How should kidney function be monitored during Crizotinib therapy?

Serum creatinine periodically (interpret with secretion artifact in mind); Serum phosphate, potassium, and electrolytes; Renal imaging if cysts are present or suspected; Cystatin C-based eGFR when true GFR is in question.

How can kidney injury from Crizotinib be prevented?

Distinguish true GFR change from reduced tubular creatinine secretion (consider cystatin C)

Who is at higher risk of kidney injury from Crizotinib?

Pre-existing renal cysts or chronic kidney disease; Longer treatment duration (for cysts); Hypertension and male sex (AKI risk factors in ALK-inhibitor cohorts); Concurrent nephrotoxins.

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Printable monograph

ALK/ROS1/MET TKI

Crizotinib

Xalkori · CRIZ

ALK/ROS1/MET TKI · approved 2011 · 10 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 10 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 10y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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 ALK/ROS1/MET inhibitor notable for reversible creatinine rises and the development or growth of complex renal cysts.

MildALK/ROS1/MET tyrosine kinase inhibitor

ALK-positive non-small-cell lung cancerROS1-positive non-small-cell lung cancer

§01

Signature kidney injury

Signature lesion

Renal Cysts

Representative incidence16%

Crizotinib commonly causes a reversible rise in serum creatinine and is distinctively associated with renal cysts: in the Halpenny series, new or enlarging cysts in 16% (9 of 57 serially imaged patients) and frankly complex cysts in 4% (2 of 57) — the 16% headline is the any-cyst rate, not a complex-cyst or AKI rate. Peripheral edema and electrolyte disturbances (including hypophosphatemia and hypokalemia) are reported. In real-world ALK-inhibitor cohorts, creatinine-based AKI/CKD events are frequent but mostly mild and reversible; frank kidney failure is uncommon.Source: Halpenny et al., Lung Cancer 2017 (renal cysts 16%); Izzedine et al., Invest New Drugs 2016

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Creatinine rises within weeks (reversible on stopping), while the renal cysts develop and enlarge over months.

Distilled from: “Creatinine rise often within weeks and reverses on discontinuation; cysts develop and grow over months.”

§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.

Renal Cysts#1 · Signature16%PMID 28285691 (opens PubMed in a new tab)
Renal cyst formation or growth in 16% of crizotinib-treated NSCLC; complex cysts ~4% (retrospective CT cohort)
Pseudo-AKISecondary12.6%PMID 30822515 (opens PubMed in a new tab)
Median eGFR fell ~15% by week 2 (creatinine-secretion effect, not true nephrotoxicity); 12.6% shifted to eGFR <45, largely reversible on discontinuation
Electrolyte DisturbanceRarequalitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

16%incidence

SeverityMild

ReversibilityReversible

Evidence10 citations

Nephron map

Proximal Tubule

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

Renal Cysts

Drug-induced complex renal cysts — the distinctive ALK-inhibitor lesion, classically crizotinib. Usually asymptomatic, dose/duration-related, and they tend to regress when the drug is stopped.

§03

Kidney injury

Deep divePseudo-AKI: the creatinine rises and the kidney is fineCreatinine does not only filter — a fifth of it is pushed into the urine by tubular transporters, and a drug that blocks those transporters raises the number without touching the glomerulus, producing a rise that looks like acute kidney injury on every axis except the one that matters.

Mechanism of kidney injury

Much of the creatinine increase reflects inhibition of tubular creatinine secretion (a rise in serum creatinine without a true fall in GFR) rather than structural injury. Separately, crizotinib promotes formation and enlargement of complex renal cysts, sometimes with hemorrhage or perinephric extension; the cyst mechanism is incompletely understood and may relate to MET-pathway inhibition in tubular/cyst epithelium.

Clinical presentation

Reversible serum creatinine elevation; new or enlarging complex renal cysts on cross-sectional imaging (which can mimic malignancy or infection); peripheral edema; occasional hypophosphatemia/hypokalemia. Overt AKI is uncommon.

Management

Most creatinine elevations are benign and reverse on discontinuation; manage cysts conservatively unless complicated (hemorrhage, infection, mass effect). Recognize cysts as a drug effect to avoid mistaking them for progression or new primary malignancy. Reduce dose or interrupt for true AKI, and correct electrolyte disturbances and edema.Lesion-level management framework

Risk factors

Pre-existing renal cysts or chronic kidney disease
Longer treatment duration (for cysts)
Hypertension and male sex (AKI risk factors in ALK-inhibitor cohorts)
Concurrent nephrotoxins

Prevention

Distinguish true GFR change from reduced tubular creatinine secretion (consider cystatin C)

Anticancer mechanism· how it treats cancer

Multitargeted ATP-competitive inhibitor of ALK, ROS1, and MET tyrosine kinases. Used in ALK-positive and ROS1-positive non-small-cell lung cancer.

Note · Complex renal cysts and a reversible (often secretion-mediated) creatinine rise are the hallmark - distinguish apparent from true GFR decline.

§04

Clinical depth

Renal dose adjustment

No starting-dose change for mild-to-moderate renal impairment (CrCl >=30). For severe renal impairment not on dialysis (CrCl <30), reduce the dose (e.g., to 250 mg once daily) per labeling. Hepatic impairment also requires adjustment.

Dialyzability & ESKD dosing

Highly protein-bound (~91%) and hepatically metabolized; not appreciably dialyzed. ESKD dosing data are limited - use clinical monitoring.

Differential diagnosis

Differentiate the secretion-mediated creatinine rise (true GFR preserved on cystatin C) from genuine AKI, and crizotinib-related complex cysts from cystic renal cell carcinoma, abscess, or metastasis - the temporal link to crizotinib and regression on cessation favor a drug effect.

