What kind of kidney injury does Telisotuzumab vedotin (Teliso-V) cause?

Acute Tubular Necrosis — Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate. Other reported patterns: Electrolyte Disturbance.

How should kidney function be monitored during Telisotuzumab vedotin (Teliso-V) therapy?

Serum albumin; Urinalysis for proteinuria/sediment if AKI develops; Volume status and peripheral edema.

How can kidney injury from Telisotuzumab vedotin (Teliso-V) be prevented?

Maintain euvolemia and correct hypoalbuminemia where possible Hold or dose-modify per label for significant toxicity

Who is at higher risk of kidney injury from Telisotuzumab vedotin (Teliso-V)?

Pre-existing chronic kidney disease; Volume depletion or hypoalbuminemia; Concomitant nephrotoxins (contrast, aminoglycosides, NSAIDs); Older age and reduced baseline renal reserve.

Back to explorer

Printable monograph

c-Met ADC (MMAE)

Telisotuzumab vedotin (Teliso-V)

Emrelis · c-Met ADC (MMAE)

c-Met ADC (MMAE) · approved 2025 · 3 citations

Up to date· through 2025

Fairly sourced4/9 · 4 signals

Not met: 3 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 2025
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.

c-Met-directed MMAE antibody-drug conjugate; renal risk is class-extrapolated from MMAE payload handling.

Moderatec-Met antibody-drug conjugate (MMAE)

Locally advanced or metastatic non-squamous EGFR wild-type non-small cell lung cancer with high c-Met protein overexpression, after at least one prior systemic therapy (accelerated approval)

§01

Signature kidney injury

Signature lesion

Acute Tubular Necrosis

Drug-specific renal toxicity data for telisotuzumab vedotin are sparse. In the pivotal LUMINOSITY trial the dominant toxicities were peripheral neuropathy, peripheral edema, hypoalbuminemia, fatigue, and nausea; clinically significant nephrotoxicity was not highlighted as a frequent or signature event. Any renal risk is therefore largely class-extrapolated from MMAE-bearing ADCs rather than measured for this agent. A precise renal incidence rate cannot be stated from existing literature.Source: 38843488

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Onset is uncharacterized, but cytotoxic ADC payload tubular injury would typically evolve over days to a few weeks of cumulative exposure.

Distilled from: “Onset is not well characterized for this agent; with cytotoxic ADC payloads, tubular injury would typically evolve over days to a few weeks of cumulative exposure.”

§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.

Acute Tubular Necrosis#1 · Signaturequalitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
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

Mechanism of kidney injury

Injury is inferred from the MMAE payload. After partial deconjugation or nonspecific uptake, free or antibody-bound MMAE can be handled by the proximal tubule, where the antimitotic payload may injure highly metabolically active tubular epithelium and produce acute tubular injury (ATN). Marked hypoalbuminemia and peripheral edema seen with the drug can also shift intravascular volume and contribute indirectly to prerenal physiology. These pathways are extrapolated from the ADC/MMAE class; agent-specific renal histopathology is not established.

Clinical presentation

When it occurs, presentation is expected to resemble nontoxic ATN: a rise in serum creatinine with bland urine sediment, possibly with low-grade proteinuria and electrolyte disturbances. Hypoalbuminemia and peripheral edema are commonly observed with the drug and may accompany or confound the renal picture.

Management

Management is supportive and follows general drug-induced ATN principles: discontinue or hold the offending agent, restore volume, remove concurrent nephrotoxins, and provide supportive care while renal function recovers. No agent-specific antidote exists. Treat associated hypoalbuminemia/edema and electrolyte abnormalities as clinically indicated.Lesion-level management framework

Risk factors

Pre-existing chronic kidney disease
Volume depletion or hypoalbuminemia
Concomitant nephrotoxins (contrast, aminoglycosides, NSAIDs)
Older age and reduced baseline renal reserve

Prevention

Maintain euvolemia and correct hypoalbuminemia where possible
Hold or dose-modify per label for significant toxicity

Anticancer mechanism· how it treats cancer

Telisotuzumab vedotin is an antibody-drug conjugate (ADC) in which an antibody against c-mesenchymal-epithelial transition factor (c-Met) is linked to the microtubule inhibitor monomethyl auristatin E (MMAE). After binding c-Met on tumor cells, the conjugate is internalized and the cleavable linker liberates MMAE, which disrupts the microtubule network and triggers cell-cycle arrest and apoptosis. It received accelerated FDA approval in May 2025 for c-Met-high, EGFR wild-type nonsquamous NSCLC after prior systemic therapy.

