Is kidney injury from Regorafenib reversible?

Reversible. Typical onset: Within the first weeks of therapy..

How should kidney function be monitored during Regorafenib therapy?

Blood pressure weekly for the first cycle, then regularly; Urine protein (dipstick/UPCR) before each cycle; Liver enzymes/bilirubin (boxed hepatotoxicity warning) and serum creatinine.

How can kidney injury from Regorafenib be prevented?

Blood pressure control before and during therapy

Who is at higher risk of kidney injury from Regorafenib?

Pre-existing hypertension; Baseline proteinuria or CKD.

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Printable monograph

VEGFR TKI

Regorafenib

Stivarga · Rego

VEGFR TKI · approved 2012 · 10 citations

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 10 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 12y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

An oral multikinase inhibitor that delivers the familiar antiangiogenic toll of hypertension and proteinuria.

ModerateVEGFR multikinase inhibitor

Metastatic colorectal cancerGastrointestinal stromal tumorHepatocellular carcinoma

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence36.8%

29.8–43.8% 95% CI

Hypertension is common and frequently grade 3. Pooling 3,813 patients across the cardiovascular-event literature puts all-grade hypertension at 36.8% (95% CI 29.8-43.8%) and high-grade at 9.9% (7.4-12.4%), against controls a relative risk of 4.10 all-grade and 5.82 high-grade. An earlier, smaller meta-analysis of 1,069 patients from five trials (750 on regorafenib) ran higher at 44.4% (30.8-59.0%) all-grade and 12.5% (5.2-27.1%) high-grade, with wider intervals; the CORRECT trial itself reported about 28% (grade 3 ~7%). Proteinuria also occurs as a VEGF-pathway class effect, but is not separately quantified for this agent.Source: Chen et al., Medicine (Baltimore) 2018 (PMID 30313066); Wang et al., Eur J Clin Pharmacol 2014 (PMID 24150533); Grothey et al., CORRECT (Lancet 2013)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Within the first weeks of therapy.

Distilled from: “Within the first weeks of therapy.”

§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.

Hypertension#1 · Signature44.4%PMID 24150533 (opens PubMed in a new tab)
All-grade hypertension 44.4% (95% CI 30.8-59.0), high-grade 12.5%, in a meta-analysis of 5 trials (n=1,069); RR 3.76 vs control. The signature VEGF-pathway toxicity.
Glomerular Injury / ProteinuriaSecondaryqualitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

36.8%incidence

SeverityModerate

ReversibilityReversible

Evidence10 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Hypertension

Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.

§03

Kidney injury

Mechanism of kidney injury

VEGFR tyrosine kinase inhibition lowers glomerular VEGF and nitric-oxide signaling, raising vascular tone (hypertension) and injuring the glomerular filtration barrier (proteinuria), with potential for a podocytopathy (FSGS/MCD pattern) and, less commonly, renal TMA.

Clinical presentation

New or worsening hypertension and proteinuria, typically within the first weeks; creatinine may rise in more severe cases. Hand-foot skin reaction and transaminitis commonly co-occur and help flag class toxicity.

Management

Antihypertensive therapy (ACE inhibitor/ARB favored); interrupt or dose-reduce per label for grade 3 hypertension or significant proteinuria; discontinue for nephrotic syndrome, hypertensive crisis or TMA. Effects generally improve with dose modification or withdrawal.Lesion-level management framework

§ Receptor target map

Which kinases Regorafenib blocks — and where the blockade reaches the kidney

8targeted

VEGFR2 is the target with documented renal consequences across every VEGFR TKI; multi-kinase breadth beyond it (PDGFR-β, FGFR, and off-target receptor kinases) adds further renal and hypertensive liability. Select a lit receptor for its renal consequence.

VEGFR family

PDGFR

PDGFR-α

Other receptor kinases

FGFRMETEGFRFLT3AXLCSF1R

VEGFR2 · renal target

Glomerular endothelial VEGFR2: loss of podocyte-derived paracrine VEGF signaling → fenestrae loss, nephrin downregulation, nitric-oxide depletion → hypertension, proteinuria, and thrombotic microangiopathy.

renal consequence (2)targetednot a target

Risk factors

Pre-existing hypertension
Baseline proteinuria or CKD

Prevention

Blood pressure control before and during therapy

Anticancer mechanism· how it treats cancer

Oral multikinase inhibitor (a fluorinated sorafenib analog) targeting VEGFR1-3, TIE2, KIT, RET, RAF-1, BRAF and PDGFR, simultaneously inhibiting angiogenic, stromal and oncogenic signaling. Used in metastatic colorectal cancer, gastrointestinal stromal tumor and hepatocellular carcinoma.

