How should kidney function be monitored during Vinflunine therapy?

Creatinine clearance before dosing to set the correct dose band; Serum sodium (SIADH/hyponatremia surveillance); Volume status and bowel function (ileus risk); CBC (neutropenia is the dominant dose-limiting toxicity).

How can kidney injury from Vinflunine be prevented?

Apply the validated CrCl-based dose schema (e.g., 280 mg/m2 for CrCl 40-60; 250 mg/m2 for CrCl 20 to <40) Aggressive bowel regimen to prevent ileus-related volume shifts

Who is at higher risk of kidney injury from Vinflunine?

Pre-existing renal impairment (the indicated population); Volume depletion from vinca-induced constipation/ileus, nausea, vomiting; Concomitant nephrotoxins or diuretics; Advanced age and poor performance status.

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Printable monograph

Vinca alkaloid

Vinflunine

Javlor · VFL

Vinca alkaloid · approved 2009 · 5 citations

Dated evidence· through 2019

Fairly sourced4/9 · 3 signals

Not met: 5 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 13y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Not met: Current through 2019
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 fluorinated vinca alkaloid used precisely because patients are too renally impaired for cisplatin — its renal story is careful dose-banding, not direct kidney injury.

Mild2009 (EMA)

Advanced/metastatic urothelial carcinoma after platinum-based therapyFirst-line cisplatin-ineligible urothelial carcinoma (investigational/combination, e.g., with gemcitabine)

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

Representative grade ≥3 incidence12%

No strong direct nephrotoxic signal. Vinflunine is given to renally impaired, cisplatin-unfit patients with a defined dose-reduction schema, and tolerability in renal impairment mirrors that of patients with normal renal function once dose-banded. SIADH/hyponatremia is a class-level vinca-alkaloid effect rather than a quantified vinflunine-specific rate. Reported rate: grade >=3 hyponatremia in 12% — 51 patients with relapse-sensitive or relapse-refractory small cell lung cancer treated with single-agent vinflunine… (Spigel 2010, PMID 20521355).Source: Spigel et al., J Thorac Oncol 2010

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Electrolyte/prerenal effects within days of a cycle.

Distilled from: “Electrolyte/prerenal effects can appear within days of a cycle; PK accumulation in renal impairment is immediate but mitigated by protocol dose reduction.”

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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.

Electrolyte Disturbance#1 · Signature12%PMID 20521355 (opens PubMed in a new tab)
Grade 3/4 hyponatremia in 12% on single-agent vinflunine 320 mg/m2 (relapsed SCLC phase II)
SIADH / HyponatremiaSecondaryqualitative — no citable incidence
Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

12%grade ≥3 incidence

SeverityMild

ReversibilityReversible

Evidence5 citations

Nephron map

Vasculature / Endothelium

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

Electrolyte Disturbance

Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

§03

Kidney injury

Mechanism of kidney injury

Vinflunine is not a recognized direct tubular toxin. The renal-relevant mechanism is pharmacokinetic: renal dysfunction modestly reduces vinflunine clearance (about a 12% decrease at CrCl 40-60 mL/min and ~28% at 20-40 mL/min), so dose banding restores comparable exposure. As a vinca alkaloid, it can be associated with SIADH (euvolemic hyponatremia) at the class level; prerenal physiology may arise from gastrointestinal toxicity and reduced intake.

Clinical presentation

Renal involvement is generally limited to electrolyte disturbance (hyponatremia, occasionally consistent with SIADH) and prerenal azotemia from constipation/ileus, nausea and reduced oral intake. Direct AKI from the drug itself is not a characteristic feature.

Management

Largely supportive: correct hyponatremia per cause (fluid restriction for SIADH), restore volume for prerenal states, and manage constipation aggressively. Continue dose-banded therapy unless intolerance arises. No drug-specific renal antidote is needed.Lesion-level management framework

Risk factors

Pre-existing renal impairment (the indicated population)
Volume depletion from vinca-induced constipation/ileus, nausea, vomiting
Concomitant nephrotoxins or diuretics
Advanced age and poor performance status

Prevention

Apply the validated CrCl-based dose schema (e.g., 280 mg/m2 for CrCl 40-60; 250 mg/m2 for CrCl 20 to <40)
Aggressive bowel regimen to prevent ileus-related volume shifts

Anticancer mechanism· how it treats cancer

Vinflunine is a third-generation, bifluorinated vinca alkaloid that binds tubulin and inhibits microtubule dynamics, arresting cells in mitosis (M phase) and triggering apoptosis. It is approved as second-line therapy for advanced/metastatic urothelial (transitional-cell) carcinoma after platinum failure, and is studied in first-line cisplatin-ineligible disease — a population defined largely by renal impairment.

