What kind of kidney injury does Tarlatamab cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Acute Tubular Necrosis.

How should kidney function be monitored during Tarlatamab therapy?

Vital signs/temperature and oxygenation intensively around initial doses (CRS watch); Serum creatinine and electrolytes through the CRS window; Inflammatory markers (ferritin, CRP) if CRS suspected; Neuro checks for ICANS.

How can kidney injury from Tarlatamab be prevented?

Step-up/priming dosing and protocol-defined monitoring per label Prompt CRS recognition and treatment Avoid nephrotoxins during the CRS window

Who is at higher risk of kidney injury from Tarlatamab?

Higher CRS grade; Volume depletion at dosing; Pre-existing CKD; Concurrent nephrotoxins; High disease burden.

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Printable monograph

Bispecific (DLL3×CD3)

Tarlatamab

Imdelltra · Tarla

Bispecific (DLL3×CD3) · approved 2024 · 8 citations

Up to date· through 2026

Fairly sourced5/9 · 5 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 5y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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 DLL3×CD3 BiTE for small-cell lung cancer — cytokine release can drive pre-renal AKI.

ModerateBispecific T-cell engager (DLL3×CD3)

Extensive-stage small-cell lung cancer (relapsed/refractory)

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Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Cytokine release syndrome is the dominant on-target toxicity — common (majority of patients in early studies), mostly low-grade, and mitigated by step-up/priming dosing and inpatient monitoring of initial doses. AKI is principally a downstream consequence of CRS (hypotension, fever, capillary leak, volume shifts) rather than a direct tubular toxin; renal-specific incidence is not separately well quantified.Source: Paz-Ares et al., J Clin Oncol 2023 (DeLLphi-300)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

CRS within the first cycle after the first full doses; AKI tracks the CRS course.

Distilled from: “CRS typically within the first cycle, often after the first full (post-priming) doses; AKI tracks the CRS course.”

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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 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

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Kidney injury

Mechanism of kidney injury

Synapse-driven T-cell activation releases a surge of inflammatory cytokines (IL-6, IFN-γ, TNF-α) — the cytokine release syndrome. The resulting vasodilation, hypotension, capillary leak and fever cause renal hypoperfusion and pre-renal azotemia; if hypotension is severe or prolonged this progresses to ischemic acute tubular necrosis. By close analogy to other T-cell-redirecting therapies, cytokine-mediated podocyte/tubulointerstitial injury (and rarely collapsing glomerulopathy, reported with CAR-T and blinatumomab) is a theoretical additional mechanism. ICANS (neurotoxicity) may co-occur.

Clinical presentation

Fever and hypotension of CRS accompanied by a rising creatinine; pre-renal urine indices (low FeNa, concentrated urine) early, evolving to muddy-brown-cast ATN if perfusion is not restored. Tachycardia, hypoxia and elevated inflammatory markers/ferritin support CRS.

Management

Treat CRS promptly: IV fluids for hypotension, antipyretics, tocilizumab (IL-6 receptor blockade) and corticosteroids per grade-based algorithms; restore perfusion early. Provide supportive AKI care and renal replacement therapy if severe. Most CRS-mediated AKI is reversible once hemodynamics normalize.Lesion-level management framework

Risk factors

Higher CRS grade
Volume depletion at dosing
Pre-existing CKD
Concurrent nephrotoxins
High disease burden

Prevention

Step-up/priming dosing and protocol-defined monitoring per label
Prompt CRS recognition and treatment
Avoid nephrotoxins during the CRS window

Anticancer mechanism· how it treats cancer

Bispecific T-cell engager (BiTE) with one arm binding DLL3 (highly expressed on small-cell lung cancer cells) and the other binding CD3 on T cells, forming an immunologic synapse that redirects polyclonal cytotoxic T cells to lyse tumor. Approved for relapsed/refractory extensive-stage small-cell lung cancer.

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Clinical depth

Renal dose adjustment

No established renal dose adjustment (T-cell engager, not renally cleared); dosing is by step-up schedule. The renal-relevant action is hemodynamic support during CRS, not dose modification for GFR.

Dialyzability & ESKD dosing

Bispecific antibody construct — not dialyzable and not renally eliminated; no ESKD dose change expected. Renal replacement therapy is for CRS-driven AKI, not drug clearance.

Differential diagnosis

CRS-driven pre-renal/ischemic ATN (fever, hypotension, high ferritin) vs sepsis-related AKI vs tumor lysis vs nephrotoxin exposure; persistent nephrotic-range proteinuria would raise the rare possibility of cytokine-mediated podocytopathy (CAR-T/blinatumomab precedent) and warrant biopsy.

Monitoring

Vital signs/temperature and oxygenation intensively around initial doses (CRS watch)
Serum creatinine and electrolytes through the CRS window
Inflammatory markers (ferritin, CRP) if CRS suspected
Neuro checks for ICANS

Key trials & series

DeLLphi-300 (Paz-Ares JCO 2023) first-in-class phase I
DeLLphi-301 phase II (registrational)
Sands Cancer 2025 practical CRS-management guidance

Clinical pearls

The AKI is CRS hemodynamics, not a tubular poison — fix the blood pressure and fever and the kidney follows.
Priming/step-up dosing with inpatient monitoring of first doses is the single most important renal-protective measure.
Tocilizumab plus fluids and steroids per CRS grade restores perfusion and reverses most AKI.
Watch for the rare cytokine-driven collapsing glomerulopathy seen with related T-cell redirectors if heavy proteinuria appears.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Acute Tubular Necrosis

Beyond the kidney — non-renal toxicities· 3 organ systems

Class-level context for the major non-renal toxicities of the Bispecific (DLL3×CD3) 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

7 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

7 references · 2021–2026 · 2 since 2024

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.

CaseB · ModerateTarlatamab-Induced Tumor Lysis Syndrome in Small Cell Carcinoma: Case Series.Lobsiger BM et al. · Clin Lung Cancer 2026 · PMID 41109815Case series of tarlatamab-induced tumor lysis syndrome in small cell carcinoma, a metabolic emergency that precipitates acute kidney injury through urate/phosphate nephropathy and hemodynamic compromise.

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 Tarlatamab 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

Talquetamab

Talvey · Bispecific (GPRC5D×CD3)

Profile

CRS-related AKI — emerging.

PREATN

Moderate#1 · 85% phenotype match

Teclistamab

Tecvayli · Bispecific (BCMA×CD3)

Profile

CRS-associated AKI in myeloma — emerging signal.

PREATN

Moderate#2 · 85% phenotype match

Tebentafusp

Kimmtrak · Bispecific T-cell engager (gp100×CD3 ImmTAC)

Profile

CRS-driven hypotension → prerenal AKI early in dosing; uveal melanoma.

PRE

Moderate#3 · 76% phenotype match

Tasonermin

Beromun · Recombinant TNF-α (cytokine)

Profile

Isolated-limb-perfusion agent; systemic leakage → SIRS/hypotension → prerenal AKI.

PREATN

Moderate#4 · 75% phenotype match

Tretinoin (ATRA)

Vesanoid · Retinoid (differentiating agent)

Profile

Differentiation syndrome → capillary leak and AKI.

PREATN

Moderate#5 · 74% phenotype match

Tagraxofusp

Elzonris · IL-3 immunotoxin

Profile

Capillary-leak syndrome → AKI.

PREATN

Moderate#6 · 74% phenotype match

Compare Tarlatamab 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.