Is kidney injury from Idarubicin reversible?

Reversible. Typical onset: Hours to days after starting induction..

Does Idarubicin need a dose adjustment in kidney impairment?

Primarily hepatobiliary elimination; reduce in hepatic dysfunction. The current label defines a GFR-based algorithm: reduce the dose by 33% for GFR =30 mL/min); clinical trials excluded serum creatinine >2 mg/dL. Cumulative anthracycline cardiotoxicity also limits dosing.

How should kidney function be monitored during Idarubicin therapy?

Tumor-lysis panel every 6-12 h during induction; CBC, LDH and renal function; Cardiac LVEF (cumulative anthracycline dose).

How can kidney injury from Idarubicin be prevented?

Hydration plus allopurinol (intermediate) or rasburicase (high-risk) before cytoreduction Leukapheresis for hyperleukocytosis Avoid urinary alkalinization

Who is at higher risk of kidney injury from Idarubicin?

High WBC/blast count and high LDH; Elevated baseline creatinine or uric acid; Bulky disease and proliferative/inv(16) AML; Volume depletion.

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Printable monograph

Anthracycline

Idarubicin

Idamycin · IDAR

Anthracycline · approved 1990 · 8 citations

Recent· through 2023

Deeply sourced7/9 · 6 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 21y)
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.

An anthracycline for AML whose AKI is the leukemia's tumor lysis, not the drug's tubular toxicity.

MildAnthracycline

Acute myeloid leukemia (in combination with cytarabine)

§01

Signature kidney injury

Signature lesion

Crystal / Obstructive Nephropathy

Minimal intrinsic nephrotoxicity; the dominant renal threat is tumor lysis syndrome in acute leukemia. In 114 consecutive adult AML patients receiving induction, fulminant tumor lysis with acute renal failure occurred in 6.1% (95% CI 2.5-12.2), most of whom required hemodialysis; five of those seven patients had inv(16), so risk in that subgroup is substantially higher than the cohort-wide rate. That cohort used cytarabine-daunorubicin induction, so the figure reflects anthracycline-based induction generally — an idarubicin-specific AKI rate is not quantified.Source: Seftel et al., Eur J Haematol 2002

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor-lysis AKI within hours to days of starting induction.

Distilled from: “Hours to days after starting induction.”

§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.

Crystal / Obstructive Nephropathy#1 · Signaturequalitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.
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).
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence8 citations

Nephron map

Distal Tubule / Collecting Duct

Tubular LumenThe urine flow path

Crystal / Obstructive Nephropathy

Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

§03

Kidney injury

Mechanism of kidney injury

Minimal intrinsic nephrotoxicity; the renal injury is tumor lysis during induction. Rapid blast lysis floods the circulation with potassium, phosphate and purines, producing uric-acid and calcium-phosphate crystal nephropathy in the distal nephron with intratubular obstruction and AKI. Leukostasis/high WBC and concomitant sepsis/nephrotoxins compound the injury.

Clinical presentation

Tumor lysis within 12-72 h of induction: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, a high LDH and oliguric AKI. Certain cytogenetics (e.g. inv(16)) are flagged as high-risk for fulminant tumor lysis in AML.

Management

Aggressive hydration, rasburicase, electrolyte management, and renal replacement therapy if refractory. Support cytopenias and treat concomitant sepsis.Lesion-level management framework

Risk factors

High WBC/blast count and high LDH
Elevated baseline creatinine or uric acid
Bulky disease and proliferative/inv(16) AML
Volume depletion

Prevention

Hydration plus allopurinol (intermediate) or rasburicase (high-risk) before cytoreduction
Leukapheresis for hyperleukocytosis
Avoid urinary alkalinization

Anticancer mechanism· how it treats cancer

Anthracycline that intercalates DNA and inhibits topoisomerase II, producing double-strand breaks; high lipophilicity (4-demethoxy) gives strong cellular uptake, and the long-lived active metabolite idarubicinol contributes to efficacy.

Note · Established (1990) anthracycline; renal events are tumor-lysis-driven in acute leukemia and not population-quantified.

§04

Clinical depth

Renal dose adjustment

Primarily hepatobiliary elimination; reduce in hepatic dysfunction. The current label defines a GFR-based algorithm: reduce the dose by 33% for GFR <30 mL/min or hemodialysis (no adjustment at GFR >=30 mL/min); clinical trials excluded serum creatinine >2 mg/dL. Cumulative anthracycline cardiotoxicity also limits dosing.

Dialyzability & ESKD dosing

Not appreciably dialyzable (large volume of distribution and tissue binding); dialysis manages tumor-lysis derangements.

Differential diagnosis

Tumor lysis versus sepsis-associated AKI versus nephrotoxic antimicrobials versus leukemic renal infiltration versus contrast.

Monitoring

Tumor-lysis panel every 6-12 h during induction
CBC, LDH and renal function
Cardiac LVEF (cumulative anthracycline dose)

Key trials & series

AML15 (Burnett, J Clin Oncol 2013) — FLAG-Ida induction in AML
QuANTUM-First (Erba, Lancet 2023) — idarubicin within the 7+3 backbone

Clinical pearls

Idarubicin AKI is the leukemia's tumor lysis, not the drug's tubular toxicity.
inv(16) AML is a recognized high-risk subgroup for fulminant tumor lysis.
Hepatobiliary clearance means hepatic, not renal, dose-cuts dominate.
Cardiotoxicity remains the long-term dose-limiting toxicity.

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

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

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

Dose-dependent cardiomyopathy and heart failure

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression

§05

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 · 2002–2023 · 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· 2

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.

