How should kidney function be monitored during Gefitinib therapy?

Urinalysis/urine protein at baseline and periodically; Serum creatinine/eGFR and serum albumin if proteinuria develops.

Who is at higher risk of kidney injury from Gefitinib?

Underlying malignancy (paraneoplastic membranous nephropathy must also be considered); Pre-existing kidney disease.

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Printable monograph

EGFR TKI

Gefitinib

Iressa · GEF

EGFR TKI · approved 2003 · 12 citations

Dated evidence· through 2018

Deeply sourced7/9 · 6 signals

Met: 12 citations
Met: 12+ references
Met: Accrued over 10+ years (span: 14y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2018
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 EGFR TKI implicated in rare nephrotic syndrome (minimal-change and membranous patterns) and occasional AKI.

MildEGFR TKI

EGFR exon 19 deletion / L858R-mutant metastatic non-small cell lung cancer

§01

Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Nephrotic syndrome (minimal-change disease and secondary membranous nephropathy patterns) and rare acute renal failure are reported only as isolated cases; not quantified in clinical-trial datasets.Source: Maruyama et al., Intern Med 2015

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Weeks to months after initiation; proteinuria resolves over weeks to months after stopping.

Distilled from: “Weeks to months after initiation in reported cases; proteinuria resolves over weeks to months after stopping the drug.”

§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.

Glomerular Injury / Proteinuria#1 · Signaturequalitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Acute Interstitial NephritisSecondaryqualitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
Hemorrhagic CystitisRarequalitative — no citable incidence
Case reports plus a prospective series attribute hemorrhagic cystitis to gefitinib, improving on discontinuation.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence12 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Interstitium

Bladder / Urothelium

Glomerular Injury / Proteinuria

Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

§03

Kidney injury

Mechanism of kidney injury

Reported as a drug-associated glomerulopathy/podocytopathy. Biopsy-confirmed cases show either minimal glomerular abnormalities with podocyte foot-process effacement (minimal-change pattern) or secondary membranous nephropathy with subepithelial immune deposits, presumed related to EGFR-pathway effects on podocyte biology and the glomerular filtration barrier; proteinuria characteristically remits after gefitinib withdrawal. Rare acute renal failure has also been described.

Clinical presentation

Nephrotic-range proteinuria with edema and hypoalbuminemia; bland urine and near-normal renal function early. Renal biopsy is needed to distinguish minimal-change versus membranous patterns and to exclude paraneoplastic membranous nephropathy.

Management

Discontinue gefitinib for significant nephrotic syndrome, which commonly leads to remission; provide supportive nephrotic-syndrome care (edema management, RAAS blockade, attention to thromboembolic risk). Switching to an alternative EGFR TKI (e.g., erlotinib) has been tolerated in reported cases without recurrence.Lesion-level management framework

Risk factors

Underlying malignancy (paraneoplastic membranous nephropathy must also be considered)
Pre-existing kidney disease

Anticancer mechanism· how it treats cancer

Selective, reversible EGFR tyrosine kinase inhibitor that blocks EGFR autophosphorylation and downstream signaling driving tumor proliferation. Used for EGFR-mutant non-small cell lung cancer.

Note · Both minimal-change and membranous patterns have been described in single cases; evidence is sparse, so incidence remains unquantified and the signal is idiosyncratic.

§04

Clinical depth

Renal dose adjustment

No defined renal dose adjustment (hepatic CYP3A4 metabolism, biliary excretion; <4% renal elimination); caution in severe impairment given limited data. The intervention for glomerular toxicity is drug discontinuation, not dose titration.

Dialyzability & ESKD dosing

Not appreciably dialyzable—highly protein-bound (~90%), lipophilic, large volume of distribution with predominantly hepatic clearance; hemodialysis is not expected to remove meaningful amounts.

Differential diagnosis

Distinguish drug-associated minimal-change disease (abrupt nephrotic syndrome, remits on withdrawal) from secondary membranous nephropathy and especially from paraneoplastic membranous nephropathy of the underlying lung cancer (where PLA2R is usually negative and the tumor, not the drug, drives disease). Biopsy with immunofluorescence is decisive.