Note · An instructive case where a drug is selected because of renal impairment. The clinical message is correct dose banding and electrolyte vigilance, not avoidance for nephrotoxicity.

§04

Clinical depth

Renal dose adjustment

Per phase I PK data: 320 mg/m2 for CrCl >60 mL/min; 280 mg/m2 for CrCl 40-60 mL/min (inclusive of both bounds); 250 mg/m2 for CrCl 20 to <40 mL/min. These bands yield exposure comparable to patients with normal renal function.

Dialyzability & ESKD dosing

Not established as dialyzable in routine practice; vinflunine is largely hepatically metabolized (CYP3A4) with a large volume of distribution, making meaningful dialytic removal unlikely. Manage by dose banding, not dialysis timing.

Differential diagnosis

Separate vinca-associated SIADH/hyponatremia and prerenal azotemia (from ileus, poor intake) from intrinsic AKI due to tumor obstruction, contrast, or concomitant nephrotoxins. Vinflunine itself is rarely the direct cause of a structural nephron lesion.

Monitoring

Creatinine clearance before dosing to set the correct dose band
Serum sodium (SIADH/hyponatremia surveillance)
Volume status and bowel function (ileus risk)
CBC (neutropenia is the dominant dose-limiting toxicity)

Key trials & series

Isambert et al. 2014 — phase I PK/tolerability defining CrCl-based dosing (280 and 250 mg/m2 bands)
De Santis et al. 2015 (JASINT1) — vinflunine-gemcitabine vs vinflunine-carboplatin in cisplatin-unfit (CrCl 30-60) urothelial carcinoma
Holmsten et al. 2019 (VINGEM) — vinflunine-gemcitabine vs carboplatin-gemcitabine in cisplatin-ineligible patients with renal impairment

Clinical pearls

Watch sodium: SIADH is a vinca-class effect.
Constipation/ileus can drive prerenal azotemia — keep the bowels moving.

Beyond the kidney — non-renal toxicities· 3 organ systems

Class-level context for the major non-renal toxicities of the Vinca alkaloid class.

Ophthalmic

Keratopathy, uveitis, retinopathy

Visual disturbance (crizotinib)

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Transaminitis

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

CNS effects (lorlatinib)

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References

5 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

5 references · 2006–2019 · 1 since 2017

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.

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 Vinflunine 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

Selinexor

Xpovio · XPO1 (nuclear export) inhibitor

Profile

Hyponatremia is common and dose-limiting.

SIADHLYTEPRE

Moderate#1 · 83% phenotype match

Sunvozertinib

Zegfrovy · EGFR exon20 TKI

Profile

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

LYTESIADHPRE

Mild#2 · 76% phenotype match

Tamoxifen

Nolvadex · SERM

Profile

Hypercalcemia flare; rare hyponatremia.

SIADHLYTEPRE

Mild#3 · 76% phenotype match

Lanreotide

Somatuline · Somatostatin analog

Profile

Kidney-neutral (CLARINET: diarrhea dominant); increased exposure in renal impairment.

LYTEPRE

Mild#4 · 73% phenotype match

Glasdegib

Daurismo · Hedgehog (SMO) inhibitor

Profile

QT prolongation and muscle spasms; AML.

PRELYTE

Mild#5 · 72% phenotype match

Darolutamide

Nubeqa · Androgen receptor inhibitor (ARSI)

Profile

Not nephrotoxic; exposure rises in severe renal impairment, so consider dose adaptation.

LYTEPRE

Mild#6 · 72% phenotype match

Compare Vinflunine 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 Microtubule 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.

1EribulinPRE — Prerenal / Hemodynamic AKIMild
2VinblastineSIADH — SIADH / HyponatremiaMild
3Vinflunine· this agentLYTE — Electrolyte DisturbanceMild
4CabazitaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
5VincristineSIADH — SIADH / HyponatremiaFAERS AKIMild
6VinorelbineSIADH — SIADH / HyponatremiaFAERS AKIMild
7DocetaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
8PaclitaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild

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.