What kind of kidney injury does Brentuximab vedotin cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Electrolyte Disturbance, Crystal / Obstructive Nephropathy.

Is kidney injury from Brentuximab vedotin reversible?

Reversible. Typical onset: Early — tumor lysis in the first cycle(s) of bulky disease..

How should kidney function be monitored during Brentuximab vedotin therapy?

Tumor lysis labs (K, phosphate, uric acid, calcium, creatinine) during early cycles of bulky disease; Neurologic exam for peripheral neuropathy and CBC (dominant direct toxicities).

How can kidney injury from Brentuximab vedotin be prevented?

Tumor lysis prophylaxis (hydration, allopurinol/rasburicase) in high-risk patients

Who is at higher risk of kidney injury from Brentuximab vedotin?

High/bulky tumor burden; Rapidly proliferative lymphoma; Volume depletion; Pre-existing CKD.

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Printable monograph

Antibody-drug conjugate (CD30/MMAE)

Brentuximab vedotin

Adcetris · BV

Antibody-drug conjugate (CD30/MMAE) · approved 2011 · 5 citations · FAERS AKI reporting ROR 2.53 (95% CI 2.19–2.92, 185 AKI reports)

Recent· through 2024

Fairly sourced6/9 · 5 signals

Not met: 5 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2024
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 CD30/MMAE conjugate whose main renal risk is tumor lysis in bulky lymphoma — direct nephrotoxicity is minimal.

MildAntibody-drug conjugate

Hodgkin lymphomaAnaplastic large-cell lymphomaCD30+ T-cell lymphomas

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is minimal. Tumor lysis syndrome occurs at low rates (<=5% in anaplastic large-cell lymphoma experience) and is the principal pathway to AKI/electrolyte disturbance; renal-specific incidence is not quantified.Source: Howard et al., Ann Hematol 2016 (systematic review)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Early — tumor lysis in the first cycle(s) of bulky disease.

Distilled from: “Early — tumor lysis in the first cycle(s) of bulky disease.”

§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.

Prerenal / Hemodynamic AKI#1 · Signature5%PMID 26758269 (opens PubMed in a new tab)
Tumor lysis syndrome (incidence <=5% in ALCL trials) is the principal indirect pathway to AKI; direct nephrotoxicity is minimal
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).
Crystal / Obstructive NephropathyRarequalitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence5 citations

Nephron map

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Tubular Lumen

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Kidney injury is largely indirect: rapid lysis of bulky CD30+ tumor causes tumor lysis with urate/phosphate crystal nephropathy and electrolyte shifts. Peripheral neuropathy and cytopenias dominate the direct toxicity profile; clinically meaningful MMAE-driven tubular nephrotoxicity is not a recognized signal at approved doses.

Clinical presentation

With tumor lysis: hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia and rising creatinine, typically early in treatment of bulky/proliferative disease.

Management

Tumor-lysis management (hydration, urate-lowering therapy, electrolyte correction); supportive AKI care.Lesion-level management framework

Risk factors

High/bulky tumor burden
Rapidly proliferative lymphoma
Volume depletion
Pre-existing CKD

Prevention

Tumor lysis prophylaxis (hydration, allopurinol/rasburicase) in high-risk patients

Anticancer mechanism· how it treats cancer

Antibody-drug conjugate targeting CD30 and delivering MMAE via a protease-cleavable linker, causing microtubule disruption and apoptosis in CD30+ tumor cells. Approved for Hodgkin lymphoma, systemic anaplastic large-cell lymphoma and other CD30-expressing lymphomas.

Note · Renal risk is mediated by tumor lysis rather than direct tubular toxicity; caution with dosing in severe renal impairment.

§04

Clinical depth

Renal dose adjustment

Per label, severe renal impairment (CrCl <30) increases MMAE exposure and adverse events - use with caution and avoid where alternatives exist; no adjustment needed for mild-moderate impairment. MMAE is a CYP3A4 substrate.

Dialyzability & ESKD dosing

Not appreciably dialyzed (large ADC; protein-bound MMAE). No supplemental dosing guidance for HD/PD.

Differential diagnosis

Tumor lysis AKI (electrolyte signature, early, bulky disease) versus prerenal AKI from intercurrent GI illness. Intrinsic tubular toxicity from MMAE is not expected.

Monitoring

Tumor lysis labs (K, phosphate, uric acid, calcium, creatinine) during early cycles of bulky disease
Neurologic exam for peripheral neuropathy and CBC (dominant direct toxicities)

Key trials & series

Howard Ann Hematol 2016 systematic review (TLS <=5% in ALCL)
ECHELON-1/ECHELON-2 registrational program (safety backbone)

Clinical pearls

The kidney risk is the tumor, not the drug: prophylax tumor lysis in bulky CD30+ disease.
Caution at CrCl <30 - MMAE exposure rises and toxicity increases even though the renal lesion itself is not tubular.
Neuropathy and neutropenia are the toxicities that actually change management.

