What kind of kidney injury does Vinblastine cause?

SIADH / Hyponatremia — Inappropriate water retention at the collecting duct — high-dose cyclophosphamide. Other reported patterns: Electrolyte Disturbance.

Is kidney injury from Vinblastine reversible?

Reversible. Typical onset: Days after administration, generally within the first cycles..

How should kidney function be monitored during Vinblastine therapy?

Serum sodium and osmolality during early cycles; Urine osmolality/sodium if hyponatremia develops; Assessment for Raynaud/digital ischemia.

How can kidney injury from Vinblastine be prevented?

Avoid excess free water in at-risk patients Plan controlled sodium correction if hyponatremia develops

Who is at higher risk of kidney injury from Vinblastine?

Concurrent SIADH-promoting medications or conditions; Excess hypotonic fluid intake; Combination vinca-containing or platinum-containing regimens (vascular events).

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Printable monograph

Vinca alkaloid

Vinblastine

Velban · VBL

Vinca alkaloid · approved 1965 · 8 citations

Recent· through 2024

Fairly sourced6/9 · 5 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 44y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2024
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 vinca alkaloid linked to SIADH-type hyponatremia and rare vascular events.

MildVinca alkaloid

Hodgkin lymphomaTesticular/germ-cell cancerBladder cancer

§01

Signature kidney injury

Signature lesion

SIADH / Hyponatremia

Vinblastine can cause SIADH with hyponatremia; this is a recognized class effect reported at case level rather than as a quantified rate. Rare Raynaud phenomenon and other vascular events (especially in germ-cell regimens) are also described.Source: Zhong et al., Expert Opin Drug Saf 2024

Onset & rechallenge

Time to injuryAcute (~1–7 days)

SIADH days after administration, generally within the first cycles.

Distilled from: “Days after administration, generally within the first cycles.”

§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.

SIADH / Hyponatremia#1 · Signaturequalitative — no citable incidence
Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

§03

Kidney injury

Deep diveDrug-induced SIADH: the sodium falls and the tumour takes the blameHyponatremia is the commonest electrolyte disorder in oncology and its commonest explanation is the cancer itself — which is exactly why a drug that impairs free-water excretion can go on being given for months while the sodium is treated as a feature of the disease.

Mechanism of kidney injury

Promotes inappropriate antidiuresis (SIADH) with enhanced collecting-duct water reabsorption, producing dilutional, euvolemic hyponatremia. No characteristic direct tubular or glomerular toxin effect; vascular events reflect endothelial/vasospastic phenomena rather than intrinsic nephrotoxicity.

Clinical presentation

Euvolemic hyponatremia with low plasma osmolality and inappropriately concentrated urine (urine osm >100, urine Na >30); symptoms scale with severity and the rate of sodium fall. Watch for digital ischemia/Raynaud as a separate vascular signal.

Management

Fluid restriction for mild cases; 3% hypertonic saline for severe/symptomatic hyponatremia with a controlled correction rate (<=8 mmol/L/24 h). Withhold the drug and manage any vascular complications supportively.Lesion-level management framework

Risk factors

Concurrent SIADH-promoting medications or conditions
Excess hypotonic fluid intake
Combination vinca-containing or platinum-containing regimens (vascular events)

Prevention

Avoid excess free water in at-risk patients
Plan controlled sodium correction if hyponatremia develops

Anticancer mechanism· how it treats cancer

Microtubule-destabilizing vinca alkaloid that binds beta-tubulin, blocks mitotic spindle formation, and arrests dividing cells at metaphase. Used in Hodgkin lymphoma (ABVD), germ-cell tumors, and bladder cancer.

Note · SIADH and rare Raynaud/vascular events define the profile; the kidneys are not directly injured.

§04

Clinical depth

Renal dose adjustment

Hepatically metabolized (CYP3A) and biliary excreted - no renal dose adjustment; reduce for hepatic impairment/hyperbilirubinemia. Never give intrathecally.

Dialyzability & ESKD dosing

Large volume of distribution and extensive tissue binding; not dialyzable. Manage hyponatremia with fluid/sodium strategies.

Differential diagnosis

Vinca-induced SIADH (euvolemic, concentrated urine) vs hypovolemic or hypervolemic hyponatremia vs paraneoplastic ectopic ADH. Volume status and urine indices distinguish them; Raynaud is a distinct vascular adverse effect.

Monitoring

Serum sodium and osmolality during early cycles
Urine osmolality/sodium if hyponatremia develops
Assessment for Raynaud/digital ischemia

Key trials & series

Zhong Expert Opin Drug Saf 2024 FAERS vinca-alkaloid disproportionality analysis

Clinical pearls

Treat vinblastine hyponatremia as SIADH - water restriction first.
Keep correction <=8 mmol/L/24 h to avoid osmotic demyelination.
Digital ischemia/Raynaud is a recognized vinca vascular effect, separate from the renal electrolyte signal.

Where it strikes· nephron segments & injury signatures

Nephron segments

Distal Tubule / Collecting Duct

Fine-tuning of Na, K, Mg, acid & water

Injury signatures

SIADH / Hyponatremia Electrolyte Disturbance

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)

§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 · 2016–2024 · 3 since 2022

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.

