What kind of kidney injury does CAR-T Cell Therapy 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.

Is kidney injury from CAR-T Cell Therapy reversible?

Reversible. Typical onset: Acute — within the CRS window (first days–weeks)..

How should kidney function be monitored during CAR-T Cell Therapy therapy?

Daily creatinine, urine output and volume status through the CRS window (roughly days 1-14 post-infusion); CRS and ICANS grading by ASTCT criteria; Tumor-lysis labs (potassium, phosphate, uric acid, calcium) before and after infusion in high-burden disease; Electrolytes and fluid balance during tocilizumab / vasopressor / IV-fluid management; Trend to recovery — most CRS-associated AKI is reversible as CRS resolves.

How can kidney injury from CAR-T Cell Therapy be prevented?

Tumor-lysis prophylaxis CRS management (tocilizumab/steroids)

Who is at higher risk of kidney injury from CAR-T Cell Therapy?

Grade ≥3 CRS; Lower baseline GFR; High tumor burden / elevated LDH; IV contrast.

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Printable monograph

CAR-T cell therapy

CAR-T Cell Therapy

Kymriah · Yescarta · CAR-T

CAR-T cell therapy · approved 2017 · 9 citations

Up to date· through 2025

Fairly sourced4/9 · 4 signals

Met: 9 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 5y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
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.

Cytokine storm reaches the kidney — AKI riding the wave of CRS.

ModerateCellular immunotherapy

B-cell lymphomaALLMultiple myeloma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Representative incidence20%

5–33% range across studies

AKI ~5–33% across cohorts (commonly ~10–30%), mostly mild and reversible.Source: Gutgarts et al., Biol Blood Marrow Transplant 2020; Kanbay et al., Clin Kidney J 2024

Onset & rechallenge

Time to injuryAcute (~1–7 days)

AKI clusters in the CRS window — the first days to weeks after infusion.

Distilled from: “Acute — within the CRS window (first days–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 · Signature10%PMID 39568416 (opens PubMed in a new tab)
AKI in 10% (any grade) and 5% (grade >=2) of 399 CD19 CAR-T-treated NHL patients; pre-renal/hemodynamic causes predominant (72%), linked to cytokine release syndrome, neurotoxicity, low albumin and high IL-6/TNF-alpha. Progression to CKD rare.
Acute Tubular NecrosisSecondaryno population incidence denominator
Intrinsic (ischemic/toxic) tubular injury is the minority pattern of CAR-T AKI; pre-renal hemodynamic causes dominate (72% of cases). PMID 39568416 (opens PubMed in a new tab)
Crystal / Obstructive NephropathyRarequalitative — 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.

20%incidence

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

Predominantly secondary to cytokine release syndrome — capillary leak and hemodynamic compromise cause prerenal AKI/ATN — compounded by tumor lysis syndrome, lymphodepleting conditioning, nephrotoxic antibiotics and sepsis.

Clinical presentation

AKI during or after CRS (fever, hypotension), often with electrolyte derangements and concurrent tumor-lysis labs.

Management

Treat CRS, supportive AKI care, manage tumor lysis, dialysis if needed.Lesion-level management framework

Risk factors

Grade ≥3 CRS
Lower baseline GFR
High tumor burden / elevated LDH
IV contrast

Prevention

Tumor-lysis prophylaxis
CRS management (tocilizumab/steroids)

Anticancer mechanism· how it treats cancer

Autologous T cells engineered to target a tumor antigen (e.g. CD19). B-cell lymphomas, leukemias and myeloma.

Note · A newer modality; incidence data are still maturing.

§04

Clinical depth

Renal dose adjustment

CAR-T is a one-time autologous cell infusion, not a dose-titrated drug, so there is no renal dose adjustment for the cells themselves; however, the lymphodepleting chemotherapy given beforehand (fludarabine/cyclophosphamide) IS renally cleared, and fludarabine should be dose-reduced in renal impairment to limit neuro/marrow toxicity. Baseline renal impairment does not preclude CAR-T but raises CRS/AKI supportive-care stakes.

