What kind of kidney injury does Ciltacabtagene autoleucel 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 Ciltacabtagene autoleucel reversible?

Reversible. Typical onset: AKI in the first 1-2 weeks; the movement disorder is delayed (weeks)..

How should kidney function be monitored during Ciltacabtagene autoleucel therapy?

Daily renal, electrolyte and tumor-lysis labs during CRS; CRS/ICANS grading (ASTCT criteria); Prolonged neurologic monitoring for the delayed movement disorder.

How can kidney injury from Ciltacabtagene autoleucel be prevented?

Tumor-lysis prophylaxis (hydration, allopurinol/rasburicase) Early tocilizumab with or without corticosteroids for CRS, to abort the hemodynamic driver of AKI Nephrotoxin avoidance and renal dosing of fludarabine conditioning

Who is at higher risk of kidney injury from Ciltacabtagene autoleucel?

High tumor burden; High-grade CRS/ICANS; Prior transplant; Baseline CKD.

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Printable monograph

BCMA CAR-T cell therapy

Ciltacabtagene autoleucel

Carvykti · CILT

BCMA CAR-T cell therapy · approved 2022 · 10 citations

Up to date· through 2026

Fairly sourced5/9 · 5 signals

Met: 10 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 6y)
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 high-avidity BCMA CAR-T sharing ide-cel's CRS-driven prerenal AKI — with a signature delayed parkinsonism not to be mistaken for uremia.

ModerateBCMA CAR-T cell therapy

Relapsed or refractory multiple myeloma (after >=1 prior line including a proteasome inhibitor and an immunomodulatory agent, lenalidomide-refractory, in the expanded indication)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

CRS-associated AKI mirrors the BCMA CAR-T class (roughly 5-30% across cohorts, mostly mild) and generally reverses with supportive care. A distinct, non-renal signature toxicity is a delayed movement-and-neurocognitive (parkinsonism-like) syndrome, named MNTs by NCCN: about 3% of ciltacabtagene recipients across CARTITUDE-1 and CARTITUDE-4 showed parkinsonism consistent with it, grade 3 or worse in 2%.Source: Berdeja et al., Lancet 2021

Onset & rechallenge

Time to injuryAcute (~1–7 days)

AKI in the first 1–2 weeks after infusion.

Distilled from: “AKI in the first 1-2 weeks; the movement disorder is delayed (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 · 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

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.

§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

The same CRS-driven, IL-6-mediated prerenal/hemodynamic AKI as ide-cel, with tumor-lysis crystal nephropathy in high-burden disease. The notable distinct toxicity is delayed neurotoxicity — a movement/neurocognitive (parkinsonism-like) syndrome hypothesized to relate to basal-ganglia BCMA expression — which is not renal but a hallmark management concern.

Clinical presentation

CRS often has a slightly later onset than ide-cel (median ~7 days), with AKI tracking CRS. A delayed parkinsonism/movement disorder can emerge weeks after infusion, frequently after ICANS.

Management

Tocilizumab with or without corticosteroids for CRS, plus hemodynamic/renal support and standard tumor-lysis management (rasburicase, allopurinol, hydration). For the movement-and-neurocognitive treatment-emergent adverse events (MNTs), NCCN v2.2024 records that the syndrome is levodopa-unresponsive — which distinguishes it from Parkinson disease — and that dexamethasone 10 mg daily may be considered for mild MNTs, with cyclophosphamide for persistent, severe or refractory disease when circulating CAR T-cell levels are high. The panel states that optimal management remains under investigation, and both agents rest on very limited data.Lesion-level management framework

Risk factors

High tumor burden
High-grade CRS/ICANS
Prior transplant
Baseline CKD

Prevention

Tumor-lysis prophylaxis (hydration, allopurinol/rasburicase)
Early tocilizumab with or without corticosteroids for CRS, to abort the hemodynamic driver of AKI
Nephrotoxin avoidance and renal dosing of fludarabine conditioning

Anticancer mechanism· how it treats cancer

Autologous BCMA-directed CAR-T bearing two BCMA-binding single-domain antibodies (bivalent) with 4-1BB and CD3-zeta domains, giving high avidity for BCMA on myeloma cells and driving T-cell activation and plasma-cell killing.

Note · Frontier-era 2022 therapy; renal mechanism is shared BCMA CAR-T CRS-driven prerenal AKI, with the distinctive delayed movement disorder flagged for differential awareness.

