What kind of kidney injury does Vemurafenib cause?

Acute Tubular Necrosis — Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate. Other reported patterns: Fanconi Syndrome, Electrolyte Disturbance, Chronic Interstitial Nephropathy.

How should kidney function be monitored during Vemurafenib therapy?

Baseline and at least monthly serum creatinine/eGFR; Serum electrolytes each cycle — potassium, sodium, phosphate, magnesium (proximal tubular wasting); Urinalysis for glycosuria, phosphaturia, or proteinuria when tubulopathy/Fanconi is suspected; Volume status and symptoms of fever/diarrhea that precipitate prerenal injury; Reassess renal recovery after any dose hold before resuming.

How can kidney injury from Vemurafenib be prevented?

Maintain euvolemia; counsel on hydration and prompt reporting of fever, diarrhea, or poor intake Avoid stacking nephrotoxins (NSAIDs, contrast, high-dose diuretics/RAAS blockade) where possible Consider combination with a MEK inhibitor (cobimetinib), which lowers AKI incidence and severity while improving efficacy Hold or bridge dosing around intercurrent volume-depleting illness

Who is at higher risk of kidney injury from Vemurafenib?

Male sex (marked predominance in pharmacovigilance data); Volume depletion from drug-related fever, diarrhea, nausea, or reduced oral intake; Concomitant nephrotoxins (NSAIDs, RAAS inhibitors, diuretics, iodinated contrast); Higher drug exposure / prolonged therapy; Pre-existing CKD (worsens tolerance of any AKI, though the Teuma cohort paradoxically found better baseline GFR in those who developed AKI — pre-existing impairment is not a prerequisite).

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Printable monograph

BRAF inhibitor

Vemurafenib

Q: How common is kidney injury with Vemurafenib?

Approximately 59.5% — Clinically meaningful AKI is a recognized but variably quantified effect, and vemurafenib is the strongest renal offender of the BRAF/MEK class. Small serum-creatinine rises are common and usually low-grade; overt AKI produced the first case series of 8 patients with significant-to-severe renal insufficiency (Launay-Vacher, Cancer 2014) and 132 vemurafenib AKI reports to FDA FAERS over 3 years, far exceeding dabrafenib's 13 (Jhaveri, JAMA Oncol 2015). The monotherapy denominator comes from a retrospective single-center cohort of 74 patients with BRAF-V600-mutant metastatic melanoma, with creatinine measured before treatment, monthly on treatment and 3 months after stopping: 44 of 74 (59.5%) met the KDIGO threshold of a 1.5-fold creatinine rise, and 40 of those 44 (91%) were stage 1. Read that figure with its definition attached — it is creatinine-based, and BRAF/MEK inhibitors also blunt tubular creatinine secretion, so a share of any such cohort is pseudo-AKI rather than tubular injury; the authors biopsied two stage-1 patients to demonstrate real tissue damage. Men were over-represented among the AKI-positive patients (75% versus 40%). Adding a MEK inhibitor lowers it substantially: in the companion cobimetinib cohort 9 of 38 (24%) developed AKI, all within three months and mostly stage 1-2, about a 60% reduction versus monotherapy. (Source: Teuma et al., Cancer Chemother Pharmacol 2016 (PMID 27371224, monotherapy, 44/74); Teuma et al., Cancer Chemother Pharmacol 2017 (PMID 28396940, plus cobimetinib, 9/38); Jhaveri et al., JAMA Oncol 2015).

Q: Is kidney injury from Vemurafenib reversible?

Partially reversible. Typical onset: Early — most cases arise within the first weeks to three months of therapy (all AKI events in the Teuma cohort occurred in the first trimester of treatment); later onset is uncommon..

Q: Does Vemurafenib need a dose adjustment in kidney impairment?

No renal-based dose adjustment is specified for mild-to-moderate impairment. Because vemurafenib is hepatically metabolized (CYP3A4) and eliminated almost entirely in feces, with only ~1% renal excretion, exposure is not expected to change materially with reduced GFR, though data in severe impairment and ESKD are lacking. Dose modification is therefore driven by toxicity, not clearance: for drug-attributable AKI or intolerable toxicity, interrupt and, on recovery, resume at reduced dose (label steps 960 -> 720 -> 480 mg twice daily); permanently discontinue for recurrent severe events. Do not reduce below 480 mg twice daily.

