What kind of kidney injury does Tebentafusp cause?

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

Is kidney injury from Tebentafusp reversible?

Reversible. Typical onset: Early — first 1–3 weekly doses, coinciding with peak CRS..

How should kidney function be monitored during Tebentafusp therapy?

Blood pressure and temperature closely during and after each early infusion; Serum creatinine around the step-up doses; Volume status; Skin toxicity assessment.

How can kidney injury from Tebentafusp be prevented?

Mandatory weekly step-up dosing and monitored administration (inpatient for first doses per label) Pre-/post-infusion hydration Prompt treatment of hypotension

Who is at higher risk of kidney injury from Tebentafusp?

Higher-grade CRS / pronounced hypotension; Pre-existing CKD or cardiovascular disease; Volume depletion; Concurrent nephrotoxins or antihypertensives amplifying hypotension.

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Printable monograph

Bispecific T-cell engager (gp100×CD3 ImmTAC)

Tebentafusp

Kimmtrak · Tebe

Bispecific T-cell engager (gp100×CD3 ImmTAC) · approved 2022 · 4 citations

Recent· through 2023

Fairly sourced4/9 · 4 signals

Not met: 4 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 2y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2023
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 gp100×CD3 ImmTAC whose renal risk is CRS-driven hypotension early in treatment — prerenal AKI.

ModerateBispecific T-cell engager (gp100×CD3 ImmTAC)

HLA-A*02:01-positive metastatic uveal melanoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Cytokine release syndrome is very common early in treatment and, with the associated hypotension, is the principal mechanism of acute kidney injury; severe sepsis-like CRS with hypotension has been reported. The pivotal phase 3 trial established CRS, hypotension and rash as defining toxicities, mitigated by weekly step-up dosing. A dedicated tebentafusp renal/AKI study does not exist; renal injury is inferred from the CRS literature.Source: Nathan et al., NEJM 2021 (pivotal phase 3); Geidel et al., JEADV 2023 (sepsis-like CRS case)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Early — first 1–3 weekly doses, coinciding with peak CRS.

Distilled from: “Early — first 1–3 weekly doses, coinciding with peak CRS.”

§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

The renal pathway is hemodynamic/prerenal. T-cell redirection triggers a cytokine release syndrome (fever, vasodilatory hypotension, capillary leak) concentrated in the first doses, reducing renal perfusion and producing prerenal azotemia that can progress to ischemic tubular injury if hypotension is sustained. Weekly step-up dosing is designed to limit the cytokine peak. There is no characteristic intrinsic tubular or glomerular lesion; tumor lysis is not a prominent feature in this low-proliferative-burden disease.

Clinical presentation

Acute creatinine rise during a CRS episode — fever, hypotension, sometimes rash — typically with the first one to three weekly infusions. Prerenal indices and fluid responsiveness are usual. Cutaneous toxicity (rash, pruritus) is a common concurrent finding.

Management

Treat CRS-related hypotension promptly with IV fluids and supportive measures (vasopressors and corticosteroids for severe cases) to restore renal perfusion; hold/delay dosing per label for severe reactions. Prerenal AKI generally recovers once hemodynamics normalize.Lesion-level management framework

Risk factors

Higher-grade CRS / pronounced hypotension
Pre-existing CKD or cardiovascular disease
Volume depletion
Concurrent nephrotoxins or antihypertensives amplifying hypotension

Prevention

Mandatory weekly step-up dosing and monitored administration (inpatient for first doses per label)
Pre-/post-infusion hydration
Prompt treatment of hypotension

Anticancer mechanism· how it treats cancer

Bispecific gp100 peptide-HLA-directed T-cell engager (ImmTAC) that fuses an affinity-enhanced T-cell receptor recognizing a gp100 peptide presented on HLA-A*02:01 to an anti-CD3 effector domain, redirecting polyclonal T cells to kill gp100+ uveal melanoma cells. Approved for HLA-A*02:01-positive unresectable or metastatic uveal melanoma.

Note · No tebentafusp-specific renal study exists; the CRS-driven hypotension to prerenal-AKI link is inferred from the pivotal trial and CRS case literature plus general onconephrology reviews. The renal risk is concentrated in the early step-up phase.

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Clinical depth

Renal dose adjustment

No dedicated renal dose adjustment is established; the fixed weekly step-up schedule is driven by CRS mitigation, not renal function. Manage AKI by hemodynamic support rather than dose change.

Dialyzability & ESKD dosing

The engineered TCR-anti-CD3 fusion protein is not meaningfully dialyzable; no ESKD dose change is defined. Dialysis would support AKI management, not drug removal.

Differential diagnosis

CRS-driven prerenal/ischemic AKI (fever, hypotension, temporal link to early infusions, fluid-responsive) vs unrelated intrinsic renal disease; the early-dose CRS time-course is the key discriminator. There is no characteristic tebentafusp tubular/glomerular lesion.

Monitoring

Blood pressure and temperature closely during and after each early infusion
Serum creatinine around the step-up doses
Volume status
Skin toxicity assessment

Key trials & series

Nathan NEJM 2021 — pivotal phase 3 (overall survival benefit)
Hassel NEJM 2023 — 3-year overall-survival follow-up

Clinical pearls

The renal danger window is the first few weekly doses — treat CRS hypotension early with fluids to protect perfusion.

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· 3 organ systems

Class-level context for the major non-renal toxicities of the Bispecific T-cell engager (gp100×CD3 ImmTAC) class.

