What kind of kidney injury does Dabrafenib cause?

Acute Interstitial Nephritis — Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors. Other reported patterns: Prerenal / Hemodynamic AKI, Electrolyte Disturbance, SIADH / Hyponatremia, Acute Tubular Necrosis.

Is kidney injury from Dabrafenib reversible?

Reversible. Typical onset: Variable and biphasic. Pyrexia-associated AKI clusters early, in the first weeks to months of therapy and coincides with febrile episodes. Biopsy-proven granulomatous/acute interstitial nephritis has appeared anywhere from a few weeks to as late as ~5 years into treatment..

How should kidney function be monitored during Dabrafenib therapy?

Serum creatinine and eGFR at baseline and periodically, and during any febrile episode; Electrolytes — sodium, potassium, phosphate, and magnesium; Temperature/pyrexia surveillance (the febrile syndrome is the leading trigger for AKI); Urinalysis when creatinine rises — sterile pyuria, WBC casts, and low-grade proteinuria suggest interstitial nephritis; Liver enzymes (transaminitis accompanies the febrile syndrome and pre-existing liver disease predicts AKI).

How can kidney injury from Dabrafenib be prevented?

Recognize the pyrexia syndrome early — interrupt dabrafenib (per label at temperature >=38.5 C), hydrate, and give antipyretics before AKI develops Maintain volume during febrile episodes and GI losses; avoid unnecessary nephrotoxins/NSAIDs and iodinated contrast when febrile Correct volume depletion promptly and review concomitant nephrotoxic or ADH-active medications

Who is at higher risk of kidney injury from Dabrafenib?

Pre-existing liver disease (the only significant baseline predictor of AKI in the largest cohort); Drug-induced pyrexia/febrile syndrome (fever, chills, GI losses, transaminitis) with volume depletion; Combination with trametinib (pyrexia and febrile-syndrome AKI are more frequent with the doublet); Prior or concurrent immune-checkpoint-inhibitor therapy (adds interstitial and glomerular injury risk; confounds attribution); Volume depletion from GI toxicity, diuretics, RAAS blockade, or intercurrent nephrotoxins/NSAIDs; Male sex (FAERS reports skew male, though this likely reflects melanoma epidemiology).

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Printable monograph

BRAF inhibitor

Dabrafenib

Tafinlar · DAB

BRAF inhibitor · approved 2013 · 9 citations · FAERS AKI reporting ROR 1.50 (95% CI 1.32–1.72, 228 AKI reports)

Aging evidence· through 2022

Fairly sourced5/9 · 5 signals

Met: 9 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 8y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2022
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 gentler BRAF inhibitor — mostly pyrexia-driven, reversible AKI, with granulomatous interstitial nephritis as its rare histologic signature.

MildTargeted therapy (2010s BRAF/MEK)

BRAF V600E/K-mutant unresectable or metastatic melanoma (with trametinib)Adjuvant treatment of resected stage III BRAF V600E/K-mutant melanoma (with trametinib)BRAF V600E-mutant metastatic non-small cell lung cancer (with trametinib)BRAF V600E anaplastic thyroid cancer (with trametinib)BRAF V600E-mutant unresectable/metastatic solid tumors, tumor-agnostic (with trametinib)Pediatric BRAF V600E low-grade glioma (with trametinib)

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Signature kidney injury

Signature lesion

Acute Interstitial Nephritis

Representative incidence21%

AKI is relatively common on dabrafenib-based therapy but usually mild and reversible. In the largest cohort, 42/199 (21%) of patients on dabrafenib/trametinib developed AKI within 12 months, and roughly 24% of those episodes occurred during the drug-induced febrile (pyrexia) syndrome (Seethapathy 2022). Pharmacovigilance places dabrafenib well below vemurafenib: FAERS acute-kidney-injury reporting-odds-ratio approximately 1.35 (95% CI 1.15–1.60) for dabrafenib versus approximately 3.28 for vemurafenib (Sanagawa 2021). Biopsy-proven granulomatous/acute interstitial nephritis and clinically significant electrolyte disorders (hyponatremia, hypokalemia, hypophosphatemia) are each individually rare — documented mainly in case reports and small FAERS counts. Registrational trials did not flag renal toxicity; the signal emerged post-marketing.Source: Seethapathy et al., Nephrol Dial Transplant 2022 (PMID 33355659): 42/199 (21%) of dabrafenib/trametinib patients developed AKI within 12 months in a single-center retrospective cohort, with ~24% of AKI episodes occurring during the drug-induced pyrexia/febrile syndrome. This is all-cause AKI on combination therapy and largely mild/reversible; drug-specific granulomatous interstitial nephritis is far rarer.

