What kind of kidney injury does Elranatamab 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, Crystal / Obstructive Nephropathy.

How should kidney function be monitored during Elranatamab therapy?

Vital signs and CRS grading during priming and early full doses; Tumor lysis labs and serum creatinine/eGFR around initiation in high-burden disease; Infection surveillance and immunoglobulin levels (hypogammaglobulinemia).

How can kidney injury from Elranatamab be prevented?

Two-step (priming) dosing with premedication and monitoring per protocol Tumor-lysis prophylaxis (hydration, uric-acid-lowering therapy) in high-burden disease; infection prophylaxis Hydration and avoidance of additional nephrotoxins

Who is at higher risk of kidney injury from Elranatamab?

Higher-grade cytokine release syndrome; Pre-existing myeloma-related CKD/cast nephropathy; High disease burden (CRS and tumor-lysis risk); Volume depletion, intercurrent infection, and concurrent nephrotoxins.

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Printable monograph

Bispecific (BCMA×CD3)

Elranatamab

Elrexfio · ELRA

Bispecific (BCMA×CD3) · approved 2023 · 10 citations

Up to date· through 2026

Deeply sourced7/9 · 6 signals

Met: 10 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 15y)
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 risk stems from cytokine release and, occasionally, tumor lysis.

ModerateBispecific antibody (BCMAxCD3)

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

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Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Cytokine release syndrome is common with elranatamab (about 58% in the pivotal MagnetisMM-3 trial, largely grade 1-2 with the two-step priming regimen); CRS-associated acute kidney injury, and occasionally tumor-lysis-related injury, are emerging case-level signals that are not separately well quantified, superimposed on frequent myeloma kidney disease.Source: Lesokhin et al., Nat Med 2023

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Early — around the two-step priming doses and the first full doses.

Distilled from: “Early, concentrated around the two-step priming doses and the first full doses.”

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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.
Crystal / Obstructive NephropathySecondaryqualitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityReversible

Evidence10 citations

Nephron map

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

Tubular Lumen

Prerenal / Hemodynamic AKI

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

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Kidney injury

Mechanism of kidney injury

T-cell activation drives cytokine release (IL-6, IFN-gamma, TNF); CRS produces hemodynamic (prerenal) hypoperfusion from vasodilation and capillary leak that can progress to ischemic acute tubular injury. Tumor lysis from rapid plasma-cell killing can add uric-acid/phosphate-mediated crystal and tubular injury; pre-existing myeloma kidney disease (cast nephropathy, light-chain tubulopathy) and infection (from BCMA-related hypogammaglobulinemia) compound risk.

Clinical presentation

Creatinine rise during CRS (fever, hypotension), sometimes with tumor-lysis metabolic derangements (hyperuricemia, hyperphosphatemia, hyperkalemia); often superimposed on baseline myeloma-related renal impairment, with septic AKI from intercurrent infection.

Management

Manage CRS by grade (supportive care, tocilizumab, corticosteroids) and tumor lysis aggressively (hydration, rasburicase/allopurinol, electrolyte correction, renal replacement if needed); hold dosing for severe CRS. Renal recovery generally follows control of the underlying syndrome; treat myeloma kidney disease and infection concurrently.Lesion-level management framework

Risk factors

Higher-grade cytokine release syndrome
Pre-existing myeloma-related CKD/cast nephropathy
High disease burden (CRS and tumor-lysis risk)
Volume depletion, intercurrent infection, and concurrent nephrotoxins

Prevention

Two-step (priming) dosing with premedication and monitoring per protocol
Tumor-lysis prophylaxis (hydration, uric-acid-lowering therapy) in high-burden disease; infection prophylaxis
Hydration and avoidance of additional nephrotoxins

Anticancer mechanism· how it treats cancer

Humanized BCMAxCD3 bispecific antibody that redirects T cells to kill BCMA-expressing myeloma cells via an immune synapse. Used in relapsed/refractory multiple myeloma.

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

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Clinical depth

Renal dose adjustment

No specific renal dose adjustment is established; elranatamab pharmacokinetics are not meaningfully renally dependent. Two-step priming dosing and holds for severe CRS, plus TLS prophylaxis, are the operative levers 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 treats AKI/TLS, not drug clearance.

Differential diagnosis

Separate CRS-driven prerenal/ischemic AKI from TLS crystal/urate nephropathy (hyperuricemia/hyperphosphatemia), from progression of myeloma cast nephropathy (rising free light chains), and from septic AKI. Timing with priming doses, CRS grade, and the tumor-lysis lab signature guide attribution.

