What kind of kidney injury does Mirvetuximab soravtansine cause?

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

Is kidney injury from Mirvetuximab soravtansine reversible?

Variable. Typical onset: Variable; tracks with GI toxicity during treatment cycles..

How should kidney function be monitored during Mirvetuximab soravtansine therapy?

Ophthalmologic exam at baseline, every other cycle for the first 8 cycles, and as indicated.

How can kidney injury from Mirvetuximab soravtansine be prevented?

Manage nausea/diarrhea and maintain hydration Prophylactic ocular surface care (lubricating and corticosteroid eye drops)

Who is at higher risk of kidney injury from Mirvetuximab soravtansine?

GI toxicity and dehydration; Pre-existing CKD; Concurrent nephrotoxins.

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Printable monograph

Antibody-drug conjugate (FRα/DM4)

Mirvetuximab soravtansine

Elahere · MIRV

Antibody-drug conjugate (FRα/DM4) · approved 2022 · 4 citations

Recent· through 2024

Fairly sourced4/9 · 4 signals

Not met: 4 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 1y)
Met: Beyond single case reports
Met: High-impact journal
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.

An FRα/DM4 conjugate for ovarian cancer — ocular and GI toxicity dominate; renal data are emerging.

MildAntibody-drug conjugate

Ovarian cancerFallopian tube cancerPrimary peritoneal cancer

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is not a prominent trial signal; ocular (keratopathy/blurred vision, ~50% any-grade across pooled trials) and GI/fatigue toxicities dominate. AKI is case-level and chiefly volume-mediated (GI toxicity). Renal-specific incidence is not quantified.Source: Moore et al., N Engl J Med 2023 (MIRASOL)

Onset & rechallenge

Time to injuryVariable / unpredictable

Prerenal injury is variable and tracks with GI toxicity during treatment cycles.

Distilled from: “Variable; tracks with GI toxicity during treatment cycles.”

§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.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Indirect/hemodynamic: nausea, vomiting and diarrhea cause volume depletion and prerenal AKI. A direct tubular mechanism is not established in humans; FRα is expressed in proximal tubule (the basis for folate-receptor tracer uptake by the kidney), but clinically meaningful tubular toxicity has not emerged at approved doses. The maytansinoid payload concentrates instead in corneal epithelium, producing the hallmark ocular toxicity.

Clinical presentation

AKI in the setting of GI toxicity/dehydration with bland sediment; renal function otherwise usually preserved. Ocular symptoms (blurred vision, keratopathy, dry eye) are the hallmark toxicity and are generally low-grade and reversible.

Management

Rehydrate, manage GI toxicity, hold drug for significant AKI, supportive care; ocular toxicity is managed by ophthalmology-guided dose modification.Lesion-level management framework

Risk factors

GI toxicity and dehydration
Pre-existing CKD
Concurrent nephrotoxins

Prevention

Manage nausea/diarrhea and maintain hydration
Prophylactic ocular surface care (lubricating and corticosteroid eye drops)

Anticancer mechanism· how it treats cancer

Antibody-drug conjugate targeting folate receptor alpha (FRα) and delivering the maytansinoid microtubule inhibitor DM4 via a cleavable disulfide linker. Approved for FRα-positive, platinum-resistant epithelial ovarian, fallopian tube or primary peritoneal cancer.

Note · Renal data are emerging; the defining toxicities are ocular and GI rather than renal.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment defined for mild-moderate impairment; data are limited in severe impairment/ESKD. DM4 is hepatically metabolized rather than renally cleared.

Dialyzability & ESKD dosing

Not appreciably dialyzed (large ADC; protein-bound maytansinoid payload).

Differential diagnosis

AKI is prerenal from GI losses (volume-responsive, bland sediment) rather than tubular; the management-defining toxicity is ocular, paralleling belantamab mafodotin. Nephron injury would be unexpected and should prompt a search for alternative causes.

