What kind of kidney injury does Lurbinectedin cause?

Acute Tubular Necrosis — Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate. Other reported patterns: Electrolyte Disturbance, Crystal / Obstructive Nephropathy.

Is kidney injury from Lurbinectedin reversible?

Reversible. Typical onset: Variable across cycles (not tightly defined) — monitor with each dose..

How should kidney function be monitored during Lurbinectedin therapy?

CBC (neutropenia is the dominant toxicity), per-cycle and as indicated; CK/CPK with any muscle symptoms; LFTs each cycle; Creatinine, electrolytes and tumor-lysis labs in high-burden disease; CK and renal function at baseline and periodically.

How can kidney injury from Lurbinectedin be prevented?

Hydration; G-CSF prophylaxis for neutropenia Avoid extravasation (vesicant — prefer a secure/central line) Tumor-lysis prophylaxis in high-burden disease

Who is at higher risk of kidney injury from Lurbinectedin?

Pre-existing renal impairment and volume depletion; Concurrent myotoxic/nephrotoxic drugs (e.g. statins); High tumor burden (tumor lysis risk); Hepatic impairment.

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Printable monograph

Marine alkylating agent

Lurbinectedin

Zepzelca · LURB

Marine alkylating agent · approved 2020 · 8 citations · FAERS AKI reporting ROR 3.70 (95% CI 2.56–5.35, 29 AKI reports)

Up to date· through 2025

Fairly sourced6/9 · 6 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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 synthetic ecteinascidin for small-cell lung cancer whose rare renal injury follows rhabdomyolysis or tumor lysis.

MildMarine alkylating agent (ecteinascidin)

Metastatic small-cell lung cancer with disease progression on or after platinum-based chemotherapy

§01

Signature kidney injury

Signature lesion

Acute Tubular Necrosis

Not directly tubulotoxic; clinically significant AKI is rare and arises from rhabdomyolysis or tumor lysis. Rhabdomyolysis was formally recognized post-approval (FDA FAERS) and as an isolated phase 1 dose-limiting toxicity; the trial rate is not quantified. The dominant toxicity is hematologic (grade >=3 neutropenia ~41%) with frequent transaminase elevations.Source: Trigo et al., Lancet Oncol 2020

Onset & rechallenge

Time to injuryVariable / unpredictable

Onset varies across cycles and is not tightly defined, warranting monitoring with each dose.

Distilled from: “Variable across cycles (not tightly defined) — monitor with each dose.”

§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.

Acute Tubular Necrosis#1 · Signaturequalitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
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

SeverityMild

ReversibilityReversible

Evidence8 citations

Nephron map

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

Distal Tubule / Collecting DuctFine-tuning of Na, K, Mg, acid & water

Tubular Lumen

Acute Tubular Necrosis

Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

§03

Kidney injury

Mechanism of kidney injury

Indirect: drug-induced rhabdomyolysis releases myoglobin causing pigment nephropathy/ATN (proximal tubular injury, intratubular cast obstruction and vasoconstriction). Tumor lysis is an alternate route to crystal/uric-acid nephropathy. The agent is not a recognized direct tubular toxin.

Clinical presentation

CK elevation with myalgia/weakness and dark urine, plus a rising creatinine; transaminase elevations are common and often concurrent. When tumor lysis drives AKI, expect hyperuricemia/hyperphosphatemia/hyperkalemia.

Management

For rhabdomyolysis: withhold/discontinue, give IV volume resuscitation, and correct hyperkalemia and metabolic derangements, with renal replacement therapy for refractory AKI. Standard tumor-lysis measures if applicable. Manage neutropenia with growth factors.Lesion-level management framework

Risk factors

Pre-existing renal impairment and volume depletion
Concurrent myotoxic/nephrotoxic drugs (e.g. statins)
High tumor burden (tumor lysis risk)
Hepatic impairment

Prevention

Hydration; G-CSF prophylaxis for neutropenia
Avoid extravasation (vesicant — prefer a secure/central line)
Tumor-lysis prophylaxis in high-burden disease

Anticancer mechanism· how it treats cancer

Synthetic ecteinascidin analog that binds the DNA minor groove and alkylates guanine N2 at CG-rich regulatory regions, stalling elongating RNA polymerase II and triggering its ubiquitination and proteasomal degradation; this induces double-strand breaks and suppresses oncogenic transcription and tumor-associated macrophages.

Note · Recent (2020) accelerated approval; renal events are uncommon and largely post-marketing/case-level, with mechanism inferred from the rhabdomyolysis/tumor-lysis pathways.

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Clinical depth

Renal dose adjustment

Standard 3.2 mg/m2 IV over 1 h every 3 weeks; dose reductions to 2.6 then 2.0 mg/m2 for toxicity. No dedicated renal adjustment for mild-moderate impairment; severe renal/hepatic impairment has not been studied, so CrCl cutoffs are not established.

