What kind of kidney injury does Lazertinib cause?

SIADH / Hyponatremia — Inappropriate water retention at the collecting duct — high-dose cyclophosphamide. Other reported patterns: Electrolyte Disturbance.

Is kidney injury from Lazertinib reversible?

Reversible. Typical onset: During therapy; case-level and variable..

How should kidney function be monitored during Lazertinib therapy?

Serum sodium periodically and whenever symptoms suggest hyponatremia; Serum magnesium, potassium and calcium (especially with amivantamab); Volume status assessment if hyponatremic.

How can kidney injury from Lazertinib be prevented?

Review and address other ADH-promoting medications Replete magnesium proactively

Who is at higher risk of kidney injury from Lazertinib?

Concurrent SIADH-promoting drugs; Combination with amivantamab (overlapping EGFR-class effects); Volume-status changes; Older age.

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Printable monograph

EGFR TKI (3rd-gen)

Lazertinib

Lazcluze · Lazer

EGFR TKI (3rd-gen) · approved 2024 · 6 citations

Recent· through 2024

Fairly sourced6/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 14y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
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 third-generation EGFR TKI — hyponatremia and EGFR-class electrolyte wasting.

MildThird-generation EGFR TKI

EGFR-mutant advanced NSCLC (with amivantamab)

§01

Signature kidney injury

Signature lesion

SIADH / Hyponatremia

Hyponatremia is a recognized signal of third-generation EGFR TKIs (an osimertinib-class effect); for lazertinib specifically the renal/sodium data are limited and not well quantified. EGFR blockade also causes electrolyte wasting (hypomagnesemia, hypokalemia), and combination with amivantamab adds to these effects.Source: Felip et al., Ann Oncol 2024 (MARIPOSA)

Onset & rechallenge

Time to injuryVariable / unpredictable

Occurs during therapy at the case level and is variable in timing.

Distilled from: “During therapy; case-level and variable.”

§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.

SIADH / Hyponatremia#1 · Signaturequalitative — no citable incidence
Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.
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).

§03

Kidney injury

Mechanism of kidney injury

Two EGFR-pathway mechanisms touch the kidney. (1) Like other third-generation EGFR TKIs, lazertinib is associated with hyponatremia, postulated to reflect SIADH-type dysregulation of water handling at the distal nephron/collecting duct (euvolemic, dilutional). (2) EGFR signaling sustains the distal-tubular magnesium channel TRPM6, so EGFR inhibition can cause renal magnesium (and potassium/calcium) wasting. Direct tubular toxicity is not characteristic; the renal footprint is water/electrolyte dysregulation.

Clinical presentation

Euvolemic hyponatremia — low serum sodium with low serum osmolality and inappropriately concentrated urine — when SIADH-type; hypomagnesemia/hypokalemia, especially in combination therapy. Serum creatinine is usually stable.

Management

For SIADH-type hyponatremia: fluid restriction, remove contributing drugs, correct sodium at a safe rate (<8–10 mEq/L per 24 h to avoid osmotic demyelination); consider drug hold for severe/symptomatic hyponatremia. Replete magnesium/potassium for EGFR-class wasting.Lesion-level management framework

Risk factors

Concurrent SIADH-promoting drugs
Combination with amivantamab (overlapping EGFR-class effects)
Volume-status changes
Older age

Prevention

Review and address other ADH-promoting medications
Replete magnesium proactively

Anticancer mechanism· how it treats cancer

Third-generation, CNS-penetrant, irreversible EGFR tyrosine-kinase inhibitor selective for EGFR-activating (exon 19 deletion, L858R) and T790M resistance mutations while sparing wild-type EGFR. Approved with amivantamab for first-line EGFR-mutant advanced NSCLC.

§04

Clinical depth

Renal dose adjustment

No established renal dose adjustment (not renally cleared to a significant degree); severe impairment/ESKD not well studied. Manage by sodium/electrolyte correction and drug hold for severe hyponatremia rather than GFR-based dosing.

Dialyzability & ESKD dosing

Highly protein-bound, hepatically metabolized small molecule; not expected to be appreciably dialyzed. No specific ESKD dosing — focus on sodium and electrolyte management.

