What kind of kidney injury does Lisocabtagene maraleucel 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, Electrolyte Disturbance.

Is kidney injury from Lisocabtagene maraleucel reversible?

Reversible. Typical onset: Early — within the first days to about two weeks after the single infusion, tracking the CRS window. In a 155-patient cohort the median time to peak creatinine was 9.5 days (range 3-30); pediatric CD19 CAR-T AKI all occurred within 14 days; TLS-associated injury clusters around days 3-9..

How should kidney function be monitored during Lisocabtagene maraleucel therapy?

Daily serum creatinine, urine output and weight through the first 2-4 weeks post-infusion; CRS grade and vital signs (temperature, blood pressure, heart rate) — the leading AKI predictor; Electrolytes: phosphate, potassium, sodium and magnesium (derangements are near-universal); TLS panel (uric acid, phosphate, potassium, calcium, LDH) in high-tumor-burden patients; Inflammatory markers (ferritin, CRP) as severity/AKI-risk surrogates.

How can kidney injury from Lisocabtagene maraleucel be prevented?

Risk-stratify for TLS (bulky/high-count disease): hydration plus allopurinol or rasburicase before and through infusion Recognize and treat CRS early (tocilizumab ± corticosteroids) to abort the hemodynamic driver of AKI Optimize volume and avoid nephrotoxins (contrast, aminoglycosides, NSAIDs) around infusion Renally dose-reduce fludarabine in impaired kidney function — it accumulates and adds tubular stress

Who is at higher risk of kidney injury from Lisocabtagene maraleucel?

High-grade (grade ≥3) cytokine release syndrome — the most consistent driver; High tumor burden / elevated LDH and ferritin (inflammatory and TLS risk); Baseline chronic kidney disease or elevated pre-infusion creatinine; ICU admission and severe multi-organ CRS; Concomitant nephrotoxins and neutropenic sepsis; Higher-grade ICANS (neurotoxicity) in some cohorts; Prior autologous/allogeneic stem-cell transplant; older age; Product choice: axicabtagene ciloleucel carried higher AKI risk than other CD19 products in at least one comparative cohort.

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Printable monograph

CD19 CAR-T cell therapy

Lisocabtagene maraleucel

Q: How common is kidney injury with Lisocabtagene maraleucel?

Approximately 22% — No liso-cel-specific AKI rate is established — the renal literature pools across CD19 and BCMA CAR-T products. In a meta-analysis of 15 studies (694 patients), 22% developed AKI, most KDIGO stage 1 and reversible (Yang, Clin Immunol 2024). Single-center CAR-T cohorts report roughly 18-34% (Sharp, Br J Haematol 2025 — 18%; Gupta, Am J Kidney Dis 2020 — 19%; Ahmed, Clin Lymphoma Myeloma Leuk 2022 — 29%; Vincendeau/Zafrani ICU cohort, Clin Kidney J 2024 — 34%), with focused reviews quoting ~30% (Khan, Clin Hematol Int 2023). Because liso-cel carries the lowest grade ≥3 CRS of the CD19 CAR-Ts (2% in TRANSCEND NHL 001) and CRS severity is the dominant AKI driver, its CRS-related renal burden is expected to track at the lower end — but this is inference, not a measured liso-cel figure. (Source: Yang et al., Clin Immunol 2024 (pooled cross-CAR-T meta-analysis; not liso-cel-specific)).

Breyanzi · LISO

CD19 CAR-T cell therapy · approved 2021 · 8 citations · FAERS AKI reporting ROR 1.97 (95% CI 1.11–3.48, 12 AKI reports)

Up to date· through 2025

Fairly sourced6/9 · 6 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 5y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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.

The CD19 CAR-T with the lowest severe-CRS rate of its class — so its kidney story is the same cytokine-and-volume prerenal hit, just dialed down.

