How should kidney function be monitored during Brigatinib therapy?

Serum creatinine periodically (interpret with secretion artifact); Electrolytes and CK/lipase per labeling; Pulmonary symptoms early in therapy.

How can kidney injury from Brigatinib be prevented?

Recognize secretion-mediated creatinine rises and consider cystatin C if true GFR is in question Use the recommended step-up dosing to mitigate early pulmonary events

Who is at higher risk of kidney injury from Brigatinib?

Pre-existing chronic kidney disease; Hypertension; Concurrent nephrotoxins.

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Printable monograph

ALK TKI

Brigatinib

Alunbrig · BRIG

ALK TKI · approved 2017 · 9 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 9 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.

A next-generation ALK inhibitor with usually benign creatinine elevations as its main renal footprint.

MildALK tyrosine kinase inhibitor

ALK-positive non-small-cell lung cancer

§01

Signature kidney injury

Signature lesion

Pseudo-AKI

As an ALK inhibitor, brigatinib is associated with creatinine elevations that are generally benign. In a real-world ALK-inhibitor cohort, creatinine-based AKI/CKD events occurred but were mostly mild and reversible across agents including brigatinib; class reviews note elevated creatinine, occasional edema, and rare electrolyte disturbances. A distinct, early-onset pulmonary event (within the first week) is a separate non-renal class concern.Source: Pinard et al., Clin Lung Cancer 2025

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Creatinine changes typically emerge within weeks and tend to reverse on discontinuation.

Distilled from: “Creatinine changes typically emerge within weeks and tend to reverse on discontinuation.”

§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.

Pseudo-AKI#1 · Signature10%PMID 40382267 (opens PubMed in a new tab)
Class-level: ~10% AKI by creatinine (KDIGO) within 90d across ALK-TKIs (incl. brigatinib); mostly reversible reduction in tubular creatinine secretion, recovers off-drug
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
HypertensionRarequalitative — no citable incidence
Drug-specific hypertension in ALK-TKI network meta-analysis, not a class effect.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence9 citations

Nephron map

Glomerulus

Vasculature / Endothelium

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

Pseudo-AKI

The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.

§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

Creatinine elevation is thought to reflect, at least in part, reduced tubular creatinine secretion (transporter inhibition) rather than true GFR loss, consistent with the ALK-inhibitor class. Peripheral edema and rare electrolyte disorders may occur; structural nephrotoxicity is uncommon.

Clinical presentation

Asymptomatic creatinine rise with reduced creatinine-based eGFR; occasional edema or mild electrolyte abnormalities; overt AKI is uncommon. Watch for early pulmonary symptoms (non-renal) in the first days of therapy.

Management

Most creatinine elevations are benign and need no specific therapy; reserve dose adjustment for true AKI. Manage edema and electrolytes supportively.Lesion-level management framework

Risk factors

Pre-existing chronic kidney disease
Hypertension
Concurrent nephrotoxins

Prevention

Recognize secretion-mediated creatinine rises and consider cystatin C if true GFR is in question
Use the recommended step-up dosing to mitigate early pulmonary events

Anticancer mechanism· how it treats cancer

Potent next-generation ALK tyrosine kinase inhibitor with activity against many resistance mutations and CNS disease; also inhibits ROS1 and EGFR variants. Used in ALK-positive non-small-cell lung cancer.

Note · Creatinine elevation is usually benign; renal data are partly extrapolated from ALK-inhibitor class experience.

§04

Clinical depth

Renal dose adjustment

Reduce the dose for severe renal impairment (eGFR <30 mL/min/1.73 m2) - e.g., decrease the maintenance dose by ~50% per labeling. No adjustment is needed for mild-to-moderate impairment. Hepatic impairment also warrants reduction.

Dialyzability & ESKD dosing

Highly protein-bound (~91%) and hepatically metabolized; not expected to be meaningfully dialyzed. ESKD data are limited - monitor clinically.

Differential diagnosis

As with other ALK inhibitors, distinguish pseudo-AKI (creatinine up, cystatin C-based eGFR preserved) from true AKI; reserve workup and dose change for genuine GFR loss.

Monitoring

Serum creatinine periodically (interpret with secretion artifact)
Electrolytes and CK/lipase per labeling
Pulmonary symptoms early in therapy

Key trials & series

Pinard et al. real-world ALK-inhibitor AKI/CKD cohort (includes brigatinib)

Clinical pearls

Brigatinib creatinine rises are usually benign secretion artifacts - confirm with cystatin C before acting.
Reduce the dose when eGFR <30; mild-to-moderate impairment needs no change.
The early pulmonary event in the first week is the more clinically urgent class concern, not the kidney.
Hypertension is a brigatinib-specific toxicity in network meta-analysis of ALK-TKI trials - not a class effect shared by alectinib or crizotinib.

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

8 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

8 references · 2015–2025 · 5 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· 1

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 · LimitedFatal Tumour Lysis Syndrome Induced by Brigatinib in a Lung Adenocarcinoma Patient Treated With Sequential ALK Inhibitors: A Case Report.Wang Y et al. · Front Pharmacol 2021 · PMID 34987411Case report of brigatinib-induced tumour lysis syndrome with oliguria and acute kidney injury in an ALK-positive lung adenocarcinoma patient.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Reduce the dose of ALUNBRIG for patients with severe renal impairment. ( 2.7 , 8.7 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 3,630 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

Hypertensioncorroborated · ROR 3.02 — on the terms that name the lesion (ROR 2.44)
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.

Hypertension

ROR 3.0295% CI 2.61–3.49· 194 reports

Hemorrhagic Cystitis

ROR 1.5995% CI 1.01–2.49· 19 reports

FAERS outcomes & reporting trend· 21.7% of reports w/ death · 27.4% w/ hospitalization

21.7%

Reported with a death outcome

786 of 3,630 reports

27.4%

Reported with hospitalization

995 of 3,630 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 3,630 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 0.6895% CI 0.43–1.08· 18 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Diarrhoea253Nausea232Vomiting129

General / constitutional

Fatigue216Asthenia94Malaise88Pain81

Respiratory

Dyspnoea131Cough117Pleural Effusion77

Vascular

Blood Pressure Increased104Hypertension92

Nervous system

Headache110Dizziness77

Skin

Rash125

Metabolic & electrolyte

Decreased Appetite120

Immune / infection

Pneumonia85

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 Brigatinib 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

Pralsetinib

Gavreto · RET inhibitor

Profile

Hypertension; rare AKI.

HTNPREPSEUDO

Mild#1 · 89% phenotype match

Alectinib

Alecensa · ALK TKI

Profile

Creatinine rise via reduced tubular secretion.

PSEUDOPRE

Mild#2 · 84% phenotype match

Ceritinib

Zykadia · ALK TKI

Profile

GI-driven prerenal AKI.

PREPSEUDO

Mild#3 · 84% phenotype match

Lorlatinib

Lorbrena · ALK TKI

Profile

Edema and metabolic effects.

PSEUDOPREGLOM

Mild#4 · 76% phenotype match

Bosutinib

Bosulif · BCR-ABL TKI

Profile

Reversible eGFR decline.

PSEUDOPRE

Mild#5 · 73% phenotype match

Niraparib

Zejula · PARP inhibitor

Profile

Hypertension and creatinine rise.

HTNPSEUDO

Mild#6 · 73% phenotype match

Compare Brigatinib 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.