Differential diagnosis

SIADH-type euvolemic hyponatremia vs hypovolemic (poor intake, GI losses) vs other-drug SIADH (urine sodium/osmolality with volume assessment); EGFR-class hypomagnesemia (low Mg with renal wasting) is distinct from the hyponatremia and may coexist, particularly in combination with amivantamab.

Monitoring

Serum sodium periodically and whenever symptoms suggest hyponatremia
Serum magnesium, potassium and calcium (especially with amivantamab)
Volume status assessment if hyponatremic

Key trials & series

MARIPOSA (Felip Ann Oncol 2024) lazertinib + amivantamab vs osimertinib
LASER301 (lazertinib monotherapy registrational)

Clinical pearls

Check sodium: third-generation EGFR TKIs carry an osimertinib-class hyponatremia (SIADH-type) signal — treat with water restriction, not saline alone.
EGFR blockade also wastes magnesium via TRPM6 — replete proactively, especially when combined with amivantamab.
Correct hyponatremia slowly (<8–10 mEq/L/24 h) to avoid osmotic demyelination.
Creatinine usually stays put; the renal story here is water and electrolytes.

Where it strikes· nephron segments & injury signatures

Nephron segments

Distal Tubule / Collecting Duct

Fine-tuning of Na, K, Mg, acid & water

Injury signatures

SIADH / Hyponatremia Electrolyte Disturbance

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

Class-level context for the major non-renal toxicities of the EGFR TKI (3rd-gen) class.

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Acneiform rash, paronychia

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Diarrhea

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Interstitial lung disease (EGFR TKIs)

§05

References

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

Evidence accrual

6 references · 2010–2024 · 2 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· renal impairment

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

Renal impairment — from the label

No dose adjustment is recommended in patients with mild or moderate renal impairment (eGFR 30 – 89 mL/min) [see Clinical Pharmacology (12.3) ] . LAZCLUZE has not been studied in patients with severe renal impairment or end-stage renal disease (eGFR < 30 mL/min).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 706 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· 4.5% of reports w/ death · 24.8% w/ hospitalization

4.5%

Reported with a death outcome

32 of 706 reports

24.8%

Reported with hospitalization

175 of 706 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 706 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 0.9795% CI 0.40–2.35· 5 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Skin

Rash134Pruritus27Dermatitis Acneiform22Skin Toxicity22Skin Disorder17

General / constitutional

Fatigue39Oedema Peripheral23Pyrexia16Oedema15Pain15

Nervous system

Neuropathy Peripheral42Dizziness22Paraesthesia18Headache15

Gastrointestinal

Diarrhoea35Nausea28Stomatitis23

Immune / infection

Infusion Related Reaction81

Respiratory

Dyspnoea27Interstitial Lung Disease17Pneumonitis16

Metabolic & electrolyte

Decreased Appetite19Hypoalbuminaemia17

Vascular

Hypotension15Deep Vein Thrombosis14

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 Lazertinib 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

Vismodegib

Erivedge · Hedgehog (SMO) inhibitor

Profile

Muscle spasms; hyponatremia reported.

SIADHLYTE

Mild#1 · 88% phenotype match

Melphalan

Alkeran · Alkylator

Profile

SIADH in high-dose myeloma conditioning; renally cleared.

SIADHLYTE

Mild#2 · 86% phenotype match

Temozolomide

Temodar · Alkylator

Profile

Occasional SIADH; generally renally well tolerated.

SIADHLYTE

Mild#3 · 86% phenotype match

Vinblastine

Velban · Vinca alkaloid

Profile

SIADH and rare Raynaud/vascular events.

SIADHLYTE

Mild#4 · 86% phenotype match

Vincristine

Oncovin · Vinca alkaloid

Profile

SIADH → hyponatremia.

SIADHLYTE

Mild#5 · 86% phenotype match

Vinorelbine

Navelbine · Vinca alkaloid

Profile

SIADH reports.

SIADHLYTE

Mild#6 · 86% phenotype match

Compare Lazertinib 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 EGFR / HER2 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.

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.