Mirvetuximab soravtansine
Elahere · Antibody-drug conjugate (FRα/DM4)
Ocular toxicity dominates; renal involvement indirect/case-level (GI volume loss).
PRE
Mild#1 · 97% phenotype match
Antibody-drug conjugate (tissue factor/MMAE)
Tisotumab vedotin
Tivdak · TV
Antibody-drug conjugate (tissue factor/MMAE) · approved 2021 · 4 citations · FAERS AKI reporting ROR 2.29 (95% CI 1.37–3.81, 15 AKI reports)
Recent· through 2024
Fairly sourced5/9 · 5 signals
- Not met: 4 citations
- Not met: 12+ references
- Not met: Accrued over 10+ years (span: 3y)
- Met: Beyond single case reports
- Met: High-impact journal
- 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 tissue-factor MMAE ADC defined by ocular and bleeding toxicity — renal involvement is essentially unreported.
MildAntibody-drug conjugate (tissue factor/MMAE)
Recurrent or metastatic cervical cancer
§01
Signature kidney injury
Signature lesion
Direct nephrotoxicity is not a recognized signal. In the pivotal innovaTV 301 and innovaTV 204 trials the defining toxicities were ocular (conjunctivitis, dry eye, keratitis), bleeding/epistaxis and peripheral neuropathy; a quantified renal-injury rate was not reported. Renal involvement, if any, is indirect/case-level.Source: Vergote et al., N Engl J Med 2024 (innovaTV 301)
Onset & rechallenge
Time to injuryAcute (~1–7 days)
Renal events are uncharacterized; any prerenal AKI would track volume depletion over days.
Distilled from: “Not characterized for renal events; any prerenal AKI would track volume depletion (days).”
§02
Renal toxicities, ranked
This agent's defining kidney lesion — its #1 signature. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
§03
Kidney injury
Mechanism of kidney injury
No characteristic intrinsic renal lesion is established. Tissue factor's role in coagulation underlies the bleeding toxicity rather than a renal one. Any renal injury is most plausibly indirect — prerenal/hemodynamic from volume depletion (GI toxicity) — while a theoretical MMAE-payload tubular concern is not supported by trial renal data. The large antibody is not renally cleared.
Clinical presentation
If present, a prerenal creatinine rise during GI volume loss; there is no signature tubular or glomerular syndrome. The dominant clinical findings are ocular surface disease, epistaxis/bleeding and peripheral neuropathy.
Management
Supportive: volume resuscitation for prerenal AKI, antiemetics, and drug-hold/dose modification per label for toxicity. Manage the dominant ocular and bleeding toxicities per protocol; there is no drug-specific renal therapy.Lesion-level management framework
Risk factors
- Volume depletion from GI toxicity
- Pre-existing CKD
- Bleeding/coagulopathy (drug-specific) compounding hemodynamic instability
- Concurrent nephrotoxins
Prevention
- Mandatory ocular prophylaxis protocol (the priority toxicity)
- Hydration and antiemetics
- Bleeding precautions
Anticancer mechanism· how it treats cancer
Antibody-drug conjugate of an anti-tissue-factor IgG1 linked via a protease-cleavable linker to monomethyl auristatin E (MMAE). After binding tissue factor (overexpressed on cervical and other tumors) and internalization, MMAE is released to disrupt microtubules and induce apoptosis with bystander killing. Approved for recurrent or metastatic cervical cancer after prior therapy.
Note · Renal-specific literature is essentially absent — ocular toxicity, hemorrhage and neuropathy dominate. The prerenal characterization is conservative and mechanistic; incidence is not quantified.
§04
Clinical depth
Renal dose adjustment
No renal dose adjustment is established; not studied in severe impairment/ESKD. Modify/hold for ocular, bleeding and other toxicities per label.
Dialyzability & ESKD dosing
The IgG–MMAE conjugate is not dialyzable; released MMAE is highly protein-bound and not meaningfully removed by dialysis. No ESKD dosing guidance exists.
Differential diagnosis
Prerenal AKI from GI volume loss (fluid-responsive) vs unrelated intrinsic renal disease; there is no characteristic tisotumab renal lesion, so significant AKI warrants a search for an alternative cause.