Q: How is kidney injury from Vemurafenib managed?

Confirm the creatinine rise and screen for reversible contributors — volume depletion (very common with vemurafenib fever/diarrhea), other nephrotoxins, obstruction, and contrast. For drug-attributable AKI, hold vemurafenib, restore volume, and replete electrolytes (potassium, phosphate, sodium, magnesium). Most low-grade injury recovers with interruption; on recovery, resume at a reduced dose with close monitoring, and permanently discontinue for recurrent or severe injury. Adding a MEK inhibitor (cobimetinib) both improves outcomes and reduces AKI frequency/severity roughly 60% versus monotherapy (Teuma 2017). If biopsy shows acute interstitial nephritis, a corticosteroid course may be considered (limited evidence). Persistent, severe, or diagnostically unclear injury warrants nephrology referral and consideration of kidney biopsy.

Zelboraf · VEM

BRAF inhibitor · approved 2011 · 9 citations · FAERS AKI reporting ROR 2.09 (95% CI 1.80–2.42, 180 AKI reports)

Aging evidence· through 2021

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
Not met: Current through 2021
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.

The first-in-class BRAF inhibitor that transformed melanoma — and, nearly alone in its class, injures the proximal tubule.

ModerateFirst-in-class BRAF inhibitor (2011)

BRAF V600E mutation-positive unresectable or metastatic melanomaErdheim-Chester disease with BRAF V600 mutationOften combined with a MEK inhibitor (cobimetinib) to improve efficacy and reduce paradoxical/off-target toxicity

§01

Signature kidney injury

Signature lesion

Acute Tubular Necrosis

Representative incidence59.5%

Clinically meaningful AKI is a recognized but variably quantified effect, and vemurafenib is the strongest renal offender of the BRAF/MEK class. Small serum-creatinine rises are common and usually low-grade; overt AKI produced the first case series of 8 patients with significant-to-severe renal insufficiency (Launay-Vacher, Cancer 2014) and 132 vemurafenib AKI reports to FDA FAERS over 3 years, far exceeding dabrafenib's 13 (Jhaveri, JAMA Oncol 2015). The monotherapy denominator comes from a retrospective single-center cohort of 74 patients with BRAF-V600-mutant metastatic melanoma, with creatinine measured before treatment, monthly on treatment and 3 months after stopping: 44 of 74 (59.5%) met the KDIGO threshold of a 1.5-fold creatinine rise, and 40 of those 44 (91%) were stage 1. Read that figure with its definition attached — it is creatinine-based, and BRAF/MEK inhibitors also blunt tubular creatinine secretion, so a share of any such cohort is pseudo-AKI rather than tubular injury; the authors biopsied two stage-1 patients to demonstrate real tissue damage. Men were over-represented among the AKI-positive patients (75% versus 40%). Adding a MEK inhibitor lowers it substantially: in the companion cobimetinib cohort 9 of 38 (24%) developed AKI, all within three months and mostly stage 1-2, about a 60% reduction versus monotherapy.Source: Teuma et al., Cancer Chemother Pharmacol 2016 (PMID 27371224, monotherapy, 44/74); Teuma et al., Cancer Chemother Pharmacol 2017 (PMID 28396940, plus cobimetinib, 9/38); Jhaveri et al., JAMA Oncol 2015

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Most AKI arises within the first weeks to three months of therapy; later onset is uncommon.

Distilled from: “Early — most cases arise within the first weeks to three months of therapy (all AKI events in the Teuma cohort occurred in the first trimester of treatment); later onset is uncommon.” · PMID 28396940 (opens PubMed in a new tab)

§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.

Acute Tubular Necrosis#1 · Signaturequalitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Fanconi SyndromeSecondaryqualitative — no citable incidence
Global failure of proximal tubule reabsorption — glucosuria, phosphaturia and acidosis, classically from ifosfamide.
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).
Chronic Interstitial NephropathySecondaryqualitative — no citable incidence
Slow, cumulative tubulointerstitial scarring — fibrosis, tubular atrophy and glomerulosclerosis with no discrete acute phase. The nitrosourea (carmustine/lomustine) lesion and delayed radioligand (radiation) nephropathy; often irreversible and detected only as a creeping creatinine months to years later.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

59.5%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence9 citations

Nephron map

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

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

Interstitium

Acute Tubular Necrosis

Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

§03

Kidney injury

Deep diveBRAF/MEK-inhibitor tubular injuryVemurafenib was built to block a mutated melanoma kinase, but in the kidney its damage is off-target: it injures the proximal tubule and can produce a Fanconi picture, usually early and usually mild — and, paradoxically, pairing it with a MEK inhibitor makes it gentler on the kidney, not harsher.