CaseC · LimitedLife-threatening hyponatremia caused by vinblastine.Zavagli G et al. · Med Oncol Tumor Pharmacother 1988 · PMID 2452936Vinblastine (ABVD) caused profound, life-threatening hyponatremia (Na 104 mEq/L) attributed to inappropriate ADH release (SIADH).CaseC · LimitedSyndrome of inappropriate antidiuretic hormone secretion associated with hepatic arterial infusion of vinblastine in three patients with breast cancer.Fraschini G et al. · Tumori 1987 · PMID 3686684Hepatic arterial vinblastine induced SIADH with hypokalemia and excessive kaliuresis in three breast cancer patients.CaseC · LimitedInappropriate antidiuretic hormone secretion after high dose vinblastine.Antony A et al. · J Urol 1980 · PMID 7420580A testicular teratocarcinoma patient developed SIADH after high-dose vinblastine, identifying high-dose vinblastine as a risk factor for this water-handling/electrolyte disturbance.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Apr 2025) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNINGS Caution: This preparation should be administered by individuals experienced in the administration of vinblastine sulfate. It is extremely important that the intravenous needle or catheter be properly positioned before any vinblastine sulfate is injected. Leakage into surrounding tissue during intravenous administration of vinblastine sulfate may cause considerable irritation. If extravasation occurs, the injection should be discontinued immediately, and any remaining portion of the dose should then be introduced into another vein. Local injection of hyaluronidase and the application of moderate heat to the area of leakage help disperse the drug and are thought to minimize discomfort and the possibility of cellulitis. FOR INTRAVENOUS USE ONLY – FATAL IF GIVEN BY OTHER ROUTES. See WARNINGS for the treatment of patients given intrathecal vinblastine sulfate injection.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,941 of them for this agent. Nobody counts the patients who were fine, so none of these numbers is an incidence, a risk, or a rate: they describe what gets reported, shaped by a drug's fame, its indication, and who was watching. How these numbers work.

Reporting odds ratio (ROR) — is kidney injury named in this agent's reports more often than in every other drug's? Above 1 means yes, disproportionately.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
Outcomes — a share of this agent's own reports, not of patients: how many were filed as involving a death or a hospitalization. Not a case-fatality rate.

FAERS reported renal phenotypes· 3 signals

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

SIADH / Hyponatremiacorroborated · ROR 4.49 — on the terms that name the lesion (ROR 4.25)
Electrolyte Disturbancecorroborated · ROR 3.05 — on the terms that name the lesion (ROR 4.69)

Acute Tubular Necrosis

ROR 5.5195% CI 2.29–13.25· 5 reports

SIADH / Hyponatremia

ROR 4.4995% CI 3.18–6.33· 33 reports

Electrolyte Disturbance

ROR 3.0595% CI 2.32–4.01· 53 reports

FAERS outcomes & reporting trend· 14.1% of reports w/ death · 40% w/ hospitalization

14.1%

Reported with a death outcome

274 of 1,941 reports

40%

Reported with hospitalization

777 of 1,941 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 1,941 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 1.4995% CI 0.97–2.30· 21 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Febrile Neutropenia170Neutropenia150Neutrophil Count Decreased75Pancytopenia75Anaemia71

Gastrointestinal

Nausea86Vomiting79Diarrhoea60Abdominal Pain51Mucosal Inflammation41

Respiratory

Pulmonary Toxicity78Dyspnoea65Interstitial Lung Disease58

General / constitutional

Pyrexia124Fatigue36Asthenia35

Immune / infection

Sepsis70Pneumonia42

Nervous system

Neuropathy Peripheral75

Endocrine

Hypothyroidism32

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 Vinblastine 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

Vincristine

Oncovin · Vinca alkaloid

Profile

SIADH → hyponatremia.

SIADHLYTE

Mild#1 · 100% phenotype match

Vinorelbine

Navelbine · Vinca alkaloid

Profile

SIADH reports.

SIADHLYTE

Mild#2 · 100% phenotype match

Melphalan

Alkeran · Alkylator

Profile

SIADH in high-dose myeloma conditioning; renally cleared.

SIADHLYTE

Mild#3 · 89% phenotype match

Temozolomide

Temodar · Alkylator

Profile

Occasional SIADH; generally renally well tolerated.

SIADHLYTE

Mild#4 · 89% phenotype match

Vismodegib

Erivedge · Hedgehog (SMO) inhibitor

Profile

Muscle spasms; hyponatremia reported.

SIADHLYTE

Mild#5 · 87% phenotype match

Chlorambucil

Leukeran · Alkylating agent (nitrogen mustard)

Profile

Minimal direct nephrotoxicity; rare drug-associated SIADH/hyponatremia is the kidney-relevant signal.

SIADHLYTE

Mild#6 · 86% phenotype match

Compare Vinblastine 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.

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 Vinblastine’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 Vinblastine; 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 32 clinical records among all 129 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.