Note · Renal effects mirror the VEGF-pathway class; quantitative renal data specific to regorafenib are limited and largely extrapolated from the class and from trial adverse-event tables.

§04

Clinical depth

Renal dose adjustment

No dose adjustment for renal impairment is recommended; regorafenib is hepatically metabolized (CYP3A4 and UGT1A9) with biliary excretion, so it carries hepatotoxicity warnings rather than renal dosing rules.

Dialyzability & ESKD dosing

Highly protein-bound (~99.5%) and hepatically/biliary cleared; not appreciably dialyzable, so no supplemental dosing for HD. Data in ESKD are limited.

Differential diagnosis

VEGFR-TKI hypertension/proteinuria/podocytopathy versus prerenal AKI versus baseline nephropathy. Within the colorectal-cancer setting, also consider overlapping toxicity from concurrent or prior antiangiogenic therapy (bevacizumab/aflibercept).

Monitoring

Blood pressure weekly for the first cycle, then regularly
Urine protein (dipstick/UPCR) before each cycle
Liver enzymes/bilirubin (boxed hepatotoxicity warning) and serum creatinine

Key trials & series

CORRECT phase III (regorafenib in refractory metastatic colorectal cancer) — hypertension a leading AE
GRID (GIST) and RESORCE (HCC) — hypertension/proteinuria safety signals

Clinical pearls

Regorafenib's renal toxicity is a class effect; expect early hypertension and watch urine protein.
Its boxed warning is hepatotoxicity — liver monitoring is as important as renal monitoring.
No renal dose adjustment is needed, but grade 3 hypertension or heavy proteinuria should trigger interruption/dose reduction.

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

Class-level context for the major non-renal toxicities of the VEGFR TKI class.

Vascular

Hypertension, VTE/ATE, bleeding, aneurysm

Hypertension, arterial/venous thrombosis, bleeding, impaired wound healing

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

LV dysfunction; QT (some TKIs)

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Diarrhea, perforation/fistula

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Hand-foot skin reaction

§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 · 2013–2021 · 3 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· 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.

CaseA · StrongClinicopathological analysis of anti-VEGF drug-associated renal thrombotic microangiopathy: A case series and review of the literature.Han Q et al. · Pathol Res Pract 2025 · PMID 39879682Biopsy-proven renal thrombotic microangiopathy case series including a previously unreported patient treated with bevacizumab plus regorafenib presenting with proteinuria, hypertension, and declining renal function.CaseB · ModerateRegorafenib-induced renal-limited thrombotic microangiopathy: a case report and review of literatures.Yin Q et al. · BMC Nephrol 2022 · PMID 35305559Biopsy-confirmed renal-limited thrombotic microangiopathy with nephrotic-range proteinuria in a patient on regorafenib for metastatic colon cancer, reported as the first such case.CaseC · LimitedLupus-Like Glomerulonephritis Associated With Regorafenib, a Multikinase Inhibitor.Strasma A et al. · Kidney Med 2021 · PMID 33851126Drug-induced lupus-like (class IV) endocapillary proliferative glomerulonephritis with acute kidney injury, proteinuria, and hematuria months after starting regorafenib, improving after drug withdrawal and corticosteroids.

FDA label — boxed warning & renal dosing· boxed warning · renal impairment

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

Boxed warning

WARNING: HEPATOTOXICITY • Severe and sometimes fatal hepatotoxicity has occurred in clinical trials [see Warnings and Precautions ( 5.1 )] . • Monitor hepatic function prior to and during treatment [see Warnings and Precautions ( 5.1 )]. • Interrupt and then reduce or discontinue STIVARGA for hepatotoxicity as manifested by elevated liver function tests or hepatocellular necrosis, depending upon severity and persistence [see Dosage and Administration ( 2.2 )] . WARNING: HEPATOTOXICITY See full prescribing information for complete boxed warning. • Severe and sometimes fatal hepatotoxicity has occurred in clinical trials. ( 5.1 ) • Monitor hepatic function prior to and during treatment. ( 5.1 ) • Interrupt and then reduce or discontinue STIVARGA for hepatotoxicity as manifested by elevated liver function tests or hepatocellular necrosis, depending upon severity and persistence. ( 2.2 )

Renal impairment — from the label

No dose adjustment is recommended for patients with renal impairment. The pharmacokinetics of regorafenib have not been studied in patients who are on dialysis and there is no recommended dose for this patient population [see Clinical Pharmacology ( 12.3 )] . 8.8 Race Based on pooled data from three placebo-controlled trials (CORRECT, GRID and CONCUR), a higher incidence of HFSR and liver function test abnormalities occurred in Asian patients treated with STIVARGA as compared with Whites [see Warnings and Precautions ( 5.1 , 5.5 )] . No starting dose adjustment is necessary based on race.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 11,542 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· 6 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