Mechanism of kidney injury

Predominantly direct, off-target (MAPK-independent) proximal tubular epithelial toxicity. In human cell work, vemurafenib reduced viability and increased cell death in proximal renal tubular epithelial cells (RPTEC) and glomerular epithelial cells (podocytes) at 10 microM — below its steady-state blood Cmax (~115 microM) — while sparing glomerular endothelial cells, and its intrinsic cytotoxicity exceeded that of dabrafenib, cobimetinib, and trametinib (Sanagawa 2021). This tubular injury manifests histologically as acute tubular injury/necrosis, with proximal tubular dysfunction (Fanconi-type glycosuria, phosphaturia, low-molecular-weight proteinuria) and electrolyte wasting in some cases; a tubulointerstitial/interstitial-nephritis component has also been described on the limited biopsy literature (Jhaveri 2015). Concurrent volume depletion from drug-related fever, diarrhea, and reduced intake frequently adds a prerenal/ischemic hit on top of the intrinsic tubular toxicity.

Clinical presentation

Usually an asymptomatic rise in serum creatinine detected on routine labs, often accompanied by electrolyte abnormalities — hypokalemia, hyponatremia, and hypophosphatemia are reported. Proximal tubulopathy (glycosuria with normal glucose, phosphaturia, aminoaciduria, LMW proteinuria) points to Fanconi-type injury. Most episodes are low-grade (CTCAE/KDIGO stage 1-2), but severe AKI requiring drug interruption and, rarely, dialysis has occurred, and some patients are left with persistent CKD. A striking, unexplained male predominance was seen in FAERS (85 men vs 47 women; p<.001).

Management

Confirm the creatinine rise and screen for reversible contributors — volume depletion (very common with vemurafenib fever/diarrhea), other nephrotoxins, obstruction, and contrast. For drug-attributable AKI, hold vemurafenib, restore volume, and replete electrolytes (potassium, phosphate, sodium, magnesium). Most low-grade injury recovers with interruption; on recovery, resume at a reduced dose with close monitoring, and permanently discontinue for recurrent or severe injury. Adding a MEK inhibitor (cobimetinib) both improves outcomes and reduces AKI frequency/severity roughly 60% versus monotherapy (Teuma 2017). If biopsy shows acute interstitial nephritis, a corticosteroid course may be considered (limited evidence). Persistent, severe, or diagnostically unclear injury warrants nephrology referral and consideration of kidney biopsy.Lesion-level management framework

Risk factors

Male sex (marked predominance in pharmacovigilance data)
Volume depletion from drug-related fever, diarrhea, nausea, or reduced oral intake
Concomitant nephrotoxins (NSAIDs, RAAS inhibitors, diuretics, iodinated contrast)
Higher drug exposure / prolonged therapy
Pre-existing CKD (worsens tolerance of any AKI, though the Teuma cohort paradoxically found better baseline GFR in those who developed AKI — pre-existing impairment is not a prerequisite)

Prevention

Maintain euvolemia; counsel on hydration and prompt reporting of fever, diarrhea, or poor intake
Avoid stacking nephrotoxins (NSAIDs, contrast, high-dose diuretics/RAAS blockade) where possible
Consider combination with a MEK inhibitor (cobimetinib), which lowers AKI incidence and severity while improving efficacy
Hold or bridge dosing around intercurrent volume-depleting illness

Anticancer mechanism· how it treats cancer

Oral small-molecule, ATP-competitive inhibitor of mutated BRAF kinase (V600E/V600K). By shutting down constitutively active RAF-MEK-ERK (MAPK) signaling in BRAF V600-mutant melanoma cells, it drives cell-cycle arrest and apoptosis. In BRAF wild-type cells it paradoxically activates ERK through CRAF, the mechanistic basis for its cutaneous squamous proliferations (and part of the rationale for co-administering a downstream MEK inhibitor).