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

Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (CD30/MMAE) class.

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression (payload-dependent)

Ophthalmic

Keratopathy, uveitis, retinopathy

Keratopathy (belantamab, mirvetuximab, tisotumab)

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Interstitial lung disease (deruxtecan ADCs)

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (MMAE payloads)

§05

References

4 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

4 references · 2013–2024 · 1 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· 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 · LimitedA case of karyomegalic interstitial nephritis without FAN1 mutations in the setting of brentuximab, ifosfamide, and carboplatin exposure.Leong M et al. · BMC Nephrol 2024 · PMID 39543462Karyomegalic interstitial nephritis with rising serum creatinine after brentuximab vedotin exposure, raising brentuximab as a possible novel cause of this tubulointerstitial injury.

Conference abstracts & journal reports· 1 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.

AbstractKaryomegalic Interstitial Nephritis in a Woman with Hodgkin Lymphoma on Brentuximab TherapyASN Kidney Week 2019 2019 · Abstract FR-PO680Biopsy-proven karyomegalic interstitial nephritis (enlarged hyperchromatic tubular nuclei with interstitial fibrosis and tubular atrophy) attributed to the MMAE antibody-drug conjugate brentuximab vedotin; renal function declined despite drug discontinuation.

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

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

Boxed warning

WARNING: PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML) JC virus infection resulting in PML and death can occur in patients receiving ADCETRIS [see Warnings and Precautions (5.9) , Adverse Reactions (6.1) ] . WARNING: PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML) See full prescribing information for complete boxed warning. JC virus infection resulting in PML and death can occur in patients receiving ADCETRIS ( 5.9 , 6.1 ).

Renal impairment — from the label

Avoid the use of ADCETRIS in patients with severe renal impairment (CrCL <30 mL/min) [see Warnings and Precautions (5.6) and Clinical Pharmacology (12.3) ]. No dosage adjustment is required for mild (CrCL >50–80 mL/min) or moderate (CrCL 30–50 mL/min) renal impairment.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 10,190 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· 4 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

Electrolyte Disturbancecorroborated · ROR 2.51 — on the terms that name the lesion (ROR 2.23)
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Crystal / Obstructive NephropathyNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

SIADH / Hyponatremia

ROR 2.9695% CI 2.46–3.56· 115 reports

Electrolyte Disturbance

ROR 2.5195% CI 2.21–2.86· 230 reports

Acute Interstitial Nephritis

ROR 2.3195% CI 1.51–3.55· 21 reports

Thrombotic Microangiopathy

ROR 1.7395% CI 1.00–2.98· 13 reports

FAERS outcomes & reporting trend· 19% of reports w/ death · 37.8% w/ hospitalization

19%

Reported with a death outcome

1,938 of 10,190 reports

37.8%

Reported with hospitalization

3,848 of 10,190 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 10,190 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 2.5395% CI 2.19–2.92· 185 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Blood & lymphatic

Febrile Neutropenia758Neutropenia586Anaemia396Thrombocytopenia380White Blood Cell Count Decreased258

General / constitutional

Pyrexia682Weight Decreased318Fatigue256Asthenia207

Gastrointestinal

Nausea393Diarrhoea382Vomiting302Abdominal Pain230

Nervous system

Neuropathy Peripheral711Polyneuropathy204

Immune / infection

Pneumonia321Sepsis263

Skin

Rash271

Respiratory

Dyspnoea238

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 Brentuximab vedotin 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

Polatuzumab vedotin

Polivy · Antibody-drug conjugate (CD79b/MMAE)

Profile

Tumor lysis; emerging renal data.

PRELYTEXTAL

Mild#1 · 100% phenotype match

Gemtuzumab ozogamicin

Mylotarg · Antibody-drug conjugate (CD33/calicheamicin)

Profile

Tumor lysis and veno-occlusive disease.

PRELYTEXTAL

Moderate#2 · 95% phenotype match

Inotuzumab ozogamicin

Besponsa · Antibody-drug conjugate (CD22/calicheamicin)

Profile

Tumor lysis and VOD in ALL.

PRELYTEXTAL

Moderate#3 · 95% phenotype match

Zanubrutinib

Brukinsa · BTK inhibitor

Profile

Tumor lysis in CLL/lymphoma.

PRELYTEXTAL

Mild#4 · 89% phenotype match

Epcoritamab

Epkinly · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#5 · 84% phenotype match

Glofitamab

Columvi · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#6 · 84% phenotype match

Compare Brentuximab vedotin 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 Antibody-drug conjugates

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 Brentuximab vedotin’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 Brentuximab vedotin; 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 10 clinical records among all 12 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.