How should kidney function be monitored during Lenvatinib therapy?

Blood pressure weekly for the first 1-2 months, then with each visit (home BP encouraged); Urine protein (dipstick/UPCR) before each cycle; quantify if >=2+.

How can kidney injury from Lenvatinib be prevented?

Pre-emptive optimization of blood pressure control (target well-controlled BP before starting)

Who is at higher risk of kidney injury from Lenvatinib?

Pre-existing hypertension; Baseline proteinuria or CKD; Diabetes.

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Printable monograph

VEGFR TKI

Lenvatinib

Lenvima · Lenva

VEGFR TKI · approved 2015 · 13 citations · FAERS AKI reporting ROR 2.22 (95% CI 2.04–2.42, 521 AKI reports)

Up to date· through 2026

Fairly sourced6/9 · 6 signals

Met: 13 citations
Met: 12+ references
Not met: Accrued over 10+ years (span: 8y)
Not met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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 multi-target VEGFR TKI ranked among the most hypertensive, frequently spilling protein into the urine.

ModerateVEGFR multikinase inhibitor

Differentiated thyroid cancerHepatocellular carcinomaRenal cell carcinoma (with everolimus or pembrolizumab)Endometrial carcinoma (with pembrolizumab)

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence68%

Hypertension is among the most common adverse events; in the SELECT thyroid-cancer trial hypertension occurred in about 68% (grade >=3 ~42%) and proteinuria in roughly 31%. In KEYNOTE-B61 (lenvatinib plus pembrolizumab) grade 3-4 hypertension occurred in ~23%. Proteinuria is a frequent renal AE with lenvatinib.Source: Schlumberger et al. (SELECT, NEJM 2015) — ~68% any-grade hypertension (grade >=3 ~42%) with single-agent lenvatinib; Albiges et al. (KEYNOTE-B61, Lancet Oncol 2023) — ~23% grade 3-4 hypertension with the pembrolizumab combination

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Hypertension early, proteinuria over the first weeks of therapy.

Distilled from: “Within the first weeks of therapy (hypertension early; proteinuria over weeks).”

§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 · Signature70%PMID 35538636 (opens PubMed in a new tab)
Meta-analysis (2483 pts): cumulative all-grade HTN 70%, high-grade (>=3) 34%; RR vs comparators 2.61 all-grade / 3.35 high-grade
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
VEGFR-TKI meta-analysis (9446 pts, 20 RCTs): lenvatinib significantly raises all-grade (pooled RR 2.35) and high-grade (RR 3.70) proteinuria; podocyte injury / VEGF-inhibition glomerulopathy, highest-risk agent of the class PMID 32105149 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

68%incidence

SeverityModerate

ReversibilityReversible

Evidence13 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

Deep diveVEGF-inhibitor thrombotic microangiopathyStarve a tumor of its blood supply and you also cut the survival signal podocytes whisper to the glomerular endothelium next door — the capillary tuft answers with thrombi, protein spilling into the urine, and a blood pressure that will not come down.

Mechanism of kidney injury

VEGFR tyrosine kinase inhibition reduces glomerular endothelial VEGF signaling and nitric-oxide-mediated vasodilation, raising blood pressure and injuring podocytes and glomerular endothelium. Unlike ligand-trapping antibodies, receptor-blocking TKIs preferentially produce podocytopathies — minimal change disease and focal segmental glomerulosclerosis (biopsy-proven with lenvatinib) — driven in part by podocyte c-mip overexpression and dysregulation, in addition to proteinuria and occasional TMA.

Clinical presentation

New or worsening hypertension (often within days to weeks) and proteinuria; occasionally nephrotic-range proteinuria with edema, hypoalbuminemia and a creatinine rise. Biopsy may show FSGS/MCD-like podocytopathy.

