

Oral selective inhibitor of mutant isocitrate dehydrogenase 1 (mIDH1, R132). It blocks the neomorphic production of the oncometabolite 2-hydroxyglutarate, relieving the differentiation block so leukemic blasts mature, inducing remission in mIDH1 AML.

Note · The renal link is indirect but clinically important — AKI arises from differentiation syndrome and tumor lysis rather than a primary tubular drug toxicity. The differentiation-syndrome rate (~14%) is real and quantified from the pivotal cohort.

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Clinical depth

Renal dose adjustment

No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well characterized (hepatic metabolism). Interruptions are driven by differentiation syndrome/TLS rather than 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, steroid-responsive) from sepsis/ATN, TLS crystalline nephropathy (early hyperuricemia/hyperphosphatemia), and prerenal azotemia. The maturation-driven systemic syndrome is the clue.

Monitoring

Blood chemistries (potassium, phosphate, uric acid, creatinine) frequently, especially early
Daily weight and assessment for edema/effusions (differentiation syndrome)
Liver tests and ECG/QTc periodically
Volume status and blood pressure

Key trials & series

Pivotal phase 2 R/R AML cohort (de Botton, Blood Adv 2023) — registrational dataset with the differentiation-syndrome (~14%) signal

Clinical pearls

Differentiation syndrome is the boxed warning — recognize early (dyspnea, edema, fever) and treat with dexamethasone before organ failure.
Like other IDH/FLT3 inhibitors, the renal hazard is differentiation-driven, not a direct tubular toxicity.
Tumor lysis is an early renal hazard in responders — risk-stratify and pre-treat.
Frequent electrolyte monitoring guards both the kidney and the QT interval.

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

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

Class-level context for the major non-renal toxicities of the IDH1 inhibitor class.

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Differentiation syndrome

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

QT prolongation

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References

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

Evidence accrual

6 references · 2010–2025 · 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.

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

Quoted verbatim from this agent's current FDA label (Nov 2025) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: DIFFERENTIATION SYNDROME Differentiation syndrome, which can be fatal, can occur with REZLIDHIA treatment. Symptoms may include dyspnea, pulmonary infiltrates/pleuropericardial effusion, kidney injury, hypotension, fever, and weight gain. If differentiation syndrome is suspected, withhold REZLIDHIA and initiate treatment with corticosteroids and hemodynamic monitoring until symptom resolution [see Warnings and Precautions ( 5.1 )] . WARNING: DIFFERENTIATION SYNDROME See full prescribing information for complete boxed warning. Differentiation syndrome, which can be fatal, can occur with REZLIDHIA treatment. If differentiation syndrome is suspected, withhold REZLIDHIA and initiate corticosteroids and hemodynamic monitoring until symptom resolution. ( 5.1 )

Renal impairment — from the label

No dosage modification is recommended for patients with mild to moderate renal impairment (creatinine clearance [CLcr] 30 to <90 mL/min, as estimated by Cockcroft-Gault). The recommended dosage of REZLIDHIA has not been established in patients with severe renal impairment (CLcr 15 to 29 mL/min as estimated by Cockcroft-Gault), kidney failure (CLcr <15 mL/min, as estimated by Cockcroft-Gault), and patients on dialysis [see Clinical Pharmacology ( 12.3 )] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 275 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.

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· 15.3% of reports w/ death · 37.8% w/ hospitalization

15.3%

Reported with a death outcome

42 of 275 reports

37.8%

Reported with hospitalization

104 of 275 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 275 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.

Gastrointestinal

Nausea27Constipation17Vomiting9Abdominal Discomfort8Diarrhoea7

General / constitutional

Fatigue26Asthenia7Malaise7

Immune / infection

Pneumonia10

Respiratory

Dyspnoea9

Metabolic & electrolyte

Decreased Appetite7

Skin

Rash7

Hepatobiliary

Hepatic Enzyme Increased6

Blood & lymphatic

White Blood Cell Count Decreased6

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 Olutasidenib 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

Tazemetostat

Tazverik · EZH2 inhibitor

Profile

Tumor lysis; generally low direct renal toxicity.

PRELYTE

Mild#1 · 94% 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#2 · 89% phenotype match

Gilteritinib

Xospata · FLT3 inhibitor

Profile

Differentiation syndrome, tumor lysis and PRES in AML.

PRELYTE

Moderate#3 · 89% 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#4 · 88% phenotype match

Ziftomenib

Komzifti · Menin inhibitor

Profile

2025 NPM1-mutated AML menin inhibitor; differentiation syndrome and tumor lysis.

PRELYTE

Moderate#5 · 88% phenotype match

Tafasitamab

Monjuvi · Anti-CD19 antibody

Profile

Tumor lysis and infusion reactions in lymphoma.

PRELYTE

Mild#6 · 83% phenotype match

Compare Olutasidenib 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.