What kind of kidney injury does Eribulin cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

How should kidney function be monitored during Eribulin therapy?

CrCl/eGFR before dosing (drives dose level); CBC with differential (neutropenia) each cycle; Peripheral neuropathy assessment; QTc per label.

How can kidney injury from Eribulin be prevented?

Dose-reduce for moderate/severe renal impairment per labeling

Who is at higher risk of kidney injury from Eribulin?

Moderate-to-severe renal impairment (CrCl <50 mL/min - reduced clearance); Volume depletion and concurrent nephrotoxins; Baseline cytopenias amplifying systemic toxicity.

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Printable monograph

Microtubule inhibitor

Eribulin

Halaven · Erib

Microtubule inhibitor · approved 2010 · 6 citations

Aging evidence· through 2022

Fairly sourced6/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2022
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 microtubule inhibitor with reduced clearance in renal impairment, not direct kidney toxicity.

MildMicrotubule inhibitor

Metastatic breast cancerLiposarcoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Eribulin is not a recognized direct nephrotoxin. Pharmacokinetic study shows reduced clearance and ~1.5-fold higher exposure with moderate-to-severe renal impairment, supporting dose adjustment; any AKI is generally prerenal and not well quantified.Source: Tan et al., Cancer Chemother Pharmacol 2015

Onset & rechallenge

Time to injuryVariable / unpredictable

Prerenal AKI follows intercurrent volume loss, with no defined onset window.

Distilled from: “Exposure-related toxicity accrues across cycles; prerenal AKI follows volume loss.”

§02

Renal toxicities, ranked

This agent's defining kidney lesion — its #1 signature. 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.

§03

Kidney injury

Also documented as kidney-sparing

Eribulin — No characteristic renal lesion. Reduced clearance in renal impairment — adjust dose; neuropathy.

The spared

Mechanism of kidney injury

No characteristic direct tubular or glomerular toxin effect. The relevant renal issue is reduced drug clearance at low GFR (increased exposure and toxicity, including myelosuppression and neuropathy); prerenal AKI arises from intercurrent volume depletion.

Clinical presentation

Renal-impairment effects are pharmacokinetic - greater exposure with more myelosuppression and neuropathy; any AKI is prerenal with bland sediment.

Management

Reduce dose in renal impairment to limit excess hematologic and neurologic toxicity; treat prerenal AKI supportively with volume optimization.Lesion-level management framework

Risk factors

Moderate-to-severe renal impairment (CrCl <50 mL/min - reduced clearance)
Volume depletion and concurrent nephrotoxins
Baseline cytopenias amplifying systemic toxicity

Prevention

Dose-reduce for moderate/severe renal impairment per labeling

Anticancer mechanism· how it treats cancer

Synthetic halichondrin-B analog that inhibits microtubule growth at the plus end (a non-taxane microtubule dynamics inhibitor distinct from the taxane binding site), sequestering tubulin and arresting cells in mitosis. Used in metastatic breast cancer and liposarcoma.

Note · Reduced clearance in renal impairment drives dosing concerns rather than intrinsic nephrotoxicity.

§04

Clinical depth

Renal dose adjustment

Reduce dose to 1.1 mg/m2 across CrCl 15-49 mL/min (moderate or severe impairment) per the label; no adjustment for mild impairment (CrCl 50-79). PK data support 1.1 mg/m2 matching the exposure seen at 1.4 mg/m2 with normal function.

Dialyzability & ESKD dosing

Highly protein-bound with a large volume of distribution and predominantly hepatobiliary elimination; not expected to be dialyzable. No HD-timed dosing established.

Differential diagnosis

Pharmacokinetic over-exposure in low GFR (cytopenias/neuropathy without renal injury) vs prerenal azotemia vs unrelated CKD. The signal is dose-exposure, not parenchymal toxicity.