Management

Antihypertensive therapy (ACE inhibitor/ARB favored for concurrent proteinuria); interrupt or dose-reduce per label for grade 3 hypertension or significant proteinuria (>=2 g/24 h) and discontinue for nephrotic syndrome or life-threatening hypertension. Switching to a less nephrotoxic VEGFR-TKI (e.g., sorafenib) has improved lenvatinib-induced nephrotic syndrome while preserving disease control in reported cases. Effects usually improve with dose modification or withdrawal, though FSGS can leave residual CKD.Lesion-level management framework

§ Receptor target map

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

7targeted

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-β

Other receptor kinases

METEGFRFLT3AXLCSF1RTIE2RAF-1/BRAF

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 (3)targetednot a target

Risk factors

Pre-existing hypertension
Baseline proteinuria or CKD
Diabetes

Prevention

Pre-emptive optimization of blood pressure control (target well-controlled BP before starting)

Anticancer mechanism· how it treats cancer

Oral multikinase inhibitor of VEGFR1-3, FGFR1-4, PDGFR-alpha, RET and KIT (with a distinctive type V binding mode), suppressing tumor angiogenesis and proliferation. Used in differentiated thyroid cancer, hepatocellular carcinoma, and renal cell and endometrial carcinoma (the latter two with pembrolizumab).

Note · Lenvatinib is consistently ranked among the most hypertensive TKIs.

§04

Clinical depth

Renal dose adjustment

Reduce the starting dose for severe renal impairment (CrCl < 30 mL/min) per label (e.g., a lower mg starting dose in thyroid/RCC indications); no adjustment for mild-moderate impairment. Lenvatinib is mainly hepatically metabolized (CYP3A and aldehyde oxidase), so hepatic impairment also drives dose reduction.

Dialyzability & ESKD dosing

Highly protein-bound (~98-99%) and hepatically cleared, so it is not appreciably removed by hemodialysis; dosing in ESKD follows the severe-renal-impairment reduction with toxicity-guided titration.

Differential diagnosis

VEGFR-TKI podocytopathy (MCD/FSGS, heavy proteinuria, hypertension) versus anti-VEGF-antibody TMA versus prerenal AKI versus diabetic/hypertensive nephropathy at baseline. Biopsy distinguishes the FSGS/MCD pattern; the temporal link to drug initiation and accompanying hypertension support attribution.

Monitoring

Blood pressure weekly for the first 1-2 months, then with each visit (home BP encouraged)
Urine protein (dipstick/UPCR) before each cycle; quantify if >=2+

Key trials & series

SELECT phase III in radioiodine-refractory differentiated thyroid cancer (hypertension ~68%, proteinuria ~31%)
KEYNOTE-B61 lenvatinib + pembrolizumab in non-clear-cell RCC (grade 3-4 hypertension ~23%)
REFLECT phase III in hepatocellular carcinoma (hypertension a leading AE)

Clinical pearls

Lenvatinib is a top-tier cause of TKI hypertension — have an antihypertensive plan before the first dose.
Its glomerular lesion is typically a podocytopathy (FSGS/MCD), which can leave residual CKD even after stopping.
Switching to sorafenib is a documented strategy to keep treating the cancer while improving lenvatinib-induced nephrotic syndrome.

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

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 · 2018–2026 · 2 since 2024

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· 5

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 · ModerateLenvatinib-associated hyaline occlusive glomerular microangiopathy.Daher A et al. · Clin Kidney J 2026 · PMID 42017032Biopsy-proven hyaline occlusive glomerular microangiopathy from lenvatinib (VEGFR2 inhibition) with extended follow-up; therapeutic modification led to reversible nephrotoxicity. Published in a dedicated nephrology venue.CaseB · ModerateCase report: Nephrotic syndrome induced by Lenvatinib treatment in a patient with von Hippel-Lindau syndrome.Zhang S et al. · BMC Nephrol 2025 · PMID 40634834Lenvatinib-induced nephrotic syndrome in a VHL patient; renal biopsy showed thrombotic microangiopathy with an FSGS-like pattern. Adds a podocyte/endothelial injury phenotype to the lenvatinib profile.CaseB · ModerateThrombotic Microangiopathy, Podocytopathy, and Damage to the Renal Tubules with Severe Proteinuria and Acute Renal Dysfunction Induced by Lenvatinib.Nakashima S et al. · Intern Med 2022 · PMID 35342129Biopsy-proven case of lenvatinib-induced renal thrombotic microangiopathy with podocytopathy, tubular damage, severe proteinuria, and acute kidney injury.CaseC · LimitedThrombotic microangiopathy associated with lenvatinib therapy.Contreras Angulo M et al. · Endocr Oncol 2023 · PMID 37434645Case report of lenvatinib-associated thrombotic microangiopathy with systemic (not solely renal) involvement, extending the recognized renal TMA risk of VEGF-pathway inhibitors.CaseC · LimitedNephrotic Syndrome Induced by Lenvatinib Treatment for Hepatocellular Carcinoma.Prasoppokakorn T et al. · Case Reports Hepatol 2022 · PMID 36106338Case report of lenvatinib-induced nephrotic-range proteinuria/nephrotic syndrome in a patient treated for hepatocellular carcinoma.

