Is kidney injury from Vandetanib reversible?

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

How should kidney function be monitored during Vandetanib therapy?

Blood pressure regularly; ECG (QTc) at baseline, 2-4 and 8-12 weeks, then periodically; Serum potassium, magnesium, calcium and TSH; Urine protein (dipstick/UPCR) periodically.

How can kidney injury from Vandetanib be prevented?

Blood pressure optimization and electrolyte repletion before and during therapy

Who is at higher risk of kidney injury from Vandetanib?

Pre-existing hypertension; Baseline proteinuria or CKD; Electrolyte abnormalities (QT risk).

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Printable monograph

VEGFR/EGFR/RET TKI

Vandetanib

Caprelsa · Vande

VEGFR/EGFR/RET TKI · approved 2011 · 6 citations

Recent· through 2023

Deeply sourced7/9 · 6 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2023
Not met: Real-world FAERS signal

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

A VEGFR/EGFR/RET inhibitor for medullary thyroid cancer whose antiangiogenic action commonly raises blood pressure.

ModerateVEGFR/EGFR/RET inhibitor

Advanced or metastatic medullary thyroid carcinoma

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence32%

In the pivotal phase III ZETA trial, any-grade hypertension occurred in about 32% of vandetanib-treated patients versus 5% with placebo; proteinuria occurs as an antiangiogenic class effect.Source: Wells et al., J Clin Oncol 2012 (ZETA, any-grade hypertension)

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 · Signaturequalitative — no citable incidence
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.
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
Vandetanib significantly increased all-grade proteinuria risk in a VEGFR-TKI meta-analysis (9,446 pts, 20 RCTs; class all-grade RR 2.35, high-grade RR 3.70) — podocyte VEGF-inhibition glomerulopathy. PMID 32105149 (opens PubMed in a new tab)
Electrolyte DisturbanceRarequalitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

32%incidence

SeverityModerate

ReversibilityReversible

Evidence6 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Distal Tubule / Collecting Duct

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

VEGFR2 tyrosine kinase inhibition reduces glomerular VEGF and nitric-oxide signaling, increasing vascular tone (hypertension) and potentially injuring the glomerular filtration barrier (proteinuria/podocytopathy). A clinically dominant non-renal hazard is QT prolongation, which interacts with drug-induced electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia) to raise arrhythmia risk.

Clinical presentation

New or worsening hypertension, sometimes with proteinuria; clinicians must also watch for QT prolongation and the electrolyte derangements (hypocalcemia, hypokalemia, hypomagnesemia) that compound cardiac risk.

Management

Antihypertensive therapy (ACE inhibitor/ARB favored); interrupt or dose-reduce per label for grade 3 hypertension or significant proteinuria; aggressively maintain potassium, magnesium and calcium to mitigate QT-related arrhythmia. Hypertension is rarely dose-limiting and improves with treatment.Lesion-level management framework

§ Receptor target map

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

3targeted

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

VEGFR1VEGFR3

PDGFR

PDGFR-αPDGFR-β

Other receptor kinases

FGFRKITMETFLT3AXLCSF1RTIE2RAF-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
Electrolyte abnormalities (QT risk)

Prevention

Blood pressure optimization and electrolyte repletion before and during therapy

Anticancer mechanism· how it treats cancer

Oral inhibitor of RET, VEGFR2 (and other VEGFRs) and EGFR signaling, blocking angiogenesis and oncogenic RET-driven proliferation. Approved for advanced/metastatic medullary thyroid carcinoma.

Note · Hypertension is the principal renal-vascular signal; proteinuria is a class effect, and QT prolongation (a boxed warning) is the key non-renal safety concern that is amplified by renal electrolyte losses.

§04

Clinical depth

Renal dose adjustment

Reduce the starting dose to 200 mg for moderate impairment (CrCl 30-49 mL/min); use in severe impairment (CrCl <30 mL/min) is not recommended per label, because vandetanib is partly renally excreted and exposure rises with impairment; titrate with ECG and electrolyte monitoring.

Dialyzability & ESKD dosing

Long half-life (~19 days), large volume of distribution and high protein binding make it essentially non-dialyzable; HD does not provide meaningful removal and is not used for dosing.

Differential diagnosis

VEGFR-TKI hypertension/proteinuria versus baseline nephropathy versus prerenal AKI. Crucially, separate drug-induced electrolyte wasting (which drives QT risk) from other causes, since correcting it is part of safe vandetanib use.

Monitoring

Blood pressure regularly
ECG (QTc) at baseline, 2-4 and 8-12 weeks, then periodically
Serum potassium, magnesium, calcium and TSH
Urine protein (dipstick/UPCR) periodically

Key trials & series

ZETA phase III trial in advanced medullary thyroid carcinoma (hypertension 32% vs 5% placebo)

Clinical pearls

Vandetanib's renal-vascular signal is hypertension, but the safety-defining toxicity is QT prolongation — monitor ECG and electrolytes together.
Hypomagnesemia/hypokalemia from VEGFR-TKI effects compound QT risk, so repletion is therapeutic and protective.