Monitoring
- Ophthalmologic examination at baseline and per protocol (the priority)
- Bleeding/hemoglobin and volume status
Key trials & series
- innovaTV 301 (Vergote NEJM 2024) — pivotal phase 3
- innovaTV 204 (Coleman Lancet Oncol 2021) — registrational phase 2
- innovaTV 205 — combination study
Clinical pearls
- Eyes and bleeding, not kidneys: tisotumab's defining toxicities are ocular and hemorrhagic.
- Any AKI is most likely prerenal from volume loss — hydrate and give antiemetics.
- Renal literature is absent; keep claims qualitative and conservative.
Where it strikes· nephron segments & injury signatures
Nephron segments
Vasculature / Endothelium
Glomerular & peritubular capillaries
Injury signatures
Beyond the kidney — non-renal toxicities· 4 organ systems
Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (tissue factor/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. Citation metadata via PubMed / NLM.
Evidence accrual
4 references · 2021–2024 · 3 since 2022Primary (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.
- 1.LandmarkTisotumab Vedotin as Second- or Third-Line Therapy for Recurrent Cervical Cancer.Vergote I et al. · N Engl J Med · 2024 · PMID 38959480Pivotal phase 3 innovaTV 301; full safety profile with ocular/bleeding/neuropathy dominance and no prominent renal signal.
- 2.Efficacy and safety of tisotumab vedotin in previously treated recurrent or metastatic cervical cancer (innovaTV 204/GOG-3023/ENGOT-cx6): a multicentre, open-label, single-arm, phase 2 study.Coleman RL et al. · Lancet Oncol · 2021 · PMID 33845034Registrational phase 2; detailed ocular-predominant adverse-event profile.
- 3.Tisotumab Vedotin Safety and Tolerability in Clinical Practice: Managing Adverse Events.Arn CR et al. · J Adv Pract Oncol · 2023 · PMID 37009403Practical AE-management review confirming ocular/bleeding/neuropathy as the key signals.
- 4.Renal Side Effects of Novel Molecular Targeted Oncologic Agents.Fenoglio R et al. · G Ital Nefrol · 2023 · PMID 38007829Onconephrology class review providing renal context for ADC/targeted agents.
FDA label — boxed warning & renal dosing· boxed warning
Quoted verbatim from this agent's current FDA label (Nov 2025) — not paraphrased or interpreted. Full label on DailyMed .
Boxed warning
WARNING: OCULAR TOXICITY • TIVDAK can cause severe ocular toxicities resulting in changes in vision, including severe vision loss, and corneal ulceration. [see Warnings and Precautions (5.1) ]. • Conduct an ophthalmic exam, including an assessment of ocular symptoms, visual acuity, and slit lamp exam of the anterior segment of the eye prior to initiation of TIVDAK, prior to every cycle for the first nine cycles, and as clinically indicated. [see Dosage and Administration (2.2) and Warnings and Precautions (5.1) ] . • Adhere to the required premedication and eye care before, during, and after infusion. [see Dosage and Administration (2.2) ]. • Withhold TIVDAK until improvement and resume, reduce the dose, or permanently discontinue, based on severity [see Dosage and Administration (2.3) , Warnings and Precautions (5.1) ]. WARNING: OCULAR TOXICITY See full prescribing information for complete boxed warning. • TIVDAK can cause severe ocular toxicities resulting in changes in vision, including severe vision loss and corneal ulceration. ( 5.1 ) • Conduct an ophthalmic exam, including an assessment of ocular symptoms, visual acuity, and slit lamp exam of the anterior segment of the eye prior to initiation of TIVDAK, prior to every cycle for the first nine cycles, and as clinically indicated. ( 2.2 , 5.1 ) • Adhere to the required premedication and eye care before, during, and after…
What gets reported — FAERS
Everything below is FAERS — adverse events someone chose to report, about 912 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
- Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Hemorrhagic Cystitis
ROR 5.3995% CI 3.29–8.83· 16 reports
Acute Tubular Necrosis
ROR 4.6995% CI 1.17–18.77· 2 reports
Crystal / Obstructive Nephropathy
ROR 2.4995% CI 1.11–5.55· 6 reports
Electrolyte Disturbance
ROR 2.1995% CI 1.37–3.49· 18 reports
FAERS outcomes & reporting trend· 7.5% of reports w/ death · 24.5% w/ hospitalization
7.5%
Reported with a death outcome
68 of 912 reports
24.5%
Reported with hospitalization
223 of 912 reports
Reports per year
- 2015: 0 reports
- 2016: 0 reports
- 2017: 0 reports
- 2018: 0 reports
- 2019: 6 reports
- 2020: 14 reports
- 2021: 24 reports
- 2022: 172 reports
- 2023: 186 reports
- 2024: 182 reports
- 2025: 232 reports
- 2026: 96 reports
Yearly FAERS report volume · most recent year is partial.