Conference abstracts & journal reports· 2 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

AbstractDelayed Presentation of Primary Podocytopathy and MPGN Pattern of Injury Secondary to Pembrolizumab and Lenvatinib UseASN Kidney Week 2025 2025 · Abstract PUB306After four years of pembrolizumab + lenvatinib, biopsy-proven diffuse podocytopathy with FSGS and an MPGN pattern (double-contoured basement membranes, hyaline microthrombi) presenting as nephrotic syndrome; complete remission on drug withdrawal plus steroids, underscoring that VEGFR-TKI/ICI glomerular injury can be delayed.AbstractAtypical Presentation of Drug-Induced Thrombotic Microangiopathy: Time Does Not MatterVeguilla Rivera NI, Dhamelia AK, Rosaly Martinez JP, Narayanankutty NP · ASN Kidney Week 2024 2024 · Abstract SA-PO223A hepatocellular-carcinoma patient on lenvatinib plus bevacizumab developed nephrotic-range proteinuria and AKI (creatinine 1.5 → 4 mg/dL); biopsy showed chronic thrombotic microangiopathy with FSGS — reinforcing the anti-angiogenic (VEGF-blockade) glomerular/TMA injury of the VEGFR-TKI class and that it can surface after prolonged exposure.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

No dose adjustment is recommended for patients with mild (CLcr 60-89 mL/min) or moderate (CLcr 30-59 mL/min) renal impairment. Lenvatinib concentrations may increase in patients with DTC, RCC, or endometrial carcinoma and severe (CLcr 15-29 mL/min) renal impairment. Reduce the dose of LENVIMA for patients with RCC, DTC, or endometrial carcinoma and severe renal impairment [see Dosage and Administration ( 2.7 )] . There is no recommended dose of LENVIMA for patients with HCC and severe renal impairment. LENVIMA has not been studied in patients with end stage renal disease [ see Warnings and Precautions ( 5.5 ) , Clinical Pharmacology ( 12.3 ) ] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 32,614 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 28.21 — on the terms that name the lesion (ROR 8.44)
Hypertensioncorroborated · ROR 12.08 — on the terms that name the lesion (ROR 12.4)

Glomerular Injury / Proteinuria

ROR 28.2195% CI 26.58–29.93· 1,183 reports

Hypertension

ROR 12.0895% CI 11.75–12.43· 5,948 reports

SIADH / Hyponatremia

ROR 4.3595% CI 3.99–4.74· 535 reports

Electrolyte Disturbance

ROR 3.0595% CI 2.85–3.26· 887 reports

Thrombotic Microangiopathy

ROR 1.8395% CI 1.36–2.46· 44 reports

Hemorrhagic Cystitis

ROR 1.6695% CI 1.43–1.92· 178 reports

FAERS outcomes & reporting trend· 13.6% of reports w/ death · 60.5% w/ hospitalization

13.6%

Reported with a death outcome

4,443 of 32,614 reports

60.5%

Reported with hospitalization

19,735 of 32,614 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 12 systems · 32,614 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. Showing the top 10 of 12 classified systems; 2 lower-ranked systems are not drawn. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 2.2295% CI 2.04–2.42· 521 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Proteinuria1,053

Gastrointestinal

Diarrhoea4,133Nausea2,464Vomiting1,994Stomatitis991Constipation904

General / constitutional

Fatigue3,333Asthenia1,610Weight Decreased1,431Malaise1,315Pyrexia1,265

Vascular

Hypertension3,703Blood Pressure Increased2,133

Metabolic & electrolyte

Decreased Appetite3,112Dehydration1,513

Skin

Rash1,016Palmar-Plantar Erythrodysaesthesia Syndrome980

Respiratory

Dysphonia885Dyspnoea837

Nervous system

Headache1,194

Endocrine

Hypothyroidism1,093

Blood & lymphatic

Platelet Count Decreased980

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 Lenvatinib 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

Regorafenib

Stivarga · VEGFR TKI

Profile

Hypertension and 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 Lenvatinib 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 Lenvatinib’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 Lenvatinib; 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 127 clinical records among all 164 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.