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

Class-level context for the major non-renal toxicities of the VEGFR/EGFR/RET 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

5 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

5 references · 2012–2023 · 2 since 2021

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

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.

CaseC · LimitedAcute tubulointerstitial nephritis induced by the tyrosine kinase inhibitor vandetanib.Pilco Teran M et al. · Invest New Drugs 2021 · PMID 32648118First reported case of immunoallergic acute tubulointerstitial nephritis caused by vandetanib in a patient treated for medullary thyroid carcinoma.

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

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

Boxed warning

WARNING: QT PROLONGATION, TORSADES DE POINTES, AND SUDDEN DEATH CAPRELSA can prolong the QT interval. Torsades de pointes and sudden death have occurred in patients receiving CAPRELSA. Do not use CAPRELSA in patients with hypocalcemia, hypokalemia, hypomagnesemia, or long QT syndrome. Correct hypocalcemia, hypokalemia and/or hypomagnesemia prior to CAPRELSA administration. Monitor electrolytes periodically. Avoid drugs known to prolong the QT interval [see Warnings and Precautions (5.1) ] . WARNING: QT PROLONGATION, TORSADES DE POINTES, AND SUDDEN DEATH See full prescribing information for complete boxed warning. CAPRELSA can prolong the QT interval. Torsades de pointes and sudden death have occurred in patients receiving CAPRELSA. Do not use CAPRELSA in patients with hypocalcemia, hypokalemia, hypomagnesemia, or long QT syndrome. Correct hypocalcemia, hypokalemia and/or hypomagnesemia prior to CAPRELSA administration. Monitor electrolytes periodically. Avoid drugs known to prolong the QT interval ( 5.1 ).

Renal impairment — from the label

Vandetanib exposure is increased in patients with impaired renal function. Reduce the starting dose to 200 mg in patients with moderate (creatinine clearance ≥30 to <50 mL/min) renal impairment [see Dosage and Administration (2.1) , Warnings and Precautions (5.12) , and Clinical Pharmacology (12.3) ] . Vandetanib is not recommended for use in patients with severe renal impairment (clearance below 30 mL/min) [see Warnings and Precautions (5.12) ] . Patients with end-stage renal disease requiring dialysis were not studied [see Adverse Reactions (6.1) ] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,794 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· 5 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

Hypertensioncorroborated · ROR 6.67 — on the terms that name the lesion (ROR 6.72)
Electrolyte Disturbancecorroborated · ROR 5.34 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Glomerular Injury / Proteinuriacorroborated · ROR 3.63 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion

Hypertension

ROR 6.6795% CI 5.75–7.72· 199 reports

Electrolyte Disturbance

ROR 5.3495% CI 4.29–6.65· 84 reports

Glomerular Injury / Proteinuria

ROR 3.6395% CI 1.89–6.99· 9 reports

Crystal / Obstructive Nephropathy

ROR 2.7495% CI 1.59–4.73· 13 reports

SIADH / Hyponatremia

ROR 2.1995% CI 1.32–3.63· 15 reports

FAERS outcomes & reporting trend· 9% of reports w/ death · 29.1% w/ hospitalization

Reported with a death outcome

161 of 1,794 reports

29.1%

Reported with hospitalization

522 of 1,794 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 11 systems · 1,794 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 11 classified systems; 1 lower-ranked system is not drawn. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 1.1595% CI 0.69–1.92· 15 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Renal & urinary

Blood Creatinine Increased48

Gastrointestinal

Diarrhoea330Nausea111Vomiting45Abdominal Distension40

General / constitutional

Fatigue176Asthenia78Pain55

Skin

Rash176Pruritus46Dry Skin41

Vascular

Hypertension115Blood Pressure Increased78

Cardiac

Electrocardiogram Qt Prolonged142

Respiratory

Dyspnoea76Cough40

Nervous system

Headache73Dizziness40

Metabolic & electrolyte

Decreased Appetite64

Psychiatric

Insomnia57

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 Vandetanib 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

Sorafenib

Nexavar · VEGFR TKI

Profile

Anti-angiogenic hypertension and proteinuria; occasional TMA.

HTNGLOMTMA

Moderate#1 · 87% phenotype match

Cabozantinib

Cabometyx · VEGFR/MET TKI

Profile

Hypertension and proteinuria; nephrotic case reports.

HTNGLOM

Moderate#2 · 84% phenotype match

Lenvatinib

Lenvima · VEGFR TKI

Profile

Highest-ranked TKI for hypertension; proteinuria.

HTNGLOM

Moderate#3 · 84% phenotype match

Regorafenib

Stivarga · VEGFR TKI

Profile

Hypertension and proteinuria.

HTNGLOM

Moderate#4 · 84% phenotype match

Tivozanib

Fotivda · VEGFR TKI

Profile

Hypertension and proteinuria in RCC.

HTNGLOM

Moderate#5 · 84% phenotype match

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate#6 · 76% phenotype match

Compare Vandetanib 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.