Monitoring

CrCl/eGFR before dosing (drives dose level)
CBC with differential (neutropenia) each cycle
Peripheral neuropathy assessment; QTc per label

Key trials & series

EMBRACE phase 3 (OS benefit in heavily pretreated metastatic breast cancer)
Tan Cancer Chemother Pharmacol 2015 renal-impairment PK study

Clinical pearls

Eribulin is dose-adjusted for the kidney to prevent over-exposure, not because it injures the kidney.
Drop to 1.1 mg/m2 across CrCl 15-49 mL/min (moderate or severe impairment); no change for mild impairment.
Watch counts and neuropathy as the readouts of excess exposure.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI

Beyond the kidney — non-renal toxicities· 3 organ systems

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

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (taxanes, vinca)

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Hypersensitivity (taxane vehicles)

§05

References

4 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

4 references · 2011–2022 · 2 since 2020

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 · LimitedTumour lysis syndrome following eribulin for metastatic uterine leiomyosarcoma.Pabon C et al. · BMJ Case Rep 2018 · PMID 30573532Eribulin precipitated tumour lysis syndrome with acute renal failure and electrolyte abnormalities on cycle 1 day 8, progressing to fatal AKI.CaseC · LimitedTumor Lysis Syndrome due to Eribulin Administration for Metastatic Undifferentiated Pleomorphic Sarcoma of the Buttock.Tsuchie H et al. · Acta Med Okayama 2021 · PMID 34511623Eribulin caused tumor lysis syndrome with deterioration of renal function plus hyperkalemia, hyperuricemia, hypocalcemia and hyperphosphatemia.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

A lower starting dose is recommended for patients with moderate (CLcr 30 to 49 mL/min) or severe (CLcr 15 to 29 mL/min) renal impairment. ( 8.7 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 3,719 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

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Electrolyte Disturbance

ROR 1.8795% CI 1.46–2.40· 63 reports

Hemorrhagic Cystitis

ROR 1.6395% CI 1.05–2.53· 20 reports

FAERS outcomes & reporting trend· 17.7% of reports w/ death · 52.4% w/ hospitalization

17.7%

Reported with a death outcome

659 of 3,719 reports

52.4%

Reported with hospitalization

1,948 of 3,719 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 3,719 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 0.7495% CI 0.48–1.15· 20 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Neutropenia537Febrile Neutropenia331Myelosuppression310Leukopenia208White Blood Cell Count Decreased176

General / constitutional

Pyrexia215Fatigue156Asthenia133Malaise91

Gastrointestinal

Nausea157Diarrhoea110Vomiting108Stomatitis103

Nervous system

Neuropathy Peripheral214Headache74

Respiratory

Interstitial Lung Disease181Dyspnoea105

Immune / infection

Pneumonia121Sepsis79

Metabolic & electrolyte

Decreased Appetite116

Skin

Alopecia102

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 Eribulin 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

Asparaginase

Elspar · Enzyme

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild#1 · 89% phenotype match

Belzutifan

Welireg · HIF-2α inhibitor

Profile

Anemia/hypoxia; emerging renal profile in VHL/RCC.

PRE

Mild#2 · 89% phenotype match

Dacarbazine

DTIC · Alkylator

Profile

Rare hepatic veno-occlusive disease; minimal direct renal injury.

PRE

Mild#3 · 89% phenotype match

Irinotecan

Camptosar · Topoisomerase I inhibitor

Profile

Diarrhea-driven prerenal AKI.

PRE

Mild#4 · 89% phenotype match

Mirvetuximab soravtansine

Elahere · Antibody-drug conjugate (FRα/DM4)

Profile

Ocular toxicity dominates; renal involvement indirect/case-level (GI volume loss).

PRE

Mild#5 · 89% phenotype match

Nilotinib

Tasigna · BCR-ABL TKI

Profile

eGFR decline over time.

PRE

Mild#6 · 89% phenotype match

Compare Eribulin 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 Microtubule 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.

1Eribulin· this agentPRE — Prerenal / Hemodynamic AKIMild
2VinblastineSIADH — SIADH / HyponatremiaMild
3VinflunineLYTE — Electrolyte DisturbanceMild
4CabazitaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
5VincristineSIADH — SIADH / HyponatremiaFAERS AKIMild
6VinorelbineSIADH — SIADH / HyponatremiaFAERS AKIMild
7DocetaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
8PaclitaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild

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.