What kind of kidney injury does Idecabtagene vicleucel 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, Electrolyte Disturbance, Crystal / Obstructive Nephropathy.

Is kidney injury from Idecabtagene vicleucel reversible?

Reversible. Typical onset: Within the first 1-2 weeks (the CRS window)..

How should kidney function be monitored during Idecabtagene vicleucel therapy?

Daily creatinine, electrolytes, uric acid and LDH during the CRS window; CRS and ICANS grading (ASTCT criteria); Volume status and blood pressure.

How can kidney injury from Idecabtagene vicleucel be prevented?

Tumor-lysis prophylaxis (hydration, allopurinol; rasburicase if high-risk) Avoid nephrotoxins and use judicious fluids Renally dose-reduce lymphodepleting fludarabine Early CRS recognition and treatment

Who is at higher risk of kidney injury from Idecabtagene vicleucel?

Grade >=3 CRS and ICU-level care; Prior autologous/allogeneic stem-cell transplant; Baseline CKD and high tumor burden; Volume depletion.

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Printable monograph

BCMA CAR-T cell therapy

Idecabtagene vicleucel

Abecma · IDEC

BCMA CAR-T cell therapy · approved 2021 · 9 citations · FAERS AKI reporting ROR 5.47 (95% CI 4.09–7.33, 47 AKI reports)

Up to date· through 2026

Fairly sourced6/9 · 6 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
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 BCMA CAR-T whose AKI is IL-6-driven and prerenal — it reverses as the cytokine-release syndrome resolves.

ModerateBCMA CAR-T cell therapy

Relapsed or refractory multiple myeloma after prior lines including an immunomodulatory agent, a proteasome inhibitor and an anti-CD38 antibody

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Published CAR-T AKI incidence runs roughly 5-30% across cohorts and is mostly mild (KDIGO stage 1); in one cohort any-grade AKI reached ~30% by day 100 with rapid recovery. Most AKI parallels cytokine-release syndrome (CRS) and reverses within ~30 days.Source: Gutgarts et al., Biol Blood Marrow Transplant 2020

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Within the first 1–2 weeks (the CRS window).

Distilled from: “Within the first 1-2 weeks (the CRS window).”

§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 · 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.
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).
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

Evidence9 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.

§03

Kidney injury

Deep diveCAR-T cytokine-release acute kidney injuryCAR-T cells cure by inflammation, and the same cytokine-release syndrome that fevers and drops the blood pressure starves the kidney of perfusion — so the acute kidney injury after CAR-T is mostly pre-renal and mostly reversible, yet the patients who develop it are the sicker ones, and they do worse.

Mechanism of kidney injury

AKI is predominantly hemodynamic/prerenal, driven by cytokine-release syndrome. Activated CAR-T and bystander myeloid cells release IL-6 (the central mediator) plus IL-1, IFN-gamma and TNF-alpha, causing vasodilation, capillary leak, hypotension and reduced renal perfusion — prerenal/ischemic AKI that can progress to ATN if severe or prolonged. Secondary contributors include tumor lysis (uric acid and calcium-phosphate crystal nephropathy in high-burden disease), nephrotoxic antimicrobials/contrast, and lymphodepleting fludarabine/cyclophosphamide.

Clinical presentation

AKI typically arises on days 1-14, paralleling CRS onset (fever, hypotension, hypoxia), with a rising creatinine and low urine output; if tumor lysis is present, expect hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia and a high LDH.

Management

Treat CRS with tocilizumab (anti-IL-6R) with or without corticosteroids, and support hemodynamics with IV fluids for the prerenal physiology. Manage tumor lysis (rasburicase, electrolyte correction). Renal replacement therapy is rarely needed; AKI usually reverses as CRS resolves.Lesion-level management framework

Risk factors

Grade >=3 CRS and ICU-level care
Prior autologous/allogeneic stem-cell transplant
Baseline CKD and high tumor burden
Volume depletion

Prevention

Tumor-lysis prophylaxis (hydration, allopurinol; rasburicase if high-risk)
Avoid nephrotoxins and use judicious fluids
Renally dose-reduce lymphodepleting fludarabine
Early CRS recognition and treatment

Anticancer mechanism· how it treats cancer

Autologous T cells transduced with a BCMA-directed chimeric antigen receptor (anti-BCMA scFv with 4-1BB costimulatory and CD3-zeta signaling domains). Binding to B-cell maturation antigen on malignant plasma cells triggers cytotoxic T-cell activation, proliferation and myeloma-cell lysis.

Note · Frontier-era 2021 therapy; the renal signal is CRS/IL-6-mediated prerenal AKI, supported by dedicated CAR-T onconephrology cohorts.

§04

Clinical depth

Renal dose adjustment

No CAR-T dose adjustment for renal function (it is a fixed cell product); the renal-relevant lever is the conditioning regimen, where fludarabine requires renal dose consideration. Cohort data show CAR-T is feasible even with reduced renal function or on dialysis.

Dialyzability & ESKD dosing

Not applicable — a living-cell product. Dialysis is used to support AKI/tumor lysis, not to remove the therapy.

Differential diagnosis

Tumor lysis versus prerenal CRS-AKI versus ATN versus fludarabine/contrast nephrotoxicity versus sepsis-associated AKI. Timing relative to CRS and the metabolic panel usually identify the dominant mechanism.

