What kind of kidney injury does Ceritinib cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Pseudo-AKI.

How should kidney function be monitored during Ceritinib therapy?

Serum creatinine and volume status, especially during GI toxicity; Liver enzymes and fasting glucose (class effects).

How can kidney injury from Ceritinib be prevented?

Aggressive antiemetic and antidiarrheal management Maintain hydration and monitor volume status Take with food per current labeling to mitigate GI effects

Who is at higher risk of kidney injury from Ceritinib?

Severe GI toxicity (vomiting/diarrhea); Inadequate oral intake / dehydration; Diuretic use and pre-existing CKD; Older age.

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Printable monograph

ALK TKI

Ceritinib

Zykadia · CERI

ALK TKI · approved 2014 · 6 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 6 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 inhibitor whose substantial GI toxicity can drive prerenal acute kidney injury through volume depletion.

MildALK tyrosine kinase inhibitor

ALK-positive non-small-cell lung cancer

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Ceritinib causes frequent gastrointestinal toxicity (nausea, vomiting, diarrhea in the majority of patients), which can lead to volume depletion and prerenal AKI; as an ALK inhibitor it can also produce generally mild, reversible creatinine elevations. The prerenal AKI risk is largely a downstream effect of GI losses and is not precisely quantified.Source: Bonilla et al., Clin Kidney J 2022; Pinard et al., Clin Lung Cancer 2025

Onset & rechallenge

Time to injuryVariable / unpredictable

Prerenal AKI whenever GI toxicity causes significant fluid loss — often early in therapy.

Distilled from: “Prerenal AKI can occur whenever GI toxicity causes significant fluid loss, often early in therapy.”

§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.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Pseudo-AKISecondary10%PMID 40382267 (opens PubMed in a new tab)
Class-level ALK-TKI creatinine rise (~10% AKI by KDIGO within 90d, incl. ceritinib); mostly reversible tubular-secretion artifact

§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

The dominant renal mechanism is prerenal: GI fluid losses cause hypovolemia and reduced renal perfusion. Like other ALK inhibitors, ceritinib may also raise serum creatinine through reduced tubular secretion (a pseudo-AKI artifact). Structural intrinsic injury is uncommon.

Clinical presentation

Volume depletion with rising creatinine, low urine output, and a prerenal urine profile (high urine osmolality, low FeNa) in the setting of significant nausea, vomiting, or diarrhea; mild creatinine elevations otherwise. Hepatotoxicity and hyperglycemia are additional class effects.

Management

Treat GI toxicity and restore volume with fluids; prerenal AKI typically reverses with rehydration. Dose-reduce or interrupt for severe or persistent toxicity, and correct electrolyte disturbances. Distinguish true volume-depletion AKI from a secretion-mediated creatinine artifact.Lesion-level management framework

Risk factors

Severe GI toxicity (vomiting/diarrhea)
Inadequate oral intake / dehydration
Diuretic use and pre-existing CKD
Older age

Prevention

Aggressive antiemetic and antidiarrheal management
Maintain hydration and monitor volume status
Take with food per current labeling to mitigate GI effects

Anticancer mechanism· how it treats cancer

Potent ALK tyrosine kinase inhibitor (also targeting IGF-1R and ROS1) used in ALK-positive non-small-cell lung cancer, including after crizotinib.

Note · Renal injury is mainly GI-driven and prerenal; correcting volume status is the key intervention.

§04

Clinical depth

Renal dose adjustment

No starting-dose change for mild-to-moderate renal impairment (negligible renal excretion); severe-impairment/ESKD data are limited, so use clinical monitoring. The practical 'renal' adjustment is interruption/reduction when GI toxicity threatens volume status. Hepatic impairment requires dose reduction.

Dialyzability & ESKD dosing

Highly protein-bound (~97%) and hepatically metabolized; not expected to be dialyzed and no supplemental dosing established.

Differential diagnosis

Distinguish GI-driven prerenal AKI (volume responsive, prerenal indices) from the ALK-class secretion artifact (cystatin C-based eGFR preserved) and from intrinsic injury (uncommon).

Monitoring

Serum creatinine and volume status, especially during GI toxicity
Liver enzymes and fasting glucose (class effects)

Key trials & series

Bonilla et al. ALK-inhibitor renal review (class context)
Pinard et al. real-world ALK-inhibitor AKI/CKD cohort (includes ceritinib)

Clinical pearls

Ceritinib’s renal risk is mostly its GI toxicity - manage nausea/diarrhea and hydration to prevent prerenal AKI.
Taking ceritinib with food (current guidance) reduces GI toxicity and the associated volume losses.
Confirm whether a creatinine rise is true volume depletion or a tubular-secretion artifact before changing dose.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Injury signatures

Pseudo-AKI Prerenal / Hemodynamic AKI

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

Class-level context for the major non-renal toxicities of the ALK 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

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

Evidence accrual

6 references · 2015–2025 · 3 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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 2,378 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

Pseudo-AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

SIADH / Hyponatremia

ROR 2.8795% CI 1.95–4.22· 26 reports

Electrolyte Disturbance

ROR 2.5795% CI 1.97–3.36· 55 reports

FAERS outcomes & reporting trend· 23.2% of reports w/ death · 24.7% w/ hospitalization

23.2%

Reported with a death outcome

552 of 2,378 reports

24.7%

Reported with hospitalization

587 of 2,378 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 2,378 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 1.3395% CI 0.89–2.01· 23 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Diarrhoea426Nausea342Vomiting224Abdominal Pain99Constipation55

General / constitutional

Fatigue134Asthenia90Pyrexia71Weight Decreased59

Hepatobiliary

Alanine Aminotransferase Increased64Aspartate Aminotransferase Increased61Hepatic Function Abnormal61

Respiratory

Dyspnoea102Pleural Effusion54

Metabolic & electrolyte

Decreased Appetite117

Immune / infection

Pneumonia65

Nervous system

Headache61

Skin

Rash56

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 Ceritinib 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

Alectinib

Alecensa · ALK TKI

Profile

Creatinine rise via reduced tubular secretion.

PSEUDOPRE

Mild#1 · 100% phenotype match

Bosutinib

Bosulif · BCR-ABL TKI

Profile

Reversible eGFR decline.

PSEUDOPRE

Mild#2 · 89% phenotype match

Capmatinib

Tabrecta · MET inhibitor

Profile

Reversible creatinine rise and edema.

PSEUDOPRE

Mild#3 · 89% phenotype match

Tepotinib

Tepmetko · MET inhibitor

Profile

Creatinine rise and peripheral edema.

PSEUDOPRE

Mild#4 · 89% phenotype match

Momelotinib

Ojjaara · JAK/ACVR1 inhibitor

Profile

2023 myelofibrosis JAK inhibitor.

PSEUDOPRE

Mild#5 · 86% phenotype match

Vimseltinib

Romvimza · CSF1R tyrosine kinase inhibitor

Profile

A clean-kidney targeted TKI — watch the CPK, not the nephron.

PSEUDOPRE

Mild#6 · 86% phenotype match

Compare Ceritinib 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.