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Cytokine release syndrome

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

ICANS / neurotoxicity

Hematologic

Cytopenias, thrombosis, TMA

Cytopenias, hypogammaglobulinemia

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References

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

Evidence accrual

4 references · 2021–2023 · 4 since 2021

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

Quoted verbatim from this agent's current FDA label (Aug 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

BOXED WARNING: CYTOKINE RELEASE SYNDROME Cytokine Release Syndrome (CRS), which may be serious or life-threatening, occurred in patients receiving KIMMTRAK. Monitor for at least 16 hours following first three infusions and then as clinically indicated [(see Dosage and Administration (2.2) , see Warnings and Precautions (5.1) ] . WARNING: CYTOKINE RELEASE SYNDROME Cytokine Release Syndrome (CRS), which may be serious or life-threatening, occurred in patients receiving KIMMTRAK. Monitor for at least 16 hours following first three infusions and then as clinically indicated ( 2.2 , 5.1 ).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 581 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.
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· 17.6% of reports w/ death · 33.6% w/ hospitalization

17.6%

Reported with a death outcome

102 of 581 reports

33.6%

Reported with hospitalization

195 of 581 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 581 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 1.1995% CI 0.49–2.86· 5 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

General / constitutional

Pyrexia104Chills57Fatigue23Asthenia17Pain13

Skin

Rash68Pruritus43Erythema13

Immune / infection

Cytokine Release Syndrome115

Vascular

Hypotension67Blood Pressure Decreased14Hypertension12

Gastrointestinal

Nausea37Vomiting32Diarrhoea16

Respiratory

Hypoxia19Oxygen Saturation Decreased15Dyspnoea14

Nervous system

Headache14Neuropathy Peripheral12

Cardiac

Tachycardia19

Psychiatric

Confusional State12

Guidelines & consensus· 19

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.

ASCOManagement of Immune-Related Adverse Events in Patients Treated With Chimeric Antigen Receptor T-Cell Therapy: ASCO GuidelineJ Clin Oncol 2021 · PMID 34724386Grade toxicities by ASTCT criteria; manage CRS with supportive care escalating to tocilizumab with or without corticosteroids, and manage moderate-to-severe ICANS with corticosteroids and supportive care given potential for rapid decline.TLS Expert PanelGuidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based reviewJ Clin Oncol 2008 · PMID 18509186Prevention is the best management: hydration plus prophylactic rasburicase for high-risk patients, hydration plus allopurinol or rasburicase for intermediate-risk, and monitoring for low-risk; for established TLS add aggressive hydration and diuresis plus allopurinol or rasburicase for hyperuricemia. Urinary alkalinization is NOT recommended.TLS Consensus PanelRecommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensusBr J Haematol 2010 · PMID 20331465Stratify each patient as low/intermediate/high TLS risk using tumor type, bulk/stage, proliferation rate, baseline laboratory TLS, and renal impairment/involvement, then match prophylaxis intensity (monitoring vs allopurinol vs rasburicase) to the assigned risk level.BCSHGuidelines for the management of tumour lysis syndrome in adults and children with haematological malignancies on behalf of the British Committee for Standards in HaematologyBr J Haematol 2015 · PMID 25876990Risk-adapted prophylaxis and management of TLS in haematological malignancy: hydration with allopurinol for lower-risk and rasburicase for high-risk patients, with monitoring of electrolytes and renal function to prevent and treat AKI.Cairo-BishopTumour lysis syndrome: new therapeutic strategies and classificationBr J Haematol 2004 · PMID 15384972Defines the Cairo-Bishop criteria distinguishing laboratory TLS (>=2 metabolic abnormalities: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia within 3 days before to 7 days after therapy) from clinical TLS (laboratory TLS plus AKI, cardiac arrhythmia, or seizure), with a severity grading scheme adopted by subsequent guidelines.ASTCTASTCT Consensus Grading for Cytokine Release Syndrome and Neurologic Toxicity Associated with Immune Effector CellsBiol Blood Marrow Transplant 2019 · PMID 30592986Grade CRS by fever, hypotension and hypoxia (grades 1-4) and grade ICANS using the ICE/encephalopathy score plus level of consciousness, seizures, motor findings and raised intracranial pressure/edema; this is the standard severity framework that triggers tocilizumab and corticosteroid escalation in CAR-T and bispecific antibody toxicity (the Lee 2019 consensus).

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 Tebentafusp 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

Denileukin diftitox

Lymphir · Immunotoxin (IL-2–diphtheria)

Profile

Capillary-leak syndrome → prerenal AKI.

PRE

Moderate#1 · 89% phenotype match

Zolbetuximab

Vyloy · Anti-Claudin-18.2 monoclonal antibody

Profile

2024 gastric mAb; severe on-target nausea/vomiting → volume-depletion prerenal AKI.

PRE

Moderate#2 · 89% phenotype match

Trifluridine/tipiracil

Lonsurf · Oral fluoropyrimidine + TP inhibitor

Profile

Tipiracil is renally cleared; reduced GFR raises exposure and early severe neutropenia; dose-reduce in renal impairment.

PRE

Moderate#3 · 88% phenotype match

Elacestrant

Orserdu · Oral selective estrogen-receptor degrader (SERD)

Profile

2023 oral SERD; nausea-dominant, minimal intrinsic nephrotoxicity.

PRE

Mild#4 · 83% phenotype match

Tisotumab vedotin

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

Profile

Ocular/bleeding toxicity dominates; renal involvement essentially unreported.

PRE

Mild#5 · 83% phenotype match

Tovorafenib

Ojemda · Type II pan-RAF (BRAF) inhibitor

Profile

2024 pediatric glioma RAF inhibitor; creatinine rise.

PRE

Mild#6 · 83% phenotype match

Compare Tebentafusp 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 Bispecifics / T-cell engagers

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.