How should kidney function be monitored during Teclistamab therapy?

Vital signs and CRS grading during step-up and early full doses; Serum creatinine/eGFR and electrolytes around dosing; Infection surveillance and immunoglobulin levels (hypogammaglobulinemia).

How can kidney injury from Teclistamab be prevented?

Mandatory step-up (priming) dosing with premedication (corticosteroid, antihistamine, antipyretic) to reduce CRS severity Inpatient or close monitoring during step-up dosing per protocol Hydration, avoidance of additional nephrotoxins, and infection prophylaxis

Who is at higher risk of kidney injury from Teclistamab?

Higher-grade cytokine release syndrome; Pre-existing myeloma-related CKD/cast nephropathy; Volume depletion and concurrent nephrotoxins; High disease burden; intercurrent infection/sepsis.

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Printable monograph

Bispecific (BCMA×CD3)

Teclistamab

Tecvayli · TECLI

Bispecific (BCMA×CD3) · approved 2022 · 9 citations

Up to date· through 2026

Fairly sourced5/9 · 5 signals

Met: 9 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
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 BCMAxCD3 bispecific for myeloma whose emerging renal signal is CRS-associated acute kidney injury on a background of myeloma kidney disease.

ModerateBispecific antibody (BCMAxCD3)

Relapsed or refractory multiple myeloma (after multiple prior lines, including triple-class exposure)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Representative incidence29%

Cytokine release syndrome is very common with teclistamab (about 72% of patients in the pivotal MajesTEC-1 trial, predominantly grade 1-2); CRS-associated acute kidney injury is an emerging, case-level signal superimposed on frequent baseline myeloma-related kidney disease, and is not separately well quantified. Reported rate: acute kidney injury in 29% — 10 of 34 patients with relapsed/refractory multiple myeloma treated with teclistamab, all of whom had received at least four prior lines of chemotherapy, versus 13% (4 of 30) after CAR-T in the same retrospective comparison; the difference was not statistically significant (HR 3.38, 95% CI 0.93-12.31, P = .065), and the authors leave open whether the excess is attributable to teclistamab or to disease progression (Charkviani 2025, PMID 39805729).Source: Charkviani et al., Nephrol Dial Transplant 2025

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Early — around step-up dosing and first full doses (first days to weeks).

Distilled from: “Early, concentrated around step-up (priming) dosing and the first full doses when CRS risk is highest (first days to weeks).”

§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.

Prerenal / Hemodynamic AKI#1 · Signature29%PMID 39805729 (opens PubMed in a new tab)
AKI in 29% (10/34) of teclistamab-treated RRMM vs 13% with CAR-T (retrospective)
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

29%incidence

SeverityModerate

ReversibilityReversible

Evidence9 citations

Nephron map

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

Prerenal / Hemodynamic AKI

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

§03

Kidney injury

Mechanism of kidney injury

T-cell activation drives cytokine release (IL-6, IFN-gamma, TNF); CRS causes hemodynamic (prerenal) renal hypoperfusion from vasodilation and capillary leak that can progress to ischemic acute tubular injury. Myeloma patients frequently have baseline cast nephropathy, light-chain proximal tubulopathy, and reduced GFR, which compound susceptibility; tumor lysis is generally less prominent than in acute leukemias.

Clinical presentation

Creatinine rise during CRS episodes (fever, hypotension, hypoxia), often superimposed on pre-existing myeloma-related kidney disease; oliguria in severe CRS. Concurrent infections (the dominant serious toxicity of BCMA bispecifics from hypogammaglobulinemia) can add septic AKI.

Management

Manage CRS by grade (supportive care, tocilizumab for the IL-6 axis, corticosteroids) and support renal perfusion with fluids; hold dosing for severe CRS. Renal recovery typically parallels CRS resolution. Address underlying myeloma kidney disease (light-chain reduction, hydration) and treat intercurrent infection concurrently.Lesion-level management framework

Risk factors

Higher-grade cytokine release syndrome
Pre-existing myeloma-related CKD/cast nephropathy
Volume depletion and concurrent nephrotoxins
High disease burden; intercurrent infection/sepsis

Prevention

Mandatory step-up (priming) dosing with premedication (corticosteroid, antihistamine, antipyretic) to reduce CRS severity
Inpatient or close monitoring during step-up dosing per protocol
Hydration, avoidance of additional nephrotoxins, and infection prophylaxis

Anticancer mechanism· how it treats cancer

T-cell-redirecting bispecific antibody binding B-cell maturation antigen (BCMA) on malignant plasma cells and CD3 on T cells, forming an immune synapse that triggers T-cell-mediated myeloma killing. Used in relapsed/refractory multiple myeloma.

Note · Renal toxicity is an emerging, indirect (CRS-mediated) signal rather than a direct nephrotoxic effect; quantitative renal data are limited for this newer agent and partly extrapolated from CAR-T/bispecific CRS-AKI cohorts.

§04

Clinical depth

Renal dose adjustment

No specific renal dose adjustment is established; teclistamab pharmacokinetics are not meaningfully renally dependent, and patients with renal impairment (including some on dialysis) have been treated. The operative levers are step-up dosing and holds for severe CRS rather than renal dose modification.

Dialyzability & ESKD dosing

Not dialyzable—an IgG-based bispecific antibody cleared by catabolism; not removed by hemodialysis and no supplemental dosing needed. Renal replacement therapy, if used, treats AKI, not drug clearance.