Glomerular Injury / Proteinuriacorroborated · ROR 7.2 — on the terms that name the lesion (ROR 4.93)
Hypertensioncorroborated · ROR 5.92 — on the terms that name the lesion (ROR 6.15)

Glomerular Injury / Proteinuria

ROR 7.2095% CI 5.99–8.67· 114 reports

Hypertension

ROR 5.9295% CI 5.57–6.30· 1,150 reports

SIADH / Hyponatremia

ROR 2.2295% CI 1.82–2.71· 98 reports

Electrolyte Disturbance

ROR 2.0095% CI 1.74–2.29· 208 reports

Hemorrhagic Cystitis

ROR 1.4295% CI 1.08–1.85· 54 reports

Crystal / Obstructive Nephropathy

ROR 1.3795% CI 1.01–1.86· 42 reports

FAERS outcomes & reporting trend· 20.5% of reports w/ death · 35% w/ hospitalization

20.5%

Reported with a death outcome

2,363 of 11,542 reports

35%

Reported with hospitalization

4,042 of 11,542 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 11,542 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 1.1795% CI 0.96–1.43· 98 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

General / constitutional

Fatigue1,769Asthenia946Pyrexia752Weight Decreased636Pain539

Gastrointestinal

Diarrhoea1,418Nausea815Vomiting570Abdominal Pain481Constipation427

Skin

Palmar-Plantar Erythrodysaesthesia Syndrome1,439Rash556Blister455

Metabolic & electrolyte

Decreased Appetite1,091Dehydration458

Respiratory

Dysphonia821Dyspnoea468

Vascular

Hypertension695Blood Pressure Increased456

Nervous system

Neuropathy Peripheral504Headache431

Musculoskeletal

Pain In Extremity774

Guidelines & consensus· 17

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.

KDIGOManagement of Blood Pressure in Patients With Chronic Kidney Disease Not Receiving Dialysis: Synopsis of the 2021 KDIGO Clinical Practice GuidelineAnn Intern Med 2021 · PMID 34152826Recommends standardized office BP measurement and a target systolic BP <120 mm Hg for most CKD patients, with RAAS inhibitors first-line when albuminuria is present — the BP-management basis for anti-VEGF/TKI-induced hypertension and proteinuria.ESC2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)Eur Heart J 2022 · PMID 36017568For VEGF/VEGFR inhibitors, perform baseline cardiovascular risk assessment, monitor blood pressure (weekly during the first cycle, then regularly) and treat to a target <140/90 mmHg with ACE inhibitors/ARBs and dihydropyridine calcium-channel blockers; manage VEGFi-associated hypertension and proteinuria with interruption/dose modification when severe.ESCEuropean Society of Cardiology quality indicators for the prevention and management of cancer therapy-related cardiovascular toxicity in cancer treatmentEur Heart J Qual Care Clin Outcomes 2022 · PMID 36316010Adherence quality indicators require documented baseline cardiovascular risk assessment and structured monitoring of cardiovascular complications (including hypertension) during cancer therapy such as VEGF-pathway inhibitors.UK Consensus PanelUsing bevacizumab to treat metastatic cancer: UK consensus guidelinesBr J Hosp Med (Lond) 2010 · PMID 21135762Assess and monitor blood pressure and proteinuria during bevacizumab therapy; treat emergent hypertension to standard targets and interrupt/discontinue the drug for uncontrolled hypertension, nephrotic-range proteinuria or other severe vascular toxicity.

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 Regorafenib 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

Cabozantinib

Cabometyx · VEGFR/MET TKI

Profile

Hypertension and proteinuria; nephrotic case reports.

HTNGLOM

Moderate#1 · 100% phenotype match

Lenvatinib

Lenvima · VEGFR TKI

Profile

Highest-ranked TKI for hypertension; proteinuria.

HTNGLOM

Moderate#2 · 100% phenotype match

Tivozanib

Fotivda · VEGFR TKI

Profile

Hypertension and proteinuria in RCC.

HTNGLOM

Moderate#3 · 100% phenotype match

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate#4 · 84% phenotype match

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#5 · 84% phenotype match

Ramucirumab

Cyramza · Anti-VEGFR2 antibody

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#6 · 84% phenotype match

Compare Regorafenib 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 Anti-angiogenic (VEGF)

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 Regorafenib’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 Regorafenib; 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 23 clinical records among all 33 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.