Note · Nephrotoxicity was not recognized in the pivotal registrational program and emerged only through post-marketing case series and FAERS pharmacovigilance. Much of the incidence evidence is combination (vemurafenib+cobimetinib) or spontaneous-report data, so quantitative estimates should be read as directional rather than precise.

§04

Clinical depth

Renal dose adjustment

No renal-based dose adjustment is specified for mild-to-moderate impairment. Because vemurafenib is hepatically metabolized (CYP3A4) and eliminated almost entirely in feces, with only ~1% renal excretion, exposure is not expected to change materially with reduced GFR, though data in severe impairment and ESKD are lacking. Dose modification is therefore driven by toxicity, not clearance: for drug-attributable AKI or intolerable toxicity, interrupt and, on recovery, resume at reduced dose (label steps 960 -> 720 -> 480 mg twice daily); permanently discontinue for recurrent severe events. Do not reduce below 480 mg twice daily.

Dialyzability & ESKD dosing

Not meaningfully dialyzable. Vemurafenib is >99% protein-bound, highly lipophilic, and eliminated predominantly in feces (~94%) with renal excretion near 1%; hemodialysis is not expected to remove appreciable drug and no post-dialysis supplemental dose is indicated. Dedicated dialysis pharmacokinetic data are lacking.

Differential diagnosis

Separate direct vemurafenib tubular toxicity/ATN from (1) prerenal azotemia due to the drug's fever, diarrhea, and anorexia (low FeNa, responds to volume — often coexists); (2) acute interstitial nephritis (sterile pyuria, eosinophiluria, rash/fever/eosinophilia, sometimes from a concomitant drug); (3) other nephrotoxins and iodinated contrast; and (4) melanoma-related obstruction or renal infiltration. Early onset (first trimester), proximal tubular electrolyte wasting (hypokalemia, hypophosphatemia, glycosuria), and the characteristic male predominance favor vemurafenib tubular toxicity; a lower renal signal with dabrafenib supports an agent-specific effect rather than a pure MAPK-pathway class effect.

Monitoring

Baseline and at least monthly serum creatinine/eGFR
Serum electrolytes each cycle — potassium, sodium, phosphate, magnesium (proximal tubular wasting)
Urinalysis for glycosuria, phosphaturia, or proteinuria when tubulopathy/Fanconi is suspected
Volume status and symptoms of fever/diarrhea that precipitate prerenal injury
Reassess renal recovery after any dose hold before resuming

Key trials & series

BRIM-3 (Chapman, NEJM 2011): phase 3 registrational trial vs dacarbazine establishing survival benefit; renal toxicity was not flagged in the pivotal safety profile, and the nephrotoxicity signal emerged post-marketing
Jhaveri (JAMA Oncol 2015): FAERS pharmacovigilance analysis defining the class signal — 132 vemurafenib AKI reports vs 13 for dabrafenib, with male predominance
Teuma (Cancer Chemother Pharmacol 2017): single-center cohort showing 24% AKI on vemurafenib+cobimetinib and ~60% AKI reduction from adding the MEK inhibitor
Sanagawa (Anticancer Drugs 2021): real-world FAERS ROR plus human-cell work localizing direct cytotoxicity to proximal tubular and glomerular epithelial cells

Clinical pearls

Vemurafenib is the outlier of the BRAF/MEK class for kidney injury — FAERS AKI ROR ~3.3 vs ~1.35 for dabrafenib (Sanagawa 2021; Jhaveri 2015). If a BRAF inhibitor is needed and kidney risk is a concern, dabrafenib carries a substantially lower renal signal.
Adding a MEK inhibitor (cobimetinib) is not just about efficacy: it cut AKI incidence roughly 60% versus vemurafenib monotherapy (Teuma 2017).
Injury is early and usually low-grade and reversible on hold, but severe episodes can leave persistent CKD — don't dismiss a creatinine bump in the first three months.
Renal excretion is trivial (~1%), so there is no pharmacokinetic reason to renally dose-adjust — dose modification is driven by the toxicity itself.
Electrolyte wasting (hypokalemia, hyponatremia, hypophosphatemia) and glycosuria are clues that the proximal tubule, not the glomerulus, is the target.
The unexplained male predominance of vemurafenib AKI is a genuine, reproducible pharmacovigilance finding, not a sampling artifact.

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

Class-level context for the major non-renal toxicities of braf inhibitors.