ModerateCD19-directed CAR-T cell therapy

Relapsed/refractory large B-cell lymphoma (DLBCL, high-grade B-cell lymphoma, primary mediastinal B-cell lymphoma, follicular lymphoma grade 3B), second-line and laterRelapsed/refractory chronic lymphocytic leukemia / small lymphocytic lymphomaRelapsed/refractory follicular lymphomaRelapsed/refractory mantle cell lymphoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Representative incidence22%

18–34% range across studies

No liso-cel-specific AKI rate is established — the renal literature pools across CD19 and BCMA CAR-T products. In a meta-analysis of 15 studies (694 patients), 22% developed AKI, most KDIGO stage 1 and reversible (Yang, Clin Immunol 2024). Single-center CAR-T cohorts report roughly 18-34% (Sharp, Br J Haematol 2025 — 18%; Gupta, Am J Kidney Dis 2020 — 19%; Ahmed, Clin Lymphoma Myeloma Leuk 2022 — 29%; Vincendeau/Zafrani ICU cohort, Clin Kidney J 2024 — 34%), with focused reviews quoting ~30% (Khan, Clin Hematol Int 2023). Because liso-cel carries the lowest grade ≥3 CRS of the CD19 CAR-Ts (2% in TRANSCEND NHL 001) and CRS severity is the dominant AKI driver, its CRS-related renal burden is expected to track at the lower end — but this is inference, not a measured liso-cel figure.Source: Yang et al., Clin Immunol 2024 (pooled cross-CAR-T meta-analysis; not liso-cel-specific)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

AKI tracks the CRS window in the first days to ~2 weeks after the single infusion; in a 155-patient CAR-T cohort, 18% developed AKI with a median time to peak creatinine of ~9.5 days.

Distilled from: “Among 155 patients undergoing CAR-T for relapsed/refractory large B-cell lymphoma, 28 (18%) developed AKI with a median time-to-peak creatinine from CAR-T of ~9.5 days — early, tracking the CRS window in the first days to about two weeks after the single infusion.” · PMID 40589093 (opens PubMed in a new tab)

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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.
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).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

22%incidence

SeverityModerate

ReversibilityReversible

Evidence8 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

The signature injury is hemodynamic and cytokine-mediated rather than a direct tubular toxin. Cytokine release syndrome (CRS) — an IL-6/IFN-γ-driven inflammatory surge as the CAR-T cells engage CD19+ targets — produces vasodilation, capillary leak, fever and hypotension, causing intravascular volume depletion and prerenal AKI that can progress to ischemic acute tubular necrosis if hypoperfusion persists; grade ≥3 CRS is the most consistently identified risk factor across cohorts. Rapid tumor cytolysis can precipitate tumor lysis syndrome (TLS) with uric-acid and calcium-phosphate crystal deposition/obstruction in the tubular lumen. The fludarabine/cyclophosphamide lymphodepletion adds prerenal and tubular stress (fludarabine is renally cleared), high peak inflammatory cytokines correlate with AKI, and neutropenic sepsis contributes ischemic injury; direct CAR-T renal infiltration is described but rare. Electrolyte wasting (hypophosphatemia, hypokalemia, hyponatremia) accompanies the systemic inflammatory/hemodynamic state and is more common than frank AKI.

Clinical presentation

A creatinine rise in the first days-to-weeks after infusion, typically coinciding with fever, tachycardia and hypotension of CRS. Early physiology is prerenal (oliguria, low fractional excretion of sodium, brisk response to fluids); persistent hypoperfusion evolves to ATN with muddy-brown granular casts. Electrolyte derangements are near-universal — hypophosphatemia (~75%), hypokalemia (~56%) and hyponatremia (~51%) in the DLBCL CAR-T series (Gupta, Am J Kidney Dis 2020). When TLS is present, hyperuricemia, hyperphosphatemia, hyperkalemia and a rising LDH appear.

Management

Largely supportive and directed at the underlying CRS. Treat CRS promptly with tocilizumab (and corticosteroids for higher grades), which relieves the capillary-leak hypotension that drives most AKI; give judicious IV fluids and, if needed, vasopressors for prerenal/distributive hypotension; support ischemic ATN. Apply standard TLS measures (aggressive hydration, rasburicase/allopurinol, electrolyte correction) when tumor lysis is present. Hold nephrotoxins and treat neutropenic sepsis. Most AKI is stage 1 and recovers; across pooled cohorts only ~10% required renal replacement therapy and renal recovery is the rule (e.g., 25/28 recovered by a median of 14 days in one series). AKI nonetheless marks a sicker, higher-inflammation course and is associated with worse survival.Lesion-level management framework

Risk factors

High-grade (grade ≥3) cytokine release syndrome — the most consistent driver
High tumor burden / elevated LDH and ferritin (inflammatory and TLS risk)
Baseline chronic kidney disease or elevated pre-infusion creatinine
ICU admission and severe multi-organ CRS
Concomitant nephrotoxins and neutropenic sepsis
Higher-grade ICANS (neurotoxicity) in some cohorts
Prior autologous/allogeneic stem-cell transplant; older age
Product choice: axicabtagene ciloleucel carried higher AKI risk than other CD19 products in at least one comparative cohort

