What kind of kidney injury does Alectinib cause?

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. Other reported patterns: Prerenal / Hemodynamic AKI.

How should kidney function be monitored during Alectinib therapy?

Serum creatinine periodically (interpret with secretion artifact); Cystatin C-based eGFR when true GFR matters (dosing of co-medications, trial eligibility); Edema and weight; Liver enzymes, CK (myalgia), bilirubin.

How can kidney injury from Alectinib be prevented?

Avoid unnecessary dose changes for isolated benign creatinine rises

Who is at higher risk of kidney injury from Alectinib?

Pre-existing chronic kidney disease; Hypertension and male sex (associated with AKI in ALK-inhibitor cohorts); Concurrent nephrotoxins.

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Printable monograph

ALK TKI

Alectinib

Alecensa · ALEC

ALK TKI · approved 2015 · 9 citations

Up to date· through 2026

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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 potent ALK inhibitor where creatinine rises largely reflect reduced tubular secretion rather than true kidney injury.

MildALK tyrosine kinase inhibitor

ALK-positive non-small-cell lung cancer

§01

Signature kidney injury

Signature lesion

Pseudo-AKI

Alectinib is associated with creatinine elevations that are usually benign. In a real-world five-agent ALK-inhibitor cohort (114 patients, 191 treatments; alectinib the most-used at 91), creatinine-based AKI/CKD events were frequent — 10% AKI within 90 days and 14% CKD at 1 year across the cohort, with no alectinib-specific rate reported — but mostly mild and reversible, with few treatment changes attributed to AKI and none requiring dialysis.Source: Pinard et al., Clin Lung Cancer 2025

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Creatinine rises within weeks of starting, with mean eGFR declining over the first 90 days and reversing after discontinuation.

Distilled from: “Creatinine rise within weeks of starting therapy (mean eGFR declines over the first 90 days); reverses after 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)
AKI by creatinine (KDIGO) within 90d in ~10% of ALK-TKI-treated NSCLC; mean eGFR dips then recovers off-drug — largely reduced tubular creatinine secretion, not true injury
Prerenal / Hemodynamic AKIRareno population incidence denominator
True intrinsic AKI (biopsy-proven ATN/AIN, anuric AKI needing dialysis) reported in <1% — case-level PMID 37021408 (opens PubMed in a new tab)

§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 creatinine rise is attributed largely to inhibition of renal tubular creatinine secretion (mediated by transporters such as MATE1/OCT2), so creatinine-based eGFR falls without a corresponding true decline in measured/cystatin C-based GFR. Edema and, rarely, electrolyte disturbances can occur; structural nephrotoxicity is uncommon.

Clinical presentation

Asymptomatic creatinine elevation with reduced creatinine-based eGFR; peripheral edema; cystatin C-based eGFR is typically discordant (higher) than creatinine-based eGFR, confirming preserved true filtration.

Management

Most creatinine elevations require no intervention and reverse on discontinuation; continue therapy when the change reflects reduced tubular secretion (the CROWN/ALEX-era data support this). Investigate and dose-adjust only for true AKI, and manage edema supportively.Lesion-level management framework

Risk factors

Pre-existing chronic kidney disease
Hypertension and male sex (associated with AKI in ALK-inhibitor cohorts)
Concurrent nephrotoxins

Prevention

Avoid unnecessary dose changes for isolated benign creatinine rises

Anticancer mechanism· how it treats cancer

Selective, CNS-penetrant ALK tyrosine kinase inhibitor with activity against several crizotinib-resistant mutations. Preferred first-line therapy for ALK-positive non-small-cell lung cancer.

Note · Apparent renal dysfunction is frequently a tubular-secretion artifact; true structural injury is uncommon.

§04

Clinical depth

Renal dose adjustment

No starting-dose change for mild-to-moderate renal impairment; data in severe impairment/ESKD are limited (alectinib is hepatically metabolized with <1% renal excretion), so no PK-based renal adjustment is mandated. Hepatic impairment requires dose reduction.

Dialyzability & ESKD dosing

Highly protein-bound (>99%) and hepatically cleared; not dialyzable and no supplemental dosing expected in ESKD.

Differential diagnosis

The key distinction is pseudo-AKI (creatinine up, cystatin C-based eGFR stable) versus true AKI. Discordant creatinine/cystatin C confirms a transporter artifact rather than nephron injury.

Monitoring

Serum creatinine periodically (interpret with secretion artifact)
Cystatin C-based eGFR when true GFR matters (dosing of co-medications, trial eligibility)
Edema and weight
Liver enzymes, CK (myalgia), bilirubin

Key trials & series

ALEX (phase 3 alectinib vs crizotinib, first-line ALK-positive NSCLC)
Pinard et al. real-world ALK-inhibitor AKI/CKD cohort (alectinib-predominant)

Clinical pearls

An isolated creatinine rise on alectinib is usually a tubular-secretion artifact - check cystatin C before changing therapy.
True structural injury is uncommon; most patients can continue alectinib despite the eGFR dip.

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. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

6 references · 2015–2025 · 2 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.

CaseB · ModerateAlectinib - induced acute renal failure.Prado-Mel E et al. · J Oncol Pharm Pract 2026 · PMID 37021408Biopsy-proven mixed acute interstitial nephritis and acute tubular necrosis causing acute renal failure 27 days after starting alectinib, resolving with corticosteroids and drug switch.CaseB · ModerateAcute kidney injury and long-term renal effects of alectinib in anaplastic lymphoma kinase-positive non-small cell lung carcinoma: a case report.van Londen M et al. · J Med Case Rep 2022 · PMID 36176005Biopsy-confirmed proximal tubular injury causing AKI 11 days after alectinib initiation, with recovery on cessation and tolerated reintroduction at reduced dose.CaseC · LimitedUnraveling the unforeseen: anuric acute kidney injury induced by alectinib.Tran VN et al. · Hosp Pract (1995) 2025 · PMID 3997727471-year-old woman developed anuric AKI (creatinine 1.0 to 3.64 mg/dL) requiring hemodialysis two months into alectinib, with renal recovery after discontinuation.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

No dose adjustment is recommended for patients with mild or moderate renal impairment. The safety of ALECENSA in patients with severe renal impairment (creatinine clearance less than 30 mL/min) or end-stage renal disease has not been studied [see Clinical Pharmacology (12.3) ].

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 7,249 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.
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 outcomes & reporting trend· 12.9% of reports w/ death · 17.7% w/ hospitalization

12.9%

Reported with a death outcome

935 of 7,249 reports

17.7%

Reported with hospitalization

1,280 of 7,249 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 10 systems · 7,249 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 0.4795% CI 0.32–0.70· 25 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

General / constitutional

Fatigue518Weight Increased208Asthenia192Peripheral Swelling178Pain162

Gastrointestinal

Constipation445Nausea161Diarrhoea149

Respiratory

Dyspnoea234Cough124

Musculoskeletal

Myalgia209Arthralgia111

Skin

Rash257

Immune / infection

Pneumonia142Covid-19105

Nervous system

Dizziness121Headache113

Blood & lymphatic

Anaemia119

Hepatobiliary

Blood Bilirubin Increased102

Cardiac

Bradycardia90

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 Alectinib 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

Ceritinib

Zykadia · ALK TKI

Profile

GI-driven prerenal AKI.

PREPSEUDO

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 Alectinib 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.