What kind of kidney injury does Obecabtagene autoleucel (Obe-cel) cause?

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

How should kidney function be monitored during Obecabtagene autoleucel (Obe-cel) therapy?

Serum creatinine and urine output through the CRS window; CRS grading (fever, hypotension, hypoxia); Tumor lysis labs: potassium, phosphate, calcium, uric acid, LDH; Volume status and weight; Baseline and serial eGFR.

How can kidney injury from Obecabtagene autoleucel (Obe-cel) be prevented?

Optimize volume status and renal function before lymphodepletion and infusion Tumor lysis prophylaxis (hydration, allopurinol or rasburicase) for high burden Early CRS recognition and grading Prompt CRS-directed therapy (tocilizumab, corticosteroids) to limit hemodynamic insult

Who is at higher risk of kidney injury from Obecabtagene autoleucel (Obe-cel)?

Higher-grade cytokine release syndrome; High leukemic/tumor burden (tumor lysis risk); Pre-existing chronic kidney disease or low baseline GFR; Volume depletion and hypotension; Concomitant nephrotoxins, contrast, and elevated baseline LDH.

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Printable monograph

CD19 CAR-T cell therapy

Obecabtagene autoleucel (Obe-cel)

Aucatzyl · CD19 CAR-T therapy

CD19 CAR-T cell therapy · approved 2024 · 5 citations

Up to date· through 2025

Fairly sourced4/9 · 4 signals

Not met: 5 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 1y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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.

CD19 CAR-T for adult B-ALL; renal risk is CRS- and tumor-lysis-associated, with notably lower high-grade CRS.

ModerateCD19 CAR-T cell therapy (fast off-rate binder)

Relapsed or refractory B-cell precursor acute lymphoblastic leukemia (B-ALL) in adults

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Obe-cel-specific renal injury rates are not separately well characterized; in the FELIX trial, CRS and immune effector cell-associated neurotoxicity were mostly low grade, with notably low high-grade rates. Across CD19 CAR-T programs, AKI is reported in roughly 5 to 33 percent of patients, driven mainly by CRS-related hemodynamics and tumor lysis, and is usually reversible. In one CAR-T AKI cohort, 18 percent developed AKI, most often from volume depletion or CRS, with renal recovery in the large majority. The lower high-grade CRS rate of obe-cel would be expected to translate into a comparatively lower burden of severe CRS-associated AKI, though direct data are limited.Source: 39602653

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Clusters with peak CRS in the first one to two weeks; early TLS as burden clears.

Distilled from: “Onset clusters with peak CRS in the first one to two weeks after infusion; tumor lysis tends to occur early as leukemic burden is cleared.”

§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.
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).

§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

Two linked mechanisms predominate. First, CRS produces fever, vasodilation, capillary leak, and hypotension that lower renal perfusion, causing prerenal azotemia and ischemic tubular injury. Second, rapid lysis of a high leukemic burden can cause tumor lysis syndrome with hyperuricemia and hyperphosphatemia, producing intratubular crystal/cast deposition and metabolic AKI. Obe-cel is not a direct tubular nephrotoxin; the kidney is injured secondarily by the inflammatory and metabolic consequences of effective tumor killing.

Clinical presentation

AKI usually presents during the CRS window with fever, hypotension, rising creatinine, and reduced urine output and a generally bland sediment. When tumor lysis dominates, hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia accompany the creatinine rise.

Management

Treat the driver: for CRS-associated AKI restore perfusion with fluids and vasopressors and give CRS-directed therapy (tocilizumab, corticosteroids per protocol); for tumor lysis use aggressive hydration and urate-lowering therapy with electrolyte correction. Most AKI is hemodynamic and reversible, with renal recovery in the majority; renal replacement therapy is reserved for severe or refractory cases.Lesion-level management framework

Risk factors

Higher-grade cytokine release syndrome
High leukemic/tumor burden (tumor lysis risk)
Pre-existing chronic kidney disease or low baseline GFR
Volume depletion and hypotension
Concomitant nephrotoxins, contrast, and elevated baseline LDH

Prevention

Optimize volume status and renal function before lymphodepletion and infusion
Tumor lysis prophylaxis (hydration, allopurinol or rasburicase) for high burden
Early CRS recognition and grading
Prompt CRS-directed therapy (tocilizumab, corticosteroids) to limit hemodynamic insult

Anticancer mechanism· how it treats cancer

Obecabtagene autoleucel is an autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy. The CAR uses a fast off-rate (low-affinity) binder designed to reduce excessive T-cell activation, allowing CD19-positive B lymphoblasts to be recognized and killed while limiting toxicity. It received FDA approval in November 2024 for relapsed or refractory adult B-cell acute lymphoblastic leukemia (B-ALL), and is notable for comparatively low rates of high-grade CRS and neurotoxicity.

§04

Clinical depth

Renal dose adjustment

Not applicable in the small-molecule sense - obe-cel is a one-time autologous cell product with no CrCl-based dose thresholds. No renal dose adjustment is established; attention to renal function is warranted for the lymphodepleting chemotherapy and supportive medications given around infusion.