Monitoring

Daily creatinine, electrolytes, uric acid and LDH during the CRS window
CRS and ICANS grading (ASTCT criteria)
Volume status and blood pressure

Key trials & series

KarMMa (Munshi, NEJM 2021) — pivotal phase 2 registrational trial
Gutgarts CAR-T AKI cohort (Biol Blood Marrow Transplant 2020) — incidence and rapid recovery

Clinical pearls

IL-6 is the linchpin — CRS-AKI is largely prerenal and reverses as CRS resolves.
Tocilizumab treats CRS but penetrates the CNS poorly, so it does not treat ICANS.
Pre-existing CKD or dialysis is not an absolute contraindication to CAR-T.
Published CAR-T AKI incidence is ~5-30%, mostly mild (KDIGO stage 1).

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

Class-level context for the major non-renal toxicities of the BCMA CAR-T cell therapy 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

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

Evidence accrual

9 references · 2019–2026 · 5 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.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Nov 2025) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: CYTOKINE RELEASE SYNDROME, NEUROLOGIC TOXICITIES, HLH/MAS, PROLONGED CYTOPENIA, AND SECONDARY HEMATOLOGICAL MALIGNANCIES • Cytokine Release Syndrome (CRS), including fatal or life-threatening reactions, occurred in patients following treatment with ABECMA. Do not administer ABECMA to patients with active infection or inflammatory disorders. Treat severe or life-threatening CRS with tocilizumab or tocilizumab and corticosteroids [see Dosage and Administration (2.2 , 2.3) , Warnings and Precautions (5.2) ] . • Neurologic toxicities, which may be severe or life-threatening, occurred following treatment with ABECMA, including concurrently with CRS, after CRS resolution, or in the absence of CRS. Monitor for neurologic events after treatment with ABECMA. Provide supportive care and/or corticosteroids as needed [see Dosage and Administration (2.2 , 2.3) and Warnings and Precautions (5.3) ] . • Hemophagocytic Lymphohistiocytosis/Macrophage Activation Syndrome (HLH/MAS) including fatal and life-threatening reactions, occurred in patients following treatment with ABECMA. HLH/MAS can occur with CRS or neurologic toxicities [see Warnings and Precautions (5.4) ] . • Prolonged Cytopenia with bleeding and infection, including fatal outcomes following stem cell transplantation for hematopoietic recovery, occurred following treatment with ABECMA [see Warnings and Precautions (5.7) ]…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,221 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· 14.1% of reports w/ death · 34.3% w/ hospitalization

14.1%

Reported with a death outcome

172 of 1,221 reports

34.3%

Reported with hospitalization

419 of 1,221 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 10 systems · 1,221 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 5.4795% CI 4.09–7.33· 47 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury47

Immune / infection

Cytokine Release Syndrome696Sepsis27

Nervous system

Immune Effector Cell-Associated Neurotoxicity Syndrome195Neurotoxicity77Headache55Somnolence34Tremor30

Blood & lymphatic

Neutropenia86Anaemia79Thrombocytopenia52Cytopenia47Pancytopenia34

General / constitutional

Fatigue160Pyrexia72

Gastrointestinal

Nausea56Diarrhoea46

Metabolic & electrolyte

Decreased Appetite55

Hepatobiliary

Aspartate Aminotransferase Increased48

Vascular

Hypotension45

Cardiac

Tachycardia29

Guidelines & consensus· 20

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.

NCCNNCCN Guidelines Insights: Management of Immunotherapy-Related Toxicities, Version 2.2024J Natl Compr Canc Netw 2024 · PMID 39536465For mild MNTs, steroids such as dexamethasone 10 mg daily can be considered. For persistent, severe, or refractory MNTs, and if high circulating CAR T-cell levels are detected, chemotherapy such as cyclophosphamide can be considered.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 Idecabtagene vicleucel 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

Ciltacabtagene autoleucel

Carvykti · BCMA CAR-T cell therapy

Profile

CRS-driven AKI; delayed neurotoxicity.

PREATNLYTE

Moderate#1 · 100% phenotype match

Lisocabtagene maraleucel

Breyanzi · CD19 CAR-T cell therapy

Profile

CRS-driven prerenal AKI and tumor-lysis crystal nephropathy in the first weeks; low severe-CRS rate softens the renal burden.

PREATNXTAL

Moderate#2 · 89% phenotype match

Odronextamab

Ordspono · Bispecific (CD20×CD3)

Profile

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

XTALPRELYTE

Moderate#3 · 81% phenotype match

Pivekimab sunirine

Decnupaz · CD123 antibody-drug conjugate

Profile

2026 CD123 ADC for BPDCN; renal risk indirect — TLS in the CD123+ disease plus the CD123-class capillary-leak concern; its own dose-limiting toxicity was reversible VOD.

PREXTALLYTE

Moderate#4 · 81% phenotype match

Obinutuzumab

Gazyva · Anti-CD20 antibody

Profile

High tumor-lysis risk in CLL.

XTALATNPRE

Moderate#5 · 78% phenotype match

Rituximab

Rituxan · Anti-CD20 antibody

Profile

Tumor lysis with bulky disease; treats some GN.

XTALATNPRE

Moderate#6 · 78% phenotype match

Compare Idecabtagene vicleucel 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 CAR-T cell therapy

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.

1Obecabtagene autoleucel (Obe-cel)PRE — Prerenal / Hemodynamic AKIModerate
2CAR-T cell therapyPRE — Prerenal / Hemodynamic AKIModerate
3Ciltacabtagene autoleucelPRE — Prerenal / Hemodynamic AKIModerate
4Idecabtagene vicleucel· this agentPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate
5Lisocabtagene maraleucelPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate

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.