What kind of kidney injury does Selumetinib cause?

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

Is kidney injury from Selumetinib reversible?

Reversible. Typical onset: Variable; adverse events can appear after prolonged dosing..

How should kidney function be monitored during Selumetinib therapy?

Creatine phosphokinase at baseline and periodically, and with myalgia; Serum creatinine and electrolytes, especially during diarrhea/vomiting; LVEF (echocardiogram) and ophthalmologic assessment per label.

How can kidney injury from Selumetinib be prevented?

Maintain hydration, especially during GI toxicity Manage diarrhea/vomiting promptly

Who is at higher risk of kidney injury from Selumetinib?

Dehydration (pediatric, GI losses); Strenuous activity (CK); Pre-existing renal disease.

Back to explorer

Printable monograph

MEK inhibitor

Selumetinib

Koselugo · Selu

MEK inhibitor · approved 2020 · 6 citations

Recent· through 2023

Fairly sourced4/9 · 4 signals

Met: 6 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 2y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2023
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 pediatric MEK inhibitor for neurofibromatosis — kidney effects are modest and rarely limiting.

MildMEK inhibitor

Neurofibromatosis type 1 with inoperable plexiform neurofibromas (pediatric)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Long-term pediatric trial data (SPRINT, up to ~5 years) show a manageable safety profile with no new safety signals; significant nephrotoxicity is not prominent, with creatinine changes generally modest. CK elevation is a recognized MEK-class laboratory effect.Source: Gross et al., Neuro Oncol 2023

Onset & rechallenge

Time to injuryVariable / unpredictable

Timing is variable, with adverse events able to appear after prolonged dosing.

Distilled from: “Variable; adverse events can appear after prolonged dosing.”

§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.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

§03

Kidney injury

Mechanism of kidney injury

No characteristic intrinsic nephrotoxic mechanism; as a MEK inhibitor it can raise CK and (rarely) cause rhabdomyolysis, a potential indirect cause of pigment tubular injury. Modest creatinine changes are within class expectations and may partly reflect tubular-secretion inhibition. GI losses (diarrhea, vomiting) can produce prerenal azotemia in children.

Clinical presentation

Generally mild; possible modest creatinine change and asymptomatic CK elevation. Diarrhea, rash, paronychia, and (rarely) reduced ejection fraction dominate the pediatric toxicity profile; dehydration from GI losses is the most common pathway to AKI.

Management

Supportive care; hold for marked CK rise/rhabdomyolysis with IV fluids; replace volume and correct electrolytes during GI losses; dose-modify per protocol for grade 3 events.Lesion-level management framework

Risk factors

Dehydration (pediatric, GI losses)
Strenuous activity (CK)
Pre-existing renal disease

Prevention

Maintain hydration, especially during GI toxicity
Manage diarrhea/vomiting promptly

Anticancer mechanism· how it treats cancer

Selective MEK1/2 inhibitor that dampens MAPK signaling driven by NF1 loss; approved for children with neurofibromatosis type 1 and symptomatic inoperable plexiform neurofibromas.

§04

Clinical depth

Renal dose adjustment

Weight/BSA-based pediatric dosing; no specific renal adjustment established (renal-impairment data are limited in this young population). Hepatic impairment, not renal, carries label dose guidance.

Dialyzability & ESKD dosing

Highly protein-bound oral small molecule; dialyzability not characterized and not clinically relevant in this indication. No ESKD dosing data.

Differential diagnosis

In a child with rising creatinine, separate prerenal azotemia from GI volume losses (responds to fluids), MEK-related CK elevation/rhabdomyolysis (check CK), and a transporter-mediated creatinine artifact.

Monitoring

Creatine phosphokinase at baseline and periodically, and with myalgia
Serum creatinine and electrolytes, especially during diarrhea/vomiting
LVEF (echocardiogram) and ophthalmologic assessment per label

Key trials & series

SPRINT phase 1/2 (pediatric NF1 plexiform neurofibromas)
Gross 2023 long-term SPRINT safety update

Clinical pearls

In NF1, the commonest route to AKI is dehydration from diarrhea/vomiting — rehydrate early rather than reflexively stopping the drug.
Check CK with myalgia; asymptomatic CK elevation is a class effect.
Renal-specific data are thin; safety is largely extrapolated from pediatric NF1 trials where nephrotoxicity was not prominent.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

Beyond the kidney — non-renal toxicities· 4 organ systems

Class-level context for the major non-renal toxicities of the MEK inhibitor class.

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Rash, photosensitivity, squamous-cell carcinomas (BRAF)

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

Reduced LVEF (MEK)

Ophthalmic

Keratopathy, uveitis, retinopathy

Retinopathy / retinal vein occlusion (MEK)

Vascular

Hypertension, VTE/ATE, bleeding, aneurysm

Pyrexia syndrome, hypertension

§05

References

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

Evidence accrual

6 references · 2021–2023 · 6 since 2021

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 1,530 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· 1 signal

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

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Electrolyte DisturbanceNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

Crystal / Obstructive Nephropathy

ROR 3.9795% CI 2.42–6.49· 16 reports

FAERS outcomes & reporting trend· 6.5% of reports w/ death · 18.9% w/ hospitalization

6.5%

Reported with a death outcome

99 of 1,530 reports

18.9%

Reported with hospitalization

289 of 1,530 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 1,530 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 0.5495% CI 0.24–1.20· 6 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Skin

Rash128Dermatitis Acneiform76Alopecia64Pruritus39Dry Skin38

Gastrointestinal

Diarrhoea82Nausea77Vomiting60Abdominal Pain43Stomatitis29

General / constitutional

Fatigue72Pain45Asthenia29

Nervous system

Headache40

Immune / infection

Pneumonia35

Blood & lymphatic

Anaemia27

Cardiac

Ejection Fraction Decreased27

Metabolic & electrolyte

Decreased Appetite26

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 Selumetinib 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

Mirdametinib

Gomekli · MEK inhibitor

Profile

2025 NF1 MEK inhibitor; creatinine rise and edema.

PRELYTE

Mild#1 · 85% phenotype match

Daratumumab

Darzalex · Anti-CD38 antibody

Profile

Tumor lysis; usable in renal impairment.

PRELYTE

Mild#2 · 78% phenotype match

Isatuximab

Sarclisa · Anti-CD38 antibody

Profile

Tumor lysis in myeloma.

PRELYTE

Mild#3 · 78% phenotype match

Teniposide

Vumon · Podophyllotoxin (topo II)

Profile

Highly protein-bound, low renal clearance (~10-25% urinary); renal relevance is PK/exposure not direct injury; not dialyzable.

LYTEPRE

Mild#4 · 77% phenotype match

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#5 · 75% phenotype match

Quizartinib

Vanflyta · FLT3 inhibitor

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild#6 · 74% phenotype match

Compare Selumetinib 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 BRAF / MEK 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.