What kind of kidney injury does Erlotinib cause?

Glomerular Injury / Proteinuria — Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade. Other reported patterns: Acute Tubular Necrosis, Prerenal / Hemodynamic AKI, Thrombotic Microangiopathy.

How should kidney function be monitored during Erlotinib therapy?

Urinalysis/urine protein at baseline and periodically; Serum creatinine/eGFR each cycle, more often during diarrhea; Volume status and electrolytes during GI toxicity.

How can kidney injury from Erlotinib be prevented?

Aggressive management of diarrhea and maintenance of hydration

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Printable monograph

EGFR TKI

Erlotinib

Tarceva · ERL

EGFR TKI · approved 2004 · 9 citations

Recent· through 2024

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 17y)
Met: Beyond single case reports
Met: High-impact journal
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.

An oral EGFR TKI rarely linked to minimal-change-type glomerular disease, AKI, and dehydration from GI toxicity.

MildEGFR TKI

EGFR-mutant non-small cell lung cancerLocally advanced/metastatic pancreatic cancer (with gemcitabine)

§01

Signature kidney injury

Signature lesion

Glomerular Injury / Proteinuria

Representative incidence3%

Glomerular disease (including minimal-change-type nephrotic syndrome) and acute kidney injury are reported rarely, at the case level; pharmacovigilance data show measurable disproportionality signals for AKI/renal failure (and rare TMA) but no robust trial-based incidence. Reported rate: proteinuria in 3% — Erlotinib-MONOTHERAPY comparator arm of 4 randomized controlled trials in EGFR-mutation-positive advanced NSCLC (Deng 2022, PMID 35985780).Source: Deng et al., BMJ Open 2022

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Weeks to months after starting; proteinuria/creatinine typically improve over weeks after discontinuation.

Distilled from: “Weeks to months after starting therapy; proteinuria/creatinine typically improve over weeks after discontinuation in reported cases.”

§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 Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Thrombotic MicroangiopathySecondaryqualitative — no citable incidence
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

3%incidence

SeverityMild

ReversibilityReversible

Evidence9 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

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

Proposed mechanisms relate to EGFR signaling in podocytes and tubular cells. Case reports describe nephrotic-range proteinuria with minimal-change/minor glomerular abnormalities (podocyte foot-process effacement on a near-normal light-microscopic background) that remit on drug withdrawal, suggesting a drug-associated podocytopathy; acute tubular injury/AKI is also described, frequently compounded by volume depletion from EGFR-TKI-associated diarrhea and anorexia, and rare thrombotic microangiopathy has been signaled.

Clinical presentation

Proteinuria (occasionally nephrotic-range with edema and hypoalbuminemia) and/or a rising creatinine. Diarrhea, mucositis, and reduced intake commonly contribute a prerenal/ischemic component with concentrated urine and low urine output.

Management

Evaluate proteinuria and renal function and consider biopsy for nephrotic syndrome or unexplained AKI; for significant nephrotic syndrome or AKI, hold or discontinue erlotinib, which often leads to remission. Provide supportive care, volume repletion, and RAAS blockade for proteinuria as appropriate.Lesion-level management framework

Risk factors

Pre-existing chronic kidney disease
Volume depletion from EGFR-TKI-associated diarrhea/anorexia
Concurrent nephrotoxins

Prevention

Aggressive management of diarrhea and maintenance of hydration

Anticancer mechanism· how it treats cancer

Reversible, ATP-competitive EGFR tyrosine kinase inhibitor that blocks EGFR autophosphorylation and downstream RAS/MAPK and PI3K/AKT proliferative signaling. Used in EGFR-mutant non-small cell lung cancer and (with gemcitabine) advanced pancreatic cancer.

Note · Renal toxicity is uncommon and largely case-based; a published case of gefitinib-associated minimal-change nephrotic syndrome was successfully switched to erlotinib without recurrence, underscoring that severe glomerular events are idiosyncratic rather than uniform across EGFR TKIs.

§04

Clinical depth

Renal dose adjustment

No specific dose reduction is established for renal impairment (erlotinib is hepatically metabolized via CYP3A4/1A2 and biliary-excreted); use caution in severe impairment as renal data are sparse, and manage GI-driven volume depletion proactively. The pancreatic-cancer regimen pairs it with gemcitabine, which has its own renal considerations.

Dialyzability & ESKD dosing

Not appreciably dialyzable—highly protein-bound (~93%), lipophilic, with predominantly hepatic clearance and minimal renal elimination; hemodialysis is not expected to remove meaningful drug.