Prevention

Risk-stratify for TLS (bulky/high-count disease): hydration plus allopurinol or rasburicase before and through infusion
Recognize and treat CRS early (tocilizumab ± corticosteroids) to abort the hemodynamic driver of AKI
Optimize volume and avoid nephrotoxins (contrast, aminoglycosides, NSAIDs) around infusion
Renally dose-reduce fludarabine in impaired kidney function — it accumulates and adds tubular stress

Anticancer mechanism· how it treats cancer

Autologous CD19-directed chimeric antigen receptor (CAR) T-cell product with 4-1BB costimulation, manufactured and infused at a defined 1:1 CD4:CD8 composition after fludarabine/cyclophosphamide lymphodepletion. The CAR redirects the patient's T cells to CD19 on malignant B cells, driving T-cell activation, proliferation and cytolysis of the tumor. It is a one-time single infusion, not a chronically dosed drug.

Note · Liso-cel-specific renal data are sparse; the incidence figures and mechanisms are drawn from the pooled CD19/BCMA CAR-T nephrotoxicity literature and are hedged accordingly. The signature signal is CRS-driven prerenal/hemodynamic AKI with TLS crystal nephropathy as the second pathway, both concentrated in the first two weeks and usually reversible. Reversibility is coded 'reversible' to reflect the dominant course (most cohorts show renal recovery), though a sicker ICU subgroup showed CKD sequelae at 6-12 months.

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Clinical depth

Renal dose adjustment

Liso-cel is a one-time, per-kilogram CAR+ T-cell dose with no renal dose adjustment for the cell product itself and no CrCl threshold on the label. The renal-relevant lever is the lymphodepletion regimen: fludarabine is renally cleared and should be dose-reduced in kidney impairment to limit accumulation and tubular toxicity. CAR-T has been delivered feasibly in patients with reduced renal function and even end-stage renal disease with careful lymphodepletion planning, and baseline renal impairment did not worsen renal or efficacy outcomes in a matched cohort (Wood, Transplant Cell Ther 2022).

Dialyzability & ESKD dosing

Not applicable to the living CAR-T cells, which are not removed by dialysis. Circulating cytokines are only partially cleared by extracorporeal modalities and this is not standard therapy. Fludarabine's active metabolite (in the conditioning regimen) is partly dialyzable but timing is not standardized. CAR-T therapy has been administered successfully to dialysis-dependent patients, so ESRD is not an absolute contraindication (Wood, Transplant Cell Ther 2022; Khan, Clin Hematol Int 2023).

Differential diagnosis

Distinguish CRS-driven prerenal AKI / ischemic ATN (hypotension, fever, timed to the CRS window) from TLS crystal nephropathy (hyperuricemia/hyperphosphatemia, rising LDH, days 3-9), from fludarabine/cyclophosphamide tubular effects and hemorrhagic cystitis, from contrast- or antimicrobial-related nephrotoxicity, and from neutropenic-sepsis ATN. Timing relative to CRS and the electrolyte/urate pattern usually identify the dominant mechanism. Across products, axicabtagene ciloleucel (axi-cel) carries a higher CRS and AKI burden than liso-cel or tisagenlecleucel (tisa-cel), whose 4-1BB constructs produce milder cytokine kinetics.

Monitoring

Daily serum creatinine, urine output and weight through the first 2-4 weeks post-infusion
CRS grade and vital signs (temperature, blood pressure, heart rate) — the leading AKI predictor
Electrolytes: phosphate, potassium, sodium and magnesium (derangements are near-universal)
TLS panel (uric acid, phosphate, potassium, calcium, LDH) in high-tumor-burden patients
Inflammatory markers (ferritin, CRP) as severity/AKI-risk surrogates

Key trials & series

TRANSCEND NHL 001 (Abramson, Lancet 2020) — registrational phase 1 in relapsed/refractory large B-cell lymphoma; grade ≥3 CRS in only 2% and grade ≥3 neurological events in 10%, the low-CRS profile that frames liso-cel's comparatively modest CRS-driven AKI risk
Gupta, Am J Kidney Dis 2020 — foundational two-center CAR-T (axi-cel/tisa-cel) nephrotoxicity series: AKI 19% (prerenal and ATN) with the electrolyte-abnormality spectrum
Sharp, Br J Haematol 2025 — 155-patient DLBCL cohort defining onset, causes (volume depletion 71%, CRS 18%, TLS 4%) and the axi-cel-versus-other-product risk difference; AKI linked to inferior survival
Yang, Clin Immunol 2024 — meta-analysis (694 patients) anchoring the ~22% pooled AKI incidence