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

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 · 2011–2021 · 1 since 2019

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· 2

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 · LimitedFanconi syndrome induced by vemurafenib: a new renal adverse event.Denis D et al. · JAMA Dermatol 2015 · PMID 25494458Proximal tubular Fanconi syndrome (glycosuria, phosphaturia, aminoaciduria) attributed to the BRAF inhibitor vemurafenib — a distinct tubular renal adverse event.CaseC · LimitedAcute kidney injury in patients with severe rash on vemurafenib treatment.Regnier-Rosencher E et al. · Br J Dermatol 2013 · PMID 23909652Acute kidney injury co-occurring with severe cutaneous reaction during vemurafenib therapy, documenting the BRAF inhibitor as the implicated agent.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

No formal clinical study has been conducted to evaluate the effect of renal impairment on the pharmacokinetics of vemurafenib. No dose adjustment is recommended for patients with mild and moderate renal impairment based on a population pharmacokinetic analysis [see Clinical Pharmacology (12.3) ]. The appropriate dose of ZELBORAF has not been established in patients with severe renal impairment.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 11,949 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· 3 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 2026-08-21.

What reporting says about this profile's documented lesions

Electrolyte Disturbancecorroborated · ROR 1.65 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Acute Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.
Fanconi SyndromeNo 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.
Chronic Interstitial NephropathyNot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Glomerular Injury / Proteinuria

ROR 1.7595% CI 1.22–2.52· 29 reports

Electrolyte Disturbance

ROR 1.6595% CI 1.43–1.92· 179 reports

SIADH / Hyponatremia

ROR 1.6495% CI 1.31–2.06· 75 reports

FAERS outcomes & reporting trend· 17.3% of reports w/ death · 28.4% w/ hospitalization

17.3%

Reported with a death outcome

2,073 of 11,949 reports

28.4%

Reported with hospitalization

3,397 of 11,949 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 11,949 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 2026-08-08.

Disproportionality (acute kidney injury):ROR 2.0995% CI 1.80–2.42· 180 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Skin

Rash1,547Alopecia561Photosensitivity Reaction414Pruritus389Erythema312

General / constitutional

Fatigue1,033Pyrexia742Asthenia348

Gastrointestinal

Diarrhoea825Nausea811Vomiting474

Musculoskeletal

Arthralgia1,039Myalgia355

Metabolic & electrolyte

Decreased Appetite532

Nervous system

Headache338

Blood & lymphatic

Anaemia231

Respiratory

Dyspnoea220

Guidelines & consensus· 12

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 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 Vemurafenib 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

Fotemustine

Muphoran · Nitrosourea (alkylating)

Profile

Class delayed cumulative tubulointerstitial/ATN; usually mild; acute signal often really cisplatin.

CINATNLYTE

Moderate#1 · 75% phenotype match

Nimustine (ACNU)

Nidran · Nitrosourea (alkylating)

Profile

Water-soluble nitrosourea; renal risk inferred at class level; cumulative delayed tubulointerstitial injury; DLT is myelosuppression.

CINATNLYTE

Moderate#2 · 74% phenotype match

BRAF / MEK inhibitors (vemurafenib · dabrafenib · trametinib)

BRAF/MEK inhibitor

Profile

Tubulointerstitial AKI; vemurafenib strongest.

ATNAINLYTE

Mild#3 · 69% phenotype match

Pemetrexed

Alimta · Antifolate

Profile

Cumulative chronic tubulointerstitial injury; RTA and nephrogenic DI.

CINATNLYTE

Moderate#4 · 68% phenotype match

Lutetium-177 PSMA-617 (vipivotide)

Pluvicto · Radioligand therapy (PSMA)

Profile

PSMA-targeted radioligand for prostate cancer; renal radiation exposure and xerostomia.

CINLYTE

Moderate#5 · 64% phenotype match

Trastuzumab deruxtecan

Enhertu · Antibody-drug conjugate (HER2/DXd)

Profile

Emerging AKI/proteinuria reports — under-published.

ATNFANCLYTE

Moderate#6 · 64% phenotype match

Compare Vemurafenib 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.

Who studies this

The leading contributors to Vemurafenib’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 Vemurafenib.

Ranked by publication volume and citation impact (NIH iCite) on this agent’s renal literature — bibliometric context, not an endorsement or a measure of clinical authority.