CaseC · LimitedAcute monoblastic leukemia presenting with striking periorbital and periauricular infiltration.Brierley CK et al. · Blood 2017 · PMID 28642361Acute monoblastic leukemia treated with idarubicin-containing chemotherapy complicated by tumor lysis syndrome and acute kidney injury, a hemodynamic/metabolic AKI occurring during idarubicin induction.CaseC · LimitedHigh cutoff membrane to reduce systemic inflammation due to differentiation syndrome: a case report.Villa G et al. · Blood Purif 2014 · PMID 25531172APL patient on idarubicin/ATRA who developed differentiation syndrome with capillary leak, hypoalbuminemia and acute kidney injury requiring hemofiltration, illustrating hemodynamic/prerenal AKI in the idarubicin induction setting.

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: CARDIOMYOPATHY, SECONDARY MALIGNANCIES, and EXTRAVASATION AND TISSUE NECROSIS • Cardiomyopathy: IDAMYCIN PFS can cause myocardial damage, including acute left ventricular failure, during or after termination of therapy. The risk of cardiomyopathy is increased in patients who have received prior anthracyclines or who have pre-existing cardiac disease. Assess left ventricular cardiac function prior to initiation of IDAMYCIN PFS and during and after treatment [see Warnings and Precautions (5.1) ] . • Secondary Malignancies: Secondary acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) occur at a higher incidence in patients treated with anthracyclines, including IDAMYCIN PFS [see Warnings and Precautions (5.2) ] . • Extravasation and Tissue Necrosis: Extravasation of IDAMYCIN PFS during administration can result in local tissue injury and necrosis. Immediately terminate the infusion of IDAMYCIN PFS and institute the recommended management procedures [see Dosage and Administration (2.6) and Warnings and Precautions (5.3) ] . WARNING: CARDIOMYOPATHY, SECONDARY MALIGNANCIES, and EXTRAVASATION AND TISSUE NECROSIS See full prescribing information for complete boxed warning. • Cardiomyopathy: Myocardial damage leading to congestive heart failure can occur with IDAMYCIN PFS. Assess left ventricular cardiac function prior to initiation of IDAMYCIN PFS and during…

Renal impairment — from the label

Reduce dosage of IDAMYCIN PFS in patients with GFR less than 30 mL/min and in patients on hemodialysis [see Dosage and Administration (2.3) ] . Renal function should be evaluated prior to and during treatment with IDAMYCIN PFS. The effect of renal impairment on idarubicin hydrochloride or idarubicinol pharmacokinetics is unknown [see Clinical Pharmacology (12.3) ] . However, renal impairment can affect the disposition of idarubicin hydrochloride based on a mechanistic understanding of idarubicin hydrochloride elimination. Treatment was not given if creatinine serum levels exceeded 2 mg/dL in multiple clinical trials.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,119 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.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
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 reported renal phenotypes· 2 signals

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Electrolyte Disturbancecorroborated · ROR 1.88 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Crystal / Obstructive NephropathyNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Thrombotic Microangiopathy

ROR 6.0895% CI 2.52–14.63· 5 reports

Electrolyte Disturbance

ROR 1.8895% CI 1.19–2.96· 19 reports

FAERS outcomes & reporting trend· 22.3% of reports w/ death · 40.9% w/ hospitalization

22.3%

Reported with a death outcome

249 of 1,119 reports

40.9%

Reported with hospitalization

458 of 1,119 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 5 systems · 1,119 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 1.3695% CI 0.75–2.46· 11 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Myelosuppression180Febrile Neutropenia147White Blood Cell Count Decreased58Neutropenia51Platelet Count Decreased50

Immune / infection

Pneumonia61Infection52Sepsis39Septic Shock26Fungal Infection24

General / constitutional

Pyrexia95Asthenia26Multiple Organ Dysfunction Syndrome24

Gastrointestinal

Nausea43Vomiting34Diarrhoea25

Respiratory

Respiratory Failure34

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 Idarubicin 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

Mitoxantrone

Novantrone · Anthracenedione

Profile

Tumor lysis; low direct renal toxicity.

XTALLYTEPRE

Mild#1 · 88% phenotype match

Dactinomycin (actinomycin D)

Cosmegen · Antitumor antibiotic

Profile

Renal risk indirect via tumor lysis in chemosensitive pediatric tumors; hepatic veno-occlusive disease is the signature organ toxicity.

LYTEPREXTAL

Moderate#2 · 85% phenotype match

Etoposide

Etopophos · Topoisomerase II inhibitor

Profile

Tumor lysis; renally cleared.

XTALPRELYTE

Mild#3 · 81% phenotype match

Hydroxyurea

Hydrea · Ribonucleotide reductase inhibitor

Profile

Tumor lysis in myeloproliferative disease.

XTALPRELYTE

Mild#4 · 81% phenotype match

Nelarabine

Arranon · Purine analog

Profile

Tumor lysis in T-ALL.

XTALPRELYTE

Mild#5 · 81% phenotype match

Pomalidomide

Pomalyst · Immunomodulatory drug (IMiD)

Profile

Tumor lysis; usable in renal impairment.

PRELYTEXTAL

Mild#6 · 81% phenotype match

Compare Idarubicin 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 Antitumor antibiotics

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.

1Idarubicin· this agentXTAL — Crystal / Obstructive NephropathyMild
2BleomycinPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
3DoxorubicinGLOM — Glomerular Injury / ProteinuriaFAERS AKIMild
4MitoxantroneXTAL — Crystal / Obstructive NephropathyFAERS AKIMild
5Plicamycin (mithramycin)ATN — Acute Tubular NecrosisModerate
6Dactinomycin (actinomycin D)LYTE — Electrolyte DisturbanceModerate
7Mitomycin CTMA — Thrombotic MicroangiopathySevere

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.

Who studies this

The leading contributors to Idarubicin’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Idarubicin; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 11 clinical records among all 20 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.