FAERS adverse-event signal — all organ systems· 8 systems · 912 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 2.2995% CI 1.37–3.81· 15 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.
Eye
Dry Eye51Conjunctivitis42Eye Disorder28Keratitis21Ocular Toxicity21
Gastrointestinal
Nausea64Diarrhoea38Vomiting25Constipation21Abdominal Pain19
General / constitutional
Fatigue34Weight Decreased26Pyrexia23Malaise21
Nervous system
Neuropathy Peripheral74
Skin
Rash44Alopecia24
Vascular
Epistaxis28Vaginal Haemorrhage20
Blood & lymphatic
Anaemia32
Metabolic & electrolyte
Decreased Appetite16
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 Tisotumab 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.
Phenotype-similar agents· the numbered markers on the map above
Profile
Elacestrant
Orserdu · Oral selective estrogen-receptor degrader (SERD)
2023 oral SERD; nausea-dominant, minimal intrinsic nephrotoxicity.
PRE
Mild#2 · 89% phenotype match
Pexidartinib
Turalio · CSF1R inhibitor
Boxed hepatotoxicity; secondary renal effects.
PRE
Mild#3 · 89% phenotype match
Tovorafenib
Ojemda · Type II pan-RAF (BRAF) inhibitor
2024 pediatric glioma RAF inhibitor; creatinine rise.
PRE
Mild#4 · 89% phenotype match
Dordaviprone
Modeyso · Imipridone (ONC201; DRD2/ClpP)
2025 imipridone for H3 K27M glioma; renally well tolerated — QT prolongation, not nephrotoxicity, is the safety focus.
PRE
Mild#5 · 89% phenotype match
Iberdomide
Zenbexus · Cereblon E3 ligase modulator (CELMoD)
2026 first-in-class CELMoD; no attributable lesion (renal impairment 11% vs 8% on the comparator arm) but exposure rises 1.8x below eGFR 30 off dialysis.
PRE
Mild#6 · 89% phenotype match
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.
- 1Mirvetuximab soravtansinePRE — Prerenal / Hemodynamic AKIMild
- 2Belantamab mafodotinGLOM — Glomerular Injury / ProteinuriaFAERS AKIMild
- 3Tisotumab vedotin· this agentPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
- 4Brentuximab vedotinPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
- 5Polatuzumab vedotinPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
- 6Datopotamab deruxtecan (Dato-DXd)ATN — Acute Tubular NecrosisModerate
- 7Loncastuximab tesirinePRE — Prerenal / Hemodynamic AKIModerate
- 8Telisotuzumab vedotin (Teliso-V)ATN — Acute Tubular NecrosisModerate
- 9Sacituzumab govitecanPRE — Prerenal / Hemodynamic AKIModerate
- 10Trastuzumab deruxtecanATN — Acute Tubular NecrosisModerate
- 11Trastuzumab emtansine (T-DM1)TMA — Thrombotic MicroangiopathyModerate
- 12Pivekimab sunirinePRE — Prerenal / Hemodynamic AKIModerate
- 13Enfortumab vedotinATN — Acute Tubular NecrosisFAERS AKIModerate
- 14Gemtuzumab ozogamicinPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate
- 15Inotuzumab ozogamicinPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate
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.