§04

Clinical depth

Renal dose adjustment

A fixed cell product with no renal dose adjustment; renal dosing applies to the lymphodepleting fludarabine.

Dialyzability & ESKD dosing

Not applicable (a living-cell product). Dialysis supports AKI/tumor lysis rather than removing the therapy.

Differential diagnosis

CRS-prerenal AKI versus tumor lysis versus ATN versus fludarabine nephrotoxicity; and for neurologic decline, ICANS versus the delayed parkinsonism — do not attribute late neuro changes to uremia.

Monitoring

Daily renal, electrolyte and tumor-lysis labs during CRS
CRS/ICANS grading (ASTCT criteria)
Prolonged neurologic monitoring for the delayed movement disorder

Key trials & series

CARTITUDE-1 (Berdeja, Lancet 2021) — pivotal phase 1b/2 registrational trial
CARTITUDE-4 (San-Miguel, NEJM 2023) — randomized trial supporting earlier-line use

Clinical pearls

Cilta-cel shares CAR-T renal physiology with ide-cel — AKI is CRS/IL-6-mediated and mostly prerenal.
The signature unique toxicity is delayed parkinsonism; renal teams should not attribute late neurologic decline to uremia.
Tumor-lysis risk is highest with bulky disease.
AKI generally reverses with supportive care as CRS resolves.

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. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

9 references · 2020–2026 · 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· 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 · ModerateMinimal Change Disease Following B-Cell Maturation Antigen-Directed Chimeric Antigen Receptor T-Cell Therapy.Shivaraj K et al. · Kidney Med 2026 · PMID 42004656Reports minimal change disease with AKI and nephrotic-range proteinuria 3 weeks after ciltacabtagene autoleucel, with biopsy-proven podocyte foot process effacement attributed to on-target off-tumor BCMA-directed CAR-T podocyte injury.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING: CYTOKINE RELEASE SYNDROME, NEUROLOGIC TOXICITIES, HLH/MAS, PROLONGED and RECURRENT CYTOPENIA, and SECONDARY HEMATOLOGICAL MALIGNANCIES Cytokine Release Syndrome (CRS), including fatal or life-threatening reactions, occurred in patients following treatment with CARVYKTI. Do not administer CARVYKTI 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) ] . Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS), which may be fatal or life-threatening, occurred following treatment with CARVYKTI, including before CRS onset, concurrently with CRS, after CRS resolution, or in the absence of CRS. Monitor for neurologic events after treatment with CARVYKTI. Provide supportive care and/or corticosteroids as needed [see Dosage and Administration (2.2 , 2.3) , Warnings and Precautions (5.3) ] . Parkinsonism and Guillain-Barré syndrome (GBS) and their associated complications resulting in fatal or life-threatening reactions have occurred following treatment with CARVYKTI [see Warnings and Precautions (5.3) ] . Hemophagocytic Lymphohistiocytosis/Macrophage Activation Syndrome (HLH/MAS), including fatal and life-threatening reactions, occurred in patients following treatment with CARVYKTI. HLH/MAS can occur…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 5,875 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· 12.7% of reports w/ death · 34.9% w/ hospitalization

12.7%

Reported with a death outcome

748 of 5,875 reports

34.9%

Reported with hospitalization

2,051 of 5,875 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 5 systems · 5,875 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 1.0195% CI 0.75–1.36· 43 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Immune / infection

Cytokine Release Syndrome813Infection122Pneumonia115Covid-1999Sepsis89

General / constitutional

Pyrexia380Malaise195Fatigue190Asthenia116

Nervous system

Immune Effector Cell-Associated Neurotoxicity Syndrome335Neurotoxicity192

Gastrointestinal

Immune-Mediated Enterocolitis146Colitis108Diarrhoea103

Blood & lymphatic

Neutropenia126Thrombocytopenia99Cytopenia94

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 Ciltacabtagene autoleucel 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

Idecabtagene vicleucel

Abecma · BCMA CAR-T cell therapy

Profile

CRS-driven AKI and tumor lysis in myeloma.

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 · 88% 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 Ciltacabtagene autoleucel 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 autoleucel· this agentPRE — Prerenal / Hemodynamic AKIModerate
4Idecabtagene vicleucelPRE — 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.