Monitoring

Serum creatinine periodically (interpret with secretion artifact in mind)
Serum phosphate, potassium, and electrolytes
Renal imaging if cysts are present or suspected
Cystatin C-based eGFR when true GFR is in question

Key trials & series

Izzedine et al. ALK-inhibitor renal-effects review
Pinard et al. real-world ALK-inhibitor AKI/CKD cohort (2025)

Clinical pearls

Crizotinib cysts can be mistaken for malignancy or progression - recognize them as a class-specific drug effect.
The creatinine bump is often pseudo-AKI from blocked tubular secretion; confirm true GFR with cystatin C before changing therapy.
Watch phosphate and potassium - ALK inhibitors can cause electrolyte wasting.

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

Class-level context for the major non-renal toxicities of the ALK/ROS1/MET TKI class.

Ophthalmic

Keratopathy, uveitis, retinopathy

Visual disturbance (crizotinib)

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Transaminitis

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

CNS effects (lorlatinib)

§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 · 2015–2025 · 1 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· 3

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 · LimitedBosniak Category III Renal Cysts Caused by Crizotinib in an Anaplastic Lymphoma Kinase Gene-Rearranged Non-Small Cell Lung Cancer Patient.Okubo K et al. · Urology 2018 · PMID 30142403Case report of complex Bosniak category III renal cysts arising during crizotinib treatment that regressed spontaneously after drug cessation.CaseC · LimitedRenal Injury during Long-Term Crizotinib Therapy.Yasuma T et al. · Int J Mol Sci 2018 · PMID 30257437Case report of ALK-positive NSCLC developing multiple renal cysts and renal dysfunction during crizotinib therapy, with mechanistic evidence of crizotinib-induced renal fibrosis.CaseC · LimitedRegression of Crizotinib-Associated Complex Cystic Lesions after Switching to Alectinib.Taima K et al. · Intern Med 2017 · PMID 28794366Case report of crizotinib-associated complex renal cyst with systemic inflammation that regressed after switching from crizotinib to alectinib.

Conference abstracts & journal reports· 1 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

AbstractCrizotinib-Induced Pseudo-AKI: A Case ReportASN Kidney Week 2019 2019 · Abstract SA-PO167Crizotinib (ALK TKI) raised serum creatinine by inhibiting tubular creatinine secretion while true GFR was preserved on Tc-99m-DTPA scintigraphy — a pseudo-AKI to recognize before stopping an effective therapy.

FDA label — boxed warning & renal dosing· renal impairment

Quoted verbatim from this agent's current FDA label (Jul 2025) — not paraphrased or interpreted. Full label on DailyMed .

Renal impairment — from the label

Increased exposure to crizotinib occurred in patients with pre-existing severe renal impairment (CL cr less than 30 mL/min calculated using the modified Cockcroft-Gault equation for adult patients and the Schwartz equation for pediatric patients) not requiring dialysis, therefore reduce dosage of XALKORI in these patients [see Dosage and Administration (2.8) , Clinical Pharmacology (12.3) ] . No dose adjustment is recommended in patients with mild to moderate renal impairment (CL cr 30 to 89 mL/min).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 12,638 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

Electrolyte Disturbancecorroborated · ROR 1.68 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Renal CystsNot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Pseudo-AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

SIADH / Hyponatremia

ROR 1.9095% CI 1.55–2.34· 92 reports

Electrolyte Disturbance

ROR 1.6895% CI 1.46–1.94· 192 reports

FAERS outcomes & reporting trend· 30% of reports w/ death · 24.3% w/ hospitalization

30%

Reported with a death outcome

3,792 of 12,638 reports

24.3%

Reported with hospitalization

3,067 of 12,638 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 12,638 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 1.0195% CI 0.83–1.24· 93 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Nausea1,118Diarrhoea846Vomiting795Constipation439

General / constitutional

Fatigue554Oedema Peripheral445Asthenia340Malaise313Peripheral Swelling294

Respiratory

Dyspnoea430Pleural Effusion309Cough249

Nervous system

Dizziness315Dysgeusia204

Eye

Visual Impairment403

Metabolic & electrolyte

Decreased Appetite380

Immune / infection

Pneumonia337

Skin

Rash208

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 Crizotinib 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

Ensartinib

Ensacove · ALK TKI

Profile

ALK TKI carrying the crizotinib-class renal signature: benign creatinine rise and possible renal cysts.

PSEUDORCYSTLYTE

Mild#1 · 97% phenotype match

Larotrectinib

Vitrakvi · TRK inhibitor

Profile

Mild creatinine rise; generally well tolerated.

PSEUDO

Mild#2 · 65% phenotype match

Entrectinib

Rozlytrek · TRK/ROS1 TKI

Profile

Creatinine rise via reduced tubular secretion.

PSEUDO

Mild#3 · 65% phenotype match

Repotrectinib

Augtyro · ROS1/TRK TKI

Profile

2023 ROS1 inhibitor; creatinine rise via secretion block.

PSEUDO

Mild#4 · 65% phenotype match

Taletrectinib

Ibtrozi · ROS1 TKI

Profile

Next-gen ROS1 TKI; benign transporter-mediated creatinine rise (pseudo-AKI), not true GFR loss.

PSEUDO

Mild#5 · 65% phenotype match

Capmatinib

Tabrecta · MET inhibitor

Profile

Reversible creatinine rise and edema.

PSEUDOPRE

Mild#6 · 64% phenotype match

Compare Crizotinib 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 ALK / ROS1 / MET / TRK 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 Crizotinib’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 Crizotinib; 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 35 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.