Onset & rechallenge

Time to injuryVariable / unpredictable

AKI most often coincides with the dabrafenib/trametinib febrile syndrome (fever, chills, GI symptoms, transaminitis), clustering in the first weeks to months; a single biopsy-proven granulomatous acute interstitial nephritis case is documented. The cited cohort defined AKI within a 12-month window, so it does not establish later onset.

Distilled from: “Forty-two patients (21%) experienced AKI within 12 months; 10 patients (5% of the total cohort, 24% of AKI patients) experienced AKI occurring during a dabrafenib/trametinib-induced febrile syndrome characterized by fever, chills, gastrointestinal symptoms and elevated liver enzymes. One patient had biopsy-proven granulomatous acute interstitial nephritis that resolved with corticosteroids.” · PMID 33355659 (opens PubMed in a new tab)

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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 Interstitial Nephritis#1 · Signaturequalitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
Prerenal / Hemodynamic AKISecondaryqualitative — 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).
SIADH / HyponatremiaSecondaryqualitative — no citable incidence
Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

21%incidence

SeverityMild

ReversibilityReversible

Evidence9 citations

Nephron map

Proximal Tubule

Distal Tubule / Collecting Duct

InterstitiumSupporting tissue around the tubules

Acute Interstitial Nephritis

Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

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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

Two dominant routes, both indirect. (1) Pre-renal/hemodynamic: dabrafenib — especially combined with trametinib — provokes a systemic pyrexia/febrile syndrome (fever, chills, rigors, GI losses, transaminitis) that causes volume depletion and hemodynamic AKI, sometimes progressing to ischemic tubular injury; about one in four AKI episodes in the largest cohort occurred during this febrile syndrome. (2) Immunoallergic tubulointerstitial: biopsy-proven acute — often granulomatous — interstitial nephritis, at times with concurrent granulomatous dermatitis, implying a T-cell/hypersensitivity mechanism rather than direct nephrotoxicity. Unlike vemurafenib, dabrafenib shows little direct proximal-tubular or glomerular-epithelial cytotoxicity in vitro, consistent with its lower FAERS AKI signal. Electrolyte wasting (hyponatremia including an SIADH-like pattern, hypokalemia, hypophosphatemia) reflects disturbed tubular handling. Rare glomerular lesions have been reported but are confounded by concomitant immune-checkpoint-inhibitor exposure.

Clinical presentation

Most often an asymptomatic serum creatinine rise found on surveillance labs. When tied to the pyrexia syndrome, patients have fever, chills, rigors, GI symptoms, and transaminitis accompanying the creatinine rise. Interstitial nephritis cases may show sterile pyuria, low-grade proteinuria/microalbuminuria, peripheral edema, and sometimes a concurrent granulomatous skin rash; the classic AIN triad (fever/rash/eosinophilia) is usually incomplete. Electrolyte abnormalities — low sodium, potassium, or phosphate — can be the presenting clue.

Management

Pyrexia-associated AKI: hold dabrafenib (and usually trametinib), give IV/oral fluids and antipyretics, and resume at the same or a reduced dose once fever and creatinine recover; corticosteroids are used for recurrent/refractory pyrexia. Suspected interstitial nephritis: discontinue the drug, refer to nephrology, and consider kidney biopsy if AKI is persistent or unexplained — biopsy-proven granulomatous/acute interstitial nephritis is treated with corticosteroids (e.g., prednisone ~1 mg/kg with a slow taper) and is generally steroid-responsive, though relapse on premature taper is described. Electrolytes: replete potassium, phosphate, and magnesium; evaluate hyponatremia for SIADH versus volume depletion and treat by cause. Rechallenge is often feasible after pyrexia-driven AKI resolves, but should be avoided after biopsy-proven granulomatous interstitial nephritis.Lesion-level management framework