§04

Clinical depth

Renal dose adjustment

No dedicated renal dose adjustment is established. The drug has not been formally studied in severe renal impairment or dialysis; mild-to-moderate impairment is not expected to require adjustment based on the antibody-conjugated pharmacology, but data are limited. Follow the current FDA label for dose modifications driven by toxicity.

Dialyzability & ESKD dosing

Not established. As a large antibody-drug conjugate, telisotuzumab vedotin is not expected to be appreciably dialyzable; the small-molecule MMAE payload is highly protein- and tissue-bound, so removal by hemodialysis is unlikely to be clinically meaningful.

Differential diagnosis

In a patient on Teliso-V with rising creatinine, distinguish class-extrapolated tubular injury (ATN) from prerenal azotemia driven by hypoalbuminemia, edema, and poor intake, and from concurrent nephrotoxins or contrast. Bland sediment favors ATN or prerenal physiology over glomerular or interstitial disease.

Monitoring

Serum albumin
Urinalysis for proteinuria/sediment if AKI develops
Volume status and peripheral edema

Key trials & series

LUMINOSITY (NCT03539536): Phase II of telisotuzumab vedotin monotherapy in previously treated c-Met-overexpressing EGFR wild-type nonsquamous NSCLC; supported accelerated approval. Predominant toxicities were peripheral neuropathy, edema, and hypoalbuminemia rather than a defined nephrotoxicity signal.

Clinical pearls

The proximal tubule is the plausible target if liberated MMAE causes injury, consistent with the proximal/ATN signature assigned here.
No renal dose adjustment is established; manage supportively and avoid stacking additional nephrotoxins.

Where it strikes· nephron segments & injury signatures

Nephron segments

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Injury signatures

Acute Tubular Necrosis Electrolyte Disturbance

§05

References

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

Evidence accrual

3 references · 2024–2025 · 3 since 2023

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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 64 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· 12.5% of reports w/ death · 23.4% w/ hospitalization

12.5%

Reported with a death outcome

8 of 64 reports

23.4%

Reported with hospitalization

15 of 64 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 64 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

Keratitis5Vision Blurred4Dry Eye1Eye Operation1

Respiratory

Interstitial Lung Disease4Pneumonitis3Pulmonary Embolism2Dyspnoea Exertional1

Nervous system

Neuropathy Peripheral6

Immune / infection

Pneumonia4Covid-191

General / constitutional

Fatigue2Pyrexia2Chills1

Blood & lymphatic

Agranulocytosis2Febrile Neutropenia1

Hepatobiliary

Alanine Aminotransferase Abnormal1Aspartate Aminotransferase Abnormal1

Vascular

Deep Vein Thrombosis1

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 Telisotuzumab vedotin (Teliso-V) 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

Melphalan flufenamide (melflufen)

Pepaxto · Peptide-conjugated alkylator

Profile

Delivers melphalan intracellularly; BRIDGE supports a reduced 30 mg dose in moderate renal impairment.

ATNLYTE

Moderate#1 · 89% phenotype match

Nedaplatin

Aqupla · Platinum agent

Profile

Second-gen platinum with reduced renal toxicity vs cisplatin.

ATNLYTE

Moderate#2 · 86% phenotype match

Enfortumab vedotin

Padcev · Antibody-drug conjugate (Nectin-4/MMAE)

Profile

Emerging AKI and electrolyte signals in urothelial cancer.

ATNLYTEPRE

Moderate#3 · 81% phenotype match

Trastuzumab deruxtecan

Enhertu · Antibody-drug conjugate (HER2/DXd)

Profile

Emerging AKI/proteinuria reports — under-published.

ATNFANCLYTE

Moderate#4 · 81% phenotype match

Trabectedin

Yondelis · Marine alkylating agent

Profile

Rhabdomyolysis → pigment nephropathy; hepatotoxicity.

ATNLYTE

Moderate#5 · 77% phenotype match

Plicamycin (mithramycin)

Mithracin · Antitumor antibiotic

Profile

Cumulative tubular ATN; hypocalcemia is an on-target antiresorptive effect.

ATNLYTE

Moderate#6 · 74% phenotype match

Compare Telisotuzumab vedotin (Teliso-V) 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.