Dialyzability & ESKD dosing

Not characterized; high protein binding and a large volume of distribution make significant dialytic removal unlikely. Dialysis would be used to support AKI, not to clear drug.

Differential diagnosis

Rhabdomyolysis/pigment nephropathy versus tumor lysis, prerenal volume depletion, concomitant nephrotoxins and sepsis-associated ATN. CK plus myoglobinuria identifies the pigment mechanism.

Monitoring

CBC (neutropenia is the dominant toxicity), per-cycle and as indicated
CK/CPK with any muscle symptoms
LFTs each cycle
Creatinine, electrolytes and tumor-lysis labs in high-burden disease
CK and renal function at baseline and periodically

Key trials & series

Trigo phase 2 basket trial (Lancet Oncol 2020) — pivotal SCLC trial supporting accelerated approval
FDA FAERS analysis (Kaland, Clin Lung Cancer 2022) — formally identified rhabdomyolysis and tumor lysis

Clinical pearls

Renal risk is indirect — an unexplained creatinine bump with myalgia or dark urine should prompt a CK.
The FDA added rhabdomyolysis and tumor lysis to the label post-approval — keep both on the differential.
Lurbinectedin is a vesicant — use a secure or central line.
The confirmatory ATLANTIS combination was negative for overall survival; single-agent 3.2 mg/m2 remains standard.

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

Class-level context for the major non-renal toxicities of the Marine alkylating agent class.

Ophthalmic

Keratopathy, uveitis, retinopathy

Visual disturbance (crizotinib)

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Transaminitis

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

CNS effects (lorlatinib)

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References

7 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

7 references · 2018–2025 · 2 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.

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.

CaseC · LimitedLurbinectedin-Induced Tumor Lysis Syndrome in Small Cell Neuroendocrine Cancer of the Cecum: A First-Ever Case Report.Wahab A et al. · Am J Case Rep 2021 · PMID 34125741Single intravenous dose of lurbinectedin precipitated grade 4 tumor lysis syndrome with anuria and acute renal failure requiring emergent hemodialysis.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,100 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· 1 signal

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

Acute Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.
Electrolyte DisturbanceNo 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.
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.

SIADH / Hyponatremia

ROR 2.1495% CI 1.11–4.12· 9 reports

FAERS outcomes & reporting trend· 25% of reports w/ death · 36.5% w/ hospitalization

25%

Reported with a death outcome

275 of 1,100 reports

36.5%

Reported with hospitalization

402 of 1,100 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 1,100 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 3.7095% CI 2.56–5.35· 29 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury29

Blood & lymphatic

Neutropenia73Thrombocytopenia60Febrile Neutropenia46Anaemia42Platelet Count Decreased25

Gastrointestinal

Nausea69Vomiting42Diarrhoea29Constipation23

General / constitutional

Fatigue51Asthenia42Pyrexia15

Respiratory

Dyspnoea29Cough18Pneumonitis17

Immune / infection

Pneumonia28Sepsis21

Metabolic & electrolyte

Decreased Appetite15

Guidelines & consensus· 14

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.

ADQIConventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupKidney Int 2026 · PMID 41881107Cisplatin is identified as a leading cytotoxic nephrotoxin; the workgroup details preventive measures (adequate isotonic hydration, correction of volume depletion, avoidance of concurrent nephrotoxins, attention to electrolyte/magnesium wasting) and management of cisplatin-associated AKI, with a research agenda for knowledge gaps.

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 Lurbinectedin 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

Trabectedin

Yondelis · Marine alkylating agent

Profile

Rhabdomyolysis → pigment nephropathy; hepatotoxicity.

ATNLYTE

Moderate#1 · 78% phenotype match

Mechlorethamine

Mustargen · Alkylating agent (nitrogen mustard)

Profile

Tumor lysis in bulky lymphoma is the main renal hazard; modern topical gel has no detectable systemic absorption.

LYTEXTAL

Moderate#2 · 72% phenotype match

Melphalan flufenamide (melflufen)

Pepaxto · Peptide-conjugated alkylator

Profile

Delivers melphalan intracellularly; BRIDGE supports a reduced 30 mg dose in moderate renal impairment.

ATNLYTE

Moderate#3 · 67% phenotype match

Raltitrexed

Tomudex · Antifolate (TS inhibitor)

Profile

Renally cleared antifolate; exposure ~doubles in renal impairment; forerunner CB3717 withdrawn for crystal nephrotoxicity.

ATNXTAL

Moderate#4 · 65% phenotype match

Methotrexate (high-dose)

Trexall · Antifolate

Profile

Crystal nephropathy; glucarpidase rescue.

XTALATN

Moderate#5 · 65% phenotype match

Amsacrine

Amsidine · Topoisomerase II inhibitor (acridine)

Profile

Predominantly hepatobiliary elimination; renal clearance minor, kidney risk mainly tumor lysis in AML; reduce dose in organ impairment.

LYTEXTAL

Moderate#6 · 65% phenotype match

Compare Lurbinectedin 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 Alkylating 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.