Risk factors

Pre-existing liver disease (the only significant baseline predictor of AKI in the largest cohort)
Drug-induced pyrexia/febrile syndrome (fever, chills, GI losses, transaminitis) with volume depletion
Combination with trametinib (pyrexia and febrile-syndrome AKI are more frequent with the doublet)
Prior or concurrent immune-checkpoint-inhibitor therapy (adds interstitial and glomerular injury risk; confounds attribution)
Volume depletion from GI toxicity, diuretics, RAAS blockade, or intercurrent nephrotoxins/NSAIDs
Male sex (FAERS reports skew male, though this likely reflects melanoma epidemiology)

Prevention

Recognize the pyrexia syndrome early — interrupt dabrafenib (per label at temperature >=38.5 C), hydrate, and give antipyretics before AKI develops
Maintain volume during febrile episodes and GI losses; avoid unnecessary nephrotoxins/NSAIDs and iodinated contrast when febrile
Correct volume depletion promptly and review concomitant nephrotoxic or ADH-active medications

Anticancer mechanism· how it treats cancer

Selective ATP-competitive inhibitor of mutant BRAF V600E/K kinase that shuts down constitutive RAF–MEK–ERK (MAPK) signaling driving BRAF-mutant tumor proliferation. Almost always paired with the MEK inhibitor trametinib to deepen and prolong response and blunt paradoxical MAPK reactivation (fewer cutaneous squamous lesions than single-agent BRAF inhibition).

Note · Dabrafenib is almost always given with trametinib, so much of the renal data reflects the combination and all-cause AKI in melanoma patients rather than a pure single-agent, drug-attributable effect. Reported incidence should be read as combination, real-world, largely mild and reversible AKI.

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Clinical depth

Renal dose adjustment

No dedicated renal dose adjustment is specified in the FDA label. Dabrafenib is cleared predominantly by hepatobiliary metabolism (CYP2C8/CYP3A4) and fecal excretion with a minority renal route, so no adjustment is recommended for mild-to-moderate renal impairment. It has not been formally studied in severe renal impairment or ESRD — use with caution and monitor. In practice, dose interruptions/reductions are driven by pyrexia, transaminitis, and other toxicities rather than by eGFR.

Dialyzability & ESKD dosing

Not expected to be removed by dialysis and not established as dialyzable. Dabrafenib is highly protein-bound (~99.7%) with a large volume of distribution and hepatic metabolism, so hemodialysis is unlikely to clear meaningful drug; no data support supplemental dosing around dialysis.

Differential diagnosis

Distinguish pyrexia/febrile-syndrome pre-renal azotemia and volume depletion (most common, fully reversible with fluids and drug hold) from intrinsic drug-induced granulomatous/acute interstitial nephritis (biopsy-confirmed, steroid-responsive). Consider concomitant or sequenced immune-checkpoint-inhibitor nephritis or glomerulonephritis — a rare atypical anti-GBM glomerulonephritis has been reported in a patient on MAPK plus checkpoint inhibitors (Kyriazis 2021), so glomerular presentations are confounded. Exclude other nephrotoxins (NSAIDs, contrast, PPIs), sepsis, and tumor-related causes (obstruction, hypercalcemia). If therapy was switched from vemurafenib, note vemurafenib carries a higher intrinsic tubular-toxicity signal.

Monitoring

Serum creatinine and eGFR at baseline and periodically, and during any febrile episode
Electrolytes — sodium, potassium, phosphate, and magnesium
Temperature/pyrexia surveillance (the febrile syndrome is the leading trigger for AKI)
Urinalysis when creatinine rises — sterile pyuria, WBC casts, and low-grade proteinuria suggest interstitial nephritis
Liver enzymes (transaminitis accompanies the febrile syndrome and pre-existing liver disease predicts AKI)

Key trials & series

COMBI-v (Robert et al., N Engl J Med 2014; PMID 25399551): dabrafenib plus trametinib improved overall survival versus vemurafenib in BRAF V600 metastatic melanoma; renal toxicity was not flagged in the pivotal data.
5-year outcomes of dabrafenib plus trametinib in metastatic melanoma (Robert et al., N Engl J Med 2019; PMID 31166680): durable long-term benefit of the doublet.
COMBI-AD (Long et al., N Engl J Med 2017; PMID 28891408): adjuvant dabrafenib plus trametinib in resected stage III BRAF-mutant melanoma.