Monitoring

Ophthalmologic exam at baseline, every other cycle for the first 8 cycles, and as indicated

Key trials & series

MIRASOL (Moore NEJM 2023, phase III)
SORAYA (Matulonis JCO 2023, registrational)
Hendershot Gynecol Oncol Rep 2023 (pooled ocular safety, n=464)

Clinical pearls

Mirvetuximab and belantamab share the ADC ocular signature - eye care and exams, not renal monitoring, define routine surveillance.
FRα is expressed in the proximal tubule (hence renal tracer uptake), yet clinical tubular toxicity has not materialized - the kidney risk is hemodynamic.
Most AKI is dehydration from GI toxicity and reverses with fluids.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI

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

Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (FRα/DM4) 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 · 2023–2024 · 4 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.

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

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

Boxed warning

WARNING: OCULAR TOXICITY ELAHERE can cause severe ocular toxicities, including visual impairment, keratopathy, dry eye, photophobia, eye pain, and uveitis [see Warnings and Precautions ( 5.1 ) and Adverse Reactions ( 6.1 )] . Conduct an ophthalmic exam including visual acuity and slit lamp exam prior to initiation of ELAHERE, every other cycle for the first 8 cycles, and as clinically indicated [see Dosage and Administration ( 2.3 )] . Administer prophylactic artificial tears and ophthalmic topical steroids [see Dosage and Administration ( 2.3 ) and Warnings and Precautions ( 5.1 )] . Withhold ELAHERE for ocular toxicities until improvement and resume at the same or reduced dose [see Dosage and Administration ( 2.4 ) and Warnings and Precautions ( 5.1 )] . Discontinue ELAHERE for Grade 4 ocular toxicities [see Dosage and Administration ( 2.4 ) and Warnings and Precautions ( 5.1 )] . WARNING: OCULAR TOXICITY See full prescribing information for complete boxed warning. ELAHERE can cause severe ocular toxicities, including visual impairment, keratopathy, dry eye, photophobia, eye pain, and uveitis. ( 5.1 , 6.1 ) Conduct an ophthalmic exam including visual acuity and slit lamp exam prior to initiation of ELAHERE, every other cycle for the first 8 cycles, and as clinically indicated. ( 2.3 ) Administer prophylactic artificial tears and ophthalmic topical steroids. ( 2.3 , 5.1 )…

Renal impairment — from the label

No dosage adjustment of ELAHERE is recommended for patients with mild to moderate renal impairment (CLcr 30 to 89 mL/min). The effect of severe renal impairment (CLcr 15 to < 30 mL/min) or end-stage renal disease on ELAHERE is unknown [see Clinical Pharmacology ( 12.3 )] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,651 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.

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 outcomes & reporting trend· 11.9% of reports w/ death · 16.1% w/ hospitalization

11.9%

Reported with a death outcome

196 of 1,651 reports

16.1%

Reported with hospitalization

265 of 1,651 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 1,651 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.

Eye

Vision Blurred114Cataract85Dry Eye55Keratitis54Keratopathy54

Gastrointestinal

Diarrhoea101Abdominal Pain96Nausea86Vomiting51Abdominal Pain Upper28

Respiratory

Pneumonitis88Interstitial Lung Disease31

Nervous system

Neuropathy Peripheral114

General / constitutional

Fatigue61Pyrexia27

Blood & lymphatic

Thrombocytopenia48Anaemia24

Immune / infection

Infusion Related Reaction43

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 Mirvetuximab soravtansine 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

Tisotumab vedotin

Tivdak · Antibody-drug conjugate (tissue factor/MMAE)

Profile

Ocular/bleeding toxicity dominates; renal involvement essentially unreported.

PRE

Mild#1 · 97% phenotype match

Asparaginase

Elspar · Enzyme

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild#2 · 89% phenotype match

Belzutifan

Welireg · HIF-2α inhibitor

Profile

Anemia/hypoxia; emerging renal profile in VHL/RCC.

PRE

Mild#3 · 89% phenotype match

Dacarbazine

DTIC · Alkylator

Profile

Rare hepatic veno-occlusive disease; minimal direct renal injury.

PRE

Mild#4 · 89% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#5 · 89% phenotype match

Irinotecan

Camptosar · Topoisomerase I inhibitor

Profile

Diarrhea-driven prerenal AKI.

PRE

Mild#6 · 89% phenotype match

Compare Mirvetuximab soravtansine 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.