Differential diagnosis

Distinguish drug-associated podocytopathy/minimal-change disease (abrupt nephrotic syndrome remitting on withdrawal) from paraneoplastic glomerulopathy of the underlying cancer, and separate true intrinsic AKI from prerenal azotemia caused by diarrhea/anorexia (low urine sodium, responds to volume). Consider rare erlotinib-associated TMA when AKI is accompanied by hemolysis and thrombocytopenia.

Monitoring

Urinalysis/urine protein at baseline and periodically
Serum creatinine/eGFR each cycle, more often during diarrhea
Volume status and electrolytes during GI toxicity

Key trials & series

Moore JCO 2007 erlotinib-gemcitabine pancreatic registration trial
Maruyama Intern Med 2015 EGFR-TKI minimal-change nephrotic case
Crosnier Cancers 2021 VigiBase EGFR renal-safety pharmacovigilance

Clinical pearls

Most erlotinib 'renal' events are prerenal from diarrhea/anorexia—rehydrate before assuming intrinsic injury.
True nephrotic syndrome is a rare minimal-change-type podocytopathy that usually remits when the drug is stopped.

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

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 · 2007–2024 · 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.

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 · ModerateTubulointerstitial nephritis associated with erlotinib therapy for lung cancer.Cho SL et al. · Nephrology (Carlton) 2020 · PMID 32364270Biopsy-confirmed acute tubulointerstitial nephritis with renal impairment in a lung-cancer patient on erlotinib, recovering after drug withdrawal and corticosteroids.CaseB · ModerateRenal-limited ANCA-associated vasculitis during erlotinib treatment for lung carcinoma.Oki R et al. · CEN Case Rep 2022 · PMID 34309804A 71-year-old man on erlotinib developed proteinuria, microscopic hematuria and rising MPO-ANCA with biopsy-proven renal-limited ANCA-associated vasculitis/glomerulonephritis attributed to persistent EGFR-TKI use.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 12,442 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· 5 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 6.14 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Thrombotic Microangiopathycorroborated · ROR 3.17
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.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Glomerular Injury / Proteinuria

ROR 6.1495% CI 5.07–7.45· 105 reports

SIADH / Hyponatremia

ROR 3.6695% CI 3.15–4.26· 173 reports

Electrolyte Disturbance

ROR 3.3895% CI 3.05–3.75· 375 reports

Thrombotic Microangiopathy

ROR 3.1795% CI 2.20–4.56· 29 reports

Hypertension

ROR 1.2695% CI 1.12–1.41· 286 reports

FAERS outcomes & reporting trend· 46.3% of reports w/ death · 31.2% w/ hospitalization

46.3%

Reported with a death outcome

5,764 of 12,442 reports

31.2%

Reported with hospitalization

3,885 of 12,442 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 12,442 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 0.9295% CI 0.74–1.14· 83 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Diarrhoea1,338Nausea696Vomiting577Abdominal Pain262

General / constitutional

Fatigue719Asthenia463Malaise379Pyrexia341Pain308

Skin

Rash1,317Dermatitis Acneiform231

Respiratory

Dyspnoea484Pleural Effusion266Cough239Pulmonary Embolism234

Metabolic & electrolyte

Decreased Appetite512Dehydration381

Blood & lymphatic

Anaemia496Neutropenia265

Immune / infection

Pneumonia419

Vascular

Hypertension246

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 Erlotinib 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

mTOR inhibitors (everolimus · temsirolimus)

mTOR inhibitor

Profile

Podocyte injury → proteinuria and FSGS.

GLOMATNTMA

Mild#1 · 77% phenotype match

Sirolimus

Rapamune · mTOR inhibitor

Profile

Proteinuria, cast nephropathy, delayed graft recovery.

GLOMATN

Moderate#2 · 60% phenotype match

Clofarabine

Clolar · Purine analog

Profile

Capillary-leak / SIRS-like AKI and tumor lysis.

PREATNGLOM

Moderate#3 · 57% phenotype match

Afatinib

Gilotrif · EGFR TKI

Profile

Diarrhea-driven prerenal AKI.

PREATNLYTE

Mild#4 · 56% phenotype match

Adagrasib

Krazati · KRAS G12C inhibitor

Profile

Creatinine rise; emerging data.

PREGLOMPSEUDO

Mild#5 · 53% phenotype match

Bleomycin

Blenoxane · Antitumor antibiotic

Profile

Renally excreted (~2/3 in urine); half-life rises exponentially below CrCl 25-35 — exposure/clearance issue amplifying pulmonary toxicity, not a direct nephrotoxin.

PRE

Mild#6 · 52% phenotype match

Compare Erlotinib 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 Erlotinib’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 Erlotinib; 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 44 clinical records among all 68 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.