Clinical pearls

Dabrafenib is the 'kinder-to-kidney' BRAF inhibitor: FAERS AKI reporting-odds-ratio is ~1.35 versus ~3.28 for vemurafenib, and in vitro it lacks vemurafenib's direct tubular cytotoxicity.
Most AKI on dabrafenib/trametinib is pyrexia-driven and pre-renal — think fever plus volume depletion and hold/hydrate before reaching for a biopsy.
The one true histologic signature is granulomatous/acute interstitial nephritis, sometimes paired with a granulomatous dermatitis; it is steroid-responsive but relapses if steroids are tapered too quickly.
Check electrolytes — hyponatremia (including an SIADH-like pattern), hypokalemia, and hypophosphatemia are reported.
Pre-existing liver disease was the only baseline predictor of AKI in the largest cohort — flag these patients for closer monitoring.
Renal signals were essentially absent in the registrational trials and emerged from post-marketing case reports and FAERS, so incidence figures should be hedged accordingly.

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

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

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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 · 2014–2022 · 4 since 2020

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.

CaseB · ModerateDabrafenib- and trametinib-associated glomerular toxicity: A case report.Jo E et al. · Medicine (Baltimore) 2022 · PMID 35029901An 80-year-old woman on dabrafenib/trametinib for melanoma developed progressive renal failure (Cr 1.59 to 5.46 mg/dL); serial biopsies showed glomerular endothelial damage then FSGS and tubulointerstitial fibrosis, progressing to dialysis.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 20,946 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 2026-10-01.

What reporting says about this profile's documented lesions

Acute Interstitial Nephritiscorroborated · ROR 2.9
SIADH / Hyponatremiacorroborated · ROR 2.43 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Electrolyte Disturbancecorroborated · ROR 1.71 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
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.

Acute Interstitial Nephritis

ROR 2.9095% CI 2.22–3.79· 54 reports

SIADH / Hyponatremia

ROR 2.4395% CI 2.11–2.80· 194 reports

Electrolyte Disturbance

ROR 1.7195% CI 1.53–1.91· 324 reports

FAERS outcomes & reporting trend· 21% of reports w/ death · 27.9% w/ hospitalization

21%

Reported with a death outcome

4,394 of 20,946 reports

27.9%

Reported with hospitalization

5,837 of 20,946 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 20,946 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 1.5095% CI 1.32–1.72· 228 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

General / constitutional

Pyrexia4,104Fatigue1,428Chills1,332Asthenia727Malaise623

Gastrointestinal

Nausea1,403Vomiting986Diarrhoea974

Skin

Rash1,174

Nervous system

Headache742Dizziness383

Metabolic & electrolyte

Decreased Appetite585Dehydration348

Respiratory

Dyspnoea411Cough357

Musculoskeletal

Arthralgia579

Eye

Visual Impairment536

Immune / infection

Pneumonia350

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 Dabrafenib 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

BRAF / MEK inhibitors (vemurafenib · dabrafenib · trametinib)

BRAF/MEK inhibitor

Profile

Tubulointerstitial AKI; vemurafenib strongest.

ATNAINLYTE

Mild#1 · 63% phenotype match

Cobimetinib

Cotellic · MEK inhibitor

Profile

Real-world AKI signal with BRAF partners.

ATNAIN

Mild#2 · 61% phenotype match

Encorafenib

Braftovi · BRAF inhibitor

Profile

Class tubular signal; usually mild.

ATNAIN

Mild#3 · 61% phenotype match

Avutometinib

Avmapki (co-packaged with defactinib as Avmapki Fakzynja) · RAF/MEK inhibitor

Profile

RAF/MEK clamp; CK elevation/rhabdomyolysis and tubular electrolyte wasting.

LYTEATNPRE

Moderate#4 · 60% phenotype match

Retifanlimab

Zynyz · PD-1 immune checkpoint inhibitor

Profile

PD-1 blockade — kidney injury is immune-mediated interstitial nephritis, not direct tubular toxicity.

AINLYTEPRE

Moderate#5 · 56% phenotype match

Sunvozertinib

Zegfrovy · EGFR exon20 TKI

Profile

2025 EGFR exon20 TKI; renal magnesium wasting (SIADH-pattern hyponatremia possible).

LYTESIADHPRE

Mild#6 · 53% phenotype match

Compare Dabrafenib 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 Dabrafenib’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 Dabrafenib; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 22 clinical records among all 27 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.