Differential diagnosis

Distinguish CRS-driven prerenal/ischemic AKI (hypotension, capillary leak) from progression of underlying myeloma cast nephropathy/light-chain tubulopathy (rising serum free light chains, Bence-Jones proteinuria) and from septic AKI due to infection. Timing relative to step-up dosing and CRS grade aids attribution.

Monitoring

Vital signs and CRS grading during step-up and early full doses
Serum creatinine/eGFR and electrolytes around dosing
Infection surveillance and immunoglobulin levels (hypogammaglobulinemia)

Key trials & series

MajesTEC-1 (Moreau NEJM 2022) registrational trial
Wen Onco Targets Ther 2024 bispecific-antibody nephrotoxicity review
Leon-Roman Clin Kidney J 2024 immune-effector-cell AKI cohort (analogous CRS-AKI)

Clinical pearls

AKI here is usually CRS hemodynamics layered on pre-existing myeloma kidney disease—evaluate both.
Step-up dosing with premedication is the key CRS-mitigation strategy and may thereby reduce AKI risk.
Tocilizumab plus supportive care manages severe CRS; renal recovery tracks CRS resolution.
Don't overlook infection: BCMA bispecifics cause profound hypogammaglobulinemia and septic AKI.

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

Class-level context for the major non-renal toxicities of the Bispecific (BCMA×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

§05

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 · 2019–2025 · 4 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.

Case reports — ranked by strength· 2

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 · ModerateSynergistic effect of teclistamab with PD-1 inhibition: a case of acute interstitial nephritis with dual immunotherapy.Mohan A et al. · Clin Kidney J 2025 · PMID 39974847Biopsy-confirmed acute interstitial nephritis with AKI in a patient on teclistamab combined with PD-1 inhibition, which the report attributes to synergistic dual-immunotherapy immune activation rather than a direct teclistamab tubulotoxic effect.CaseB · ModerateRecurrent cytokine release syndrome in patients receiving bispecific antibody therapy for multiple myeloma: a case series.Della Pepa R et al. · Ann Hematol 2026 · PMID 41882240A teclistamab-treated myeloma patient developed recurrent cyclic CRS that contributed to renal complications leading to treatment discontinuation, consistent with CRS-driven prerenal/hemodynamic kidney injury.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING: CYTOKINE RELEASE SYNDROME and NEUROLOGIC TOXICITY, including IMMUNE EFFECTOR CELL-ASSOCIATED NEUROTOXICITY SYNDROME Cytokine release syndrome (CRS), including life-threatening or fatal reactions, can occur in patients receiving TECVAYLI. Initiate treatment with TECVAYLI step-up dosing schedule to reduce risk of CRS. Withhold TECVAYLI until CRS resolves or permanently discontinue based on severity [see Dosage and Administration (2.1 , 2.5) and Warnings and Precautions (5.1) ] . Neurologic toxicity, including Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS) and serious, life-threatening, or fatal reactions, can occur in patients receiving TECVAYLI. Monitor patients for signs or symptoms of neurologic toxicity, including ICANS, during treatment. Withhold TECVAYLI until neurologic toxicity resolves or permanently discontinue based on severity [see Dosage and Administration (2.5) and Warnings and Precautions (5.2) ] . Because of the risk of CRS and neurologic toxicity, including ICANS, TECVAYLI is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called the TECVAYLI and TALVEY REMS [see Warnings and Precautions (5.3) ] . WARNING: CYTOKINE RELEASE SYNDROME and NEUROLOGIC TOXICITY including IMMUNE EFFECTOR CELL-ASSOCIATED NEUROTOXICITY SYNDROME See full prescribing information for complete boxed warning. Cytokine…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 2,119 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· 19.9% of reports w/ death · 24.5% w/ hospitalization

19.9%

Reported with a death outcome

421 of 2,119 reports

24.5%

Reported with hospitalization

519 of 2,119 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 2,119 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 1.0495% CI 0.64–1.70· 16 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Immune / infection

Cytokine Release Syndrome508Infection112Covid-1979Pneumonia78Sepsis47

Nervous system

Immune Effector Cell-Associated Neurotoxicity Syndrome196Neuropathy Peripheral45Headache35Neurotoxicity32Progressive Multifocal Leukoencephalopathy32

General / constitutional

Fatigue93Pyrexia87Weight Decreased31

Blood & lymphatic

Neutropenia93Thrombocytopenia44Anaemia40Cytopenia32

Gastrointestinal

Diarrhoea56Nausea35

Skin

Rash36

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 Teclistamab 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 · 100% phenotype match

Tretinoin (ATRA)

Vesanoid · Retinoid (differentiating agent)

Profile

Differentiation syndrome → capillary leak and AKI.

PREATN

Moderate#2 · 89% phenotype match

Tagraxofusp

Elzonris · IL-3 immunotoxin

Profile

Capillary-leak syndrome → AKI.

PREATN

Moderate#3 · 89% phenotype match

Tasonermin

Beromun · Recombinant TNF-α (cytokine)

Profile

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

PREATN

Moderate#4 · 88% phenotype match

Tarlatamab

Imdelltra · Bispecific (DLL3×CD3)

Profile

2024 small-cell lung BiTE; CRS-driven AKI risk.

PREATN

Moderate#5 · 85% phenotype match

Blinatumomab

Blincyto · BiTE (CD19×CD3)

Profile

CRS and tumor lysis → AKI.

PREATNXTAL

Moderate#6 · 84% phenotype match

Compare Teclistamab 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.