Monitoring

Urinalysis/urine protein at baseline and periodically
Serum creatinine/eGFR and serum albumin if proteinuria develops

Key trials & series

IPASS (Mok NEJM 2009) registrational EGFR-mutant NSCLC trial
Maruyama Intern Med 2015 minimal-change case; Kaneko CEN Case Rep 2014 membranous case
Kumasaka JCO 2004 early gefitinib nephrotic-syndrome report

Clinical pearls

Two glomerular phenotypes are reported—minimal-change disease and secondary membranous nephropathy—so biopsy matters.
Always weigh paraneoplastic membranous nephropathy from the lung cancer itself before attributing it to gefitinib.
The predominant lesion is a podocyte/filtration-barrier glomerulopathy with characteristically bland urine (protein only), though rare tubulointerstitial nephritis with hematuria has also been reported.
Gefitinib causes hemorrhagic cystitis, sometimes with an inflammatory contracted bladder — several case reports plus a prospective series, improving on discontinuation; agent-specific rather than an EGFR class effect.

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

Class-level context for the major non-renal toxicities of the EGFR TKI 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

10 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

10 references · 2004–2015 · 5 since 2013

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.

CaseB · ModerateCase of Proteinuria, Worsening Hypertension, and Glomerular Endotheliosis With Erlotinib and Gefitinib.Latcha S et al. · Kidney Int Rep 2018 · PMID 30450475EGFR-TKI therapy including gefitinib caused proteinuria, worsening hypertension, and biopsy-proven glomerular endotheliosis, a glomerular endothelial injury.CaseB · ModerateTubulointerstitial nephritis and IgA nephropathy in a patient with advanced lung cancer treated with long-term gefitinib.Masutani K et al. · Clin Exp Nephrol 2008 · PMID 18575950Long-term gefitinib was associated with biopsy-proven IgA nephropathy and tubulointerstitial nephritis presenting with proteinuria, hematuria, and glomerular mesangial IgA deposition.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Less than four percent (<4%) of gefitinib and its metabolites are excreted via the kidney. No clinical studies were conducted with gefitinib tablets in patients with severe renal impairment.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 8,974 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· 4 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

Glomerular Injury / Proteinuriacorroborated · ROR 4.12 — on the terms that name the lesion (ROR 2.57)
Hemorrhagic Cystitiscorroborated · ROR 2.85 — on the terms that name the lesion (ROR 20)
Acute Interstitial NephritisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.

Glomerular Injury / Proteinuria

ROR 4.1295% CI 3.13–5.42· 51 reports

Hemorrhagic Cystitis

ROR 2.8595% CI 2.30–3.54· 84 reports

SIADH / Hyponatremia

ROR 1.9895% CI 1.56–2.52· 68 reports

Electrolyte Disturbance

ROR 1.8295% CI 1.55–2.15· 148 reports

FAERS outcomes & reporting trend· 21.8% of reports w/ death · 28.7% w/ hospitalization

21.8%

Reported with a death outcome

1,952 of 8,974 reports

28.7%

Reported with hospitalization

2,577 of 8,974 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 8,974 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 0.3295% CI 0.21–0.49· 21 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Gastrointestinal

Diarrhoea903Nausea379Vomiting326

Respiratory

Interstitial Lung Disease419Dyspnoea330Pleural Effusion243Lung Disorder217Cough193

Skin

Rash642Dry Skin193Pruritus174

General / constitutional

Pyrexia270Fatigue242Asthenia208

Hepatobiliary

Hepatic Function Abnormal247Liver Disorder166

Metabolic & electrolyte

Decreased Appetite233Dehydration174

Immune / infection

Pneumonia273

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 Gefitinib 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

Atezolizumab

Tecentriq · Anti-PD-L1 antibody

Profile

Interstitial nephritis; rare glomerular disease.

AINGLOMCYST

Moderate#1 · 60% phenotype match

Belantamab mafodotin

Blenrep · Antibody-drug conjugate (BCMA/MMAF)

Profile

Myeloma ADC; renal data emerging.

GLOM

Mild#2 · 57% phenotype match

Avelumab

Bavencio · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#3 · 56% phenotype match

Cemiplimab

Libtayo · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#4 · 56% phenotype match

Dostarlimab

Jemperli · Anti-PD-1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#5 · 56% phenotype match

Durvalumab

Imfinzi · Anti-PD-L1 antibody

Profile

ICI-associated AIN.

AINGLOM

Moderate#6 · 56% phenotype match

Compare Gefitinib 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.

Who studies this

The leading contributors to Gefitinib’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 Gefitinib; 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 31 clinical records among all 53 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.