Dialyzability & ESKD dosing

Not applicable. The CAR-T product is a living-cell therapy and is not dialyzable; dialysis serves only to support severe AKI or tumor-lysis metabolic derangements.

Differential diagnosis

Distinguish CRS-driven prerenal/ischemic AKI from tumor lysis syndrome (hyperuricemia, hyperphosphatemia, hyperkalemia) and from lymphodepletion-related or concomitant nephrotoxin injury. Timing relative to CRS and the tumor-lysis lab panel separate the two dominant mechanisms; bland sediment argues against primary glomerular or interstitial disease.

Monitoring

Serum creatinine and urine output through the CRS window
CRS grading (fever, hypotension, hypoxia)
Tumor lysis labs: potassium, phosphate, calcium, uric acid, LDH
Volume status and weight
Baseline and serial eGFR

Key trials & series

FELIX (NCT04404660): pivotal phase 1b/2 of obecabtagene autoleucel in relapsed/refractory adult B-ALL; high response rates with notably low rates of high-grade CRS and neurotoxicity, framing CRS/TLS-associated renal risk as comparatively modest.

Clinical pearls

High leukemic burden makes tumor lysis a key early renal threat - prophylax with hydration and urate-lowering therapy.
Most CAR-T AKI is hemodynamic and reversible; controlling CRS and TLS is the main renal-protective strategy.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Tubular Lumen

The urine flow path

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

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

Class-level context for the major non-renal toxicities of the CD19 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

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

Evidence accrual

5 references · 2024–2025 · 5 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.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING: CYTOKINE RELEASE SYNDROME, NEUROLOGIC TOXICITIES, and SECONDARY HEMATOLOGICAL MALIGNANCIES Cytokine Release Syndrome (CRS) occurred in patients receiving AUCATZYL. Do not administer AUCATZYL to patients with active infection or inflammatory disorders. Prior to administering AUCATZYL, ensure that healthcare providers have immediate access to medications and resuscitative equipment to manage CRS [see Dosage and Administration (2.2 , 2.3) , Warnings and Precautions (5.1) ]. Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS), including fatal or life-threatening reactions, occurred in patients receiving AUCATZYL, including concurrently with CRS or after CRS resolution. Monitor for neurologic signs and symptoms after treatment with AUCATZYL. Prior to administering AUCATZYL, ensure that healthcare providers have immediate access to medications and resuscitative equipment to manage neurologic toxicities. Provide supportive care and/or corticosteroids, as needed [see Dosage and Administration (2.2 , 2.3) , Warnings and Precautions (5.2) ]. T cell malignancies have occurred following treatment of hematologic malignancies with BCMA- and CD19-directed genetically modified autologous T cell immunotherapies [see Warnings and Precautions (5.8) ]. WARNING: CYTOKINE RELEASE SYNDROME, NEUROLOGIC TOXICITIES, and SECONDARY HEMATOLOGICAL MALIGNANCIES See full prescribing…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 52 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· 25% of reports w/ death · 69.2% w/ hospitalization

25%

Reported with a death outcome

13 of 52 reports

69.2%

Reported with hospitalization

36 of 52 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 52 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 2.6895% CI 0.37–19.39· 1 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Immune / infection

Cytokine Release Syndrome15Infection3Sepsis3Adenovirus Infection2Respiratory Syncytial Virus Infection2

Nervous system

Immune Effector Cell-Associated Neurotoxicity Syndrome7Immune Effector Cell-Associated Hlh-Like Syndrome3Headache2Neurotoxicity2

Blood & lymphatic

Pancytopenia8Febrile Neutropenia3Cytopenia2

General / constitutional

Pyrexia6Asthenia3Back Pain2

Musculoskeletal

Arthralgia2Myalgia2

Respiratory

Acute Respiratory Failure2

Hepatobiliary

Hyperbilirubinaemia2

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 Obecabtagene autoleucel (Obe-cel) 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

Olutasidenib

Rezlidhi · IDH1 inhibitor

Profile

Differentiation syndrome and tumor lysis in AML.

PRELYTE

Moderate#1 · 89% phenotype match

Gilteritinib

Xospata · FLT3 inhibitor

Profile

Differentiation syndrome, tumor lysis and PRES in AML.

PRELYTE

Moderate#2 · 89% phenotype match

Tafasitamab

Monjuvi · Anti-CD19 antibody

Profile

Tumor lysis and infusion reactions in lymphoma.

PRELYTE

Mild#3 · 83% phenotype match

Tazemetostat

Tazverik · EZH2 inhibitor

Profile

Tumor lysis; generally low direct renal toxicity.

PRELYTE

Mild#4 · 83% phenotype match

Mogamulizumab

Poteligeo · Anti-CCR4 antibody

Profile

Tumor lysis and rare AKI; cutaneous T-cell lymphoma.

PRELYTE

Mild#5 · 83% phenotype match

Midostaurin

Rydapt · FLT3 / multikinase inhibitor

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild#6 · 83% phenotype match

Compare Obecabtagene autoleucel (Obe-cel) 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)· this agentPRE — Prerenal / Hemodynamic AKIModerate
2CAR-T cell therapyPRE — Prerenal / Hemodynamic AKIModerate
3Ciltacabtagene autoleucelPRE — 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.