Monitoring

Vital signs and CRS grading during priming and early full doses
Tumor lysis labs and serum creatinine/eGFR around initiation in high-burden disease
Infection surveillance and immunoglobulin levels (hypogammaglobulinemia)

Key trials & series

MagnetisMM-3 (Lesokhin Nat Med 2023) 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

Among the myeloma bispecifics, elranatamab carries a more explicit tumor-lysis as well as CRS-AKI signal—give TLS prophylaxis in high burden.
AKI is usually CRS hemodynamics layered on myeloma kidney disease, not direct tubular toxicity.
Two-step priming with premedication mitigates CRS and downstream AKI.
Watch for septic AKI from BCMA-related hypogammaglobulinemia and infection.

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

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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 · 2011–2026 · 4 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· 3

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.

CaseC · Limited[Elranatamab treatment in a refractory multiple myeloma patient on maintenance hemodialysis].Nagahama Y et al. · Rinsho Ketsueki 2026 · PMID 41621964Case report of elranatamab in a myeloma patient with acute kidney injury from cast nephropathy who became hemodialysis-dependent, experiencing grade 1 cytokine release syndrome, relevant to CRS-related hemodynamic effects on the kidney.CaseC · LimitedEfficacy and safety of bispecific antibodies in multiple myeloma patients with end-stage renal disease undergoing hemodialysis: a case report of elranatamab and a literature review.Ogiya D et al. · Ann Hematol 2025 · PMID 41152534Case report of elranatamab in a hemodialysis-dependent ESRD myeloma patient who developed grade 1 cytokine release syndrome with mild hypotension, illustrating the hemodynamic/prerenal vulnerability of renally impaired patients on this BCMAxCD3 bispecific.CaseC · LimitedElranatamab for Relapsed/Refractory Multiple Myeloma With Severe Renal Impairment Requiring Hemodialysis.Hoffmann M et al. · Hematol Oncol 2025 · PMID 40684380Case report of a dialysis-dependent end-stage renal disease myeloma patient treated with elranatamab who developed grade I cytokine release syndrome requiring tocilizumab/dexamethasone, documenting the CRS-driven hemodynamic risk in a severely renally impaired patient.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (May 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 ELREXFIO. Initiate treatment with ELREXFIO step-up dosing schedule to reduce the risk of CRS. Withhold ELREXFIO until CRS resolves or permanently discontinue based on severity [see Dosage and Administration (2.2 , 2.5 ), Warnings and Precautions (5.1) ] . • Neurologic toxicity, including Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS), and serious and life-threatening reactions, can occur in patients receiving ELREXFIO. Monitor patients for signs and symptoms of neurologic toxicity, including ICANS, during treatment. Withhold ELREXFIO until the neurologic toxicity resolves or permanently discontinue based on severity [see Dosage and Administration (2.5) , Warnings and Precautions (5.2) ] . • Because of the risk of CRS and neurologic toxicity, including ICANS, ELREXFIO is available only through a restricted program under a Risk Evaluation and Mitigation Strategy (REMS) called ELREXFIO 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 Release…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,037 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· 23.5% of reports w/ death · 28.8% w/ hospitalization

23.5%

Reported with a death outcome

244 of 1,037 reports

28.8%

Reported with hospitalization

299 of 1,037 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 1,037 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 0.9395% CI 0.44–1.95· 7 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Immune / infection

Cytokine Release Syndrome184Cytomegalovirus Infection Reactivation54Pneumonia46Infection43Cytomegalovirus Infection25

General / constitutional

Pyrexia70Fatigue51Asthenia23Pain18

Blood & lymphatic

Neutropenia35Anaemia26White Blood Cell Count Decreased21

Nervous system

Immune Effector Cell-Associated Neurotoxicity Syndrome51Neuropathy Peripheral19

Skin

Rash39Skin Exfoliation27

Gastrointestinal

Diarrhoea38

Vascular

Hypotension30

Metabolic & electrolyte

Decreased Appetite28

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 Elranatamab 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

Blinatumomab

Blincyto · BiTE (CD19×CD3)

Profile

CRS and tumor lysis → AKI.

PREATNXTAL

Moderate#1 · 100% phenotype match

Talquetamab

Talvey · Bispecific (GPRC5D×CD3)

Profile

CRS-related AKI — emerging.

PREATN

Moderate#2 · 84% phenotype match

Teclistamab

Tecvayli · Bispecific (BCMA×CD3)

Profile

CRS-associated AKI in myeloma — emerging signal.

PREATN

Moderate#3 · 84% phenotype match

CAR-T cell therapy

Kymriah · Yescarta · CAR-T cell therapy

Profile

CRS-driven prerenal AKI and tumor lysis.

PREATNXTAL

Moderate#4 · 81% phenotype match

Odronextamab

Ordspono · Bispecific (CD20×CD3)

Profile

CD20×CD3 bispecific; tumor-lysis urate crystal nephropathy with CRS.

XTALPRELYTE

Moderate#5 · 77% phenotype match

Tretinoin (ATRA)

Vesanoid · Retinoid (differentiating agent)

Profile

Differentiation syndrome → capillary leak and AKI.

PREATN

Moderate#6 · 73% phenotype match

Compare Elranatamab 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.