Clinical pearls

Liso-cel's grade ≥3 CRS rate is the lowest of the CD19 CAR-Ts (2% in TRANSCEND), so its CRS-driven AKI should track lower — but the mechanism is identical to axi-cel/tisa-cel, just less intense.
Most post-CAR-T AKI is prerenal from CRS capillary-leak hypotension and reverses as CRS is controlled with tocilizumab — treat the cytokine storm, not just the creatinine.
Electrolyte derangements (hypophosphatemia, hypokalemia, hyponatremia) are more common than frank AKI and are easy to miss.
AKI after CAR-T is a red flag for a severe-inflammation phenotype and is associated with worse progression-free and overall survival — it is prognostic, not merely renal.
Dialysis dependence and reduced eGFR are not absolute contraindications: CAR-T has been delivered safely with careful, dose-adjusted lymphodepletion planning.

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

Class-level context for the major non-renal toxicities of cd19 car-t cell therapys.

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

8 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

8 references · 2020–2025 · 4 since 2023

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Feb 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), including fatal or life-threatening reactions, occurred in patients receiving BREYANZI. Do not administer BREYANZI to patients with active infection or inflammatory disorders. Treat severe or life-threatening CRS with tocilizumab with or without corticosteroids [see Dosage and Administration ( 2.2 , 2.3 ) and Warnings and Precautions ( 5.1 )] . • Neurologic toxicities, including fatal or life-threatening reactions, occurred in patients receiving BREYANZI, including concurrently with CRS, after CRS resolution, or in the absence of CRS. Monitor for neurologic events after treatment with BREYANZI. Provide supportive care and/or corticosteroids as needed [see Dosage and Administration ( 2.2 , 2.3 ) and 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, including BREYANZI [see Warnings and Precautions ( 5.7 )] . WARNING: CYTOKINE RELEASE SYNDROME, NEUROLOGIC TOXICITIES, AND SECONDARY HEMATOLOGICAL MALIGNANCIES See full prescribing information for complete boxed warning. • Cytokine Release Syndrome (CRS), including fatal or life-threatening reactions, occurred in patients receiving BREYANZI. Do not…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 846 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· 17.8% of reports w/ death · 50.6% w/ hospitalization

17.8%

Reported with a death outcome

151 of 846 reports

50.6%

Reported with hospitalization

428 of 846 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 846 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 2026-08-08.

Disproportionality (acute kidney injury):ROR 1.9795% CI 1.11–3.48· 12 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Immune / infection

Cytokine Release Syndrome352Pneumonia18

Nervous system

Immune Effector Cell-Associated Neurotoxicity Syndrome162Neurotoxicity104Aphasia25Tremor23Encephalopathy21

Blood & lymphatic

Febrile Neutropenia26Platelet Count Decreased26Neutropenia21Neutrophil Count Decreased17Haemoglobin Decreased15

General / constitutional

Pyrexia50Fatigue39

Vascular

Hypotension41

Psychiatric

Confusional State31

Metabolic & electrolyte

Decreased Appetite17

Respiratory

Pleural Effusion15

Gastrointestinal

Nausea14

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.

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 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 Lisocabtagene maraleucel 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 · 89% phenotype match

Ciltacabtagene autoleucel

Carvykti · BCMA CAR-T cell therapy

Profile

CRS-driven AKI; delayed neurotoxicity.

PREATNLYTE

Moderate#2 · 88% phenotype match

Odronextamab

Ordspono · Bispecific (CD20×CD3)

Profile

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

XTALPRELYTE

Moderate#3 · 83% 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 · 83% phenotype match

Obinutuzumab

Gazyva · Anti-CD20 antibody

Profile

High tumor-lysis risk in CLL.

XTALATNPRE

Moderate#5 · 80% phenotype match

Rituximab

Rituxan · Anti-CD20 antibody

Profile

Tumor lysis with bulky disease; treats some GN.

XTALATNPRE

Moderate#6 · 80% phenotype match

Compare Lisocabtagene maraleucel 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 vicleucelPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate
5Lisocabtagene maraleucel· this agentPRE — 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.