Dialyzability & ESKD dosing

Not applicable to the cell product; AKI is driven by cytokine-release-syndrome hemodynamics and tumor lysis and is managed supportively, with continuous renal replacement therapy (CRRT) used for severe AKI in the ICU. Tocilizumab and corticosteroids used for CRS are not removed by dialysis.

Differential diagnosis

CAR-T AKI is usually CRS-driven hemodynamic/prerenal injury that can progress to acute tubular injury (hypotension, capillary leak, cytokine storm), distinguished from tumor-lysis crystalline nephropathy (hyperuricemia/hyperphosphatemia in high tumor burden) and from contrast/nephrotoxin exposure during the admission; timing relative to the CRS peak is the key clue.

Monitoring

Daily creatinine, urine output and volume status through the CRS window (roughly days 1-14 post-infusion)
CRS and ICANS grading by ASTCT criteria
Tumor-lysis labs (potassium, phosphate, uric acid, calcium) before and after infusion in high-burden disease
Electrolytes and fluid balance during tocilizumab / vasopressor / IV-fluid management
Trend to recovery — most CRS-associated AKI is reversible as CRS resolves

Key trials & series

ZUMA-1 (axicabtagene ciloleucel, N Engl J Med 2017) - pivotal large-B-cell lymphoma trial defining the CRS/ICANS profile that drives secondary AKI
ELIANA (tisagenlecleucel, N Engl J Med 2018) - pediatric/young-adult B-ALL trial with frequent high-grade CRS and attendant renal/electrolyte derangement
JULIET (tisagenlecleucel, N Engl J Med 2019) - DLBCL registrational trial
KarMMa (idecabtagene vicleucel, N Engl J Med 2021) - BCMA CAR-T in multiple myeloma, a renally vulnerable population

Clinical pearls

AKI tracks CRS severity - grade the CRS (ASTCT) and the kidney usually follows
Most CAR-T AKI is reversible hemodynamic injury; prompt CRS control (tocilizumab, steroids, fluids/pressors) protects the kidney
Screen for and pre-empt tumor lysis in high-burden disease - a second, crystal-mediated AKI mechanism distinct from CRS
ESKD/dialysis patients have received CAR-T successfully; renal impairment is not an absolute barrier but raises the supportive-care stakes

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

Class-level context for the major non-renal toxicities of the 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. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

5 references · 2020–2025 · 3 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.

Case reports — ranked by strength· 4

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 · ModerateAcute Kidney Injury Following Chimeric Antigen Receptor T-Cell Therapy for B-Cell Lymphoma in a Kidney Transplant Recipient.Melilli E et al. · Kidney Med 2021 · PMID 34401733Kidney transplant recipient developed asymptomatic AKI after anti-CD19 CAR-T, with biopsy showing borderline immunoallergic-pattern tubulointerstitial nephritis and no CAR-T/lymphoma graft infiltration, indicating an indirect mechanism.CaseB · ModerateCollapsing Focal Segmental Glomerulosclerosis and Acute Kidney Injury Associated With Chimeric Antigen Receptor T-Cell (CAR-T) Therapy: A Case Report.Acharya R et al. · Kidney Med 2021 · PMID 34939018Young man developed severe cytokine release syndrome with new nephrotic syndrome and AKI after CD19 CAR-T, with biopsy-proven collapsing glomerulopathy and interstitial nephritis.CaseB · ModerateCAR-T therapy in solid organ transplant recipients with treatment refractory posttransplant lymphoproliferative disorder.Krishnamoorthy S et al. · Am J Transplant 2021 · PMID 33089906Case series of 3 solid-organ-transplant recipients given CD19 CAR-T for refractory PTLD; all developed CRS/ICANS and AKI, with 2 of 3 requiring renal replacement therapy. No kidney biopsy, so the lesion is not histologically defined, but it documents CAR-T-associated severe AKI in an under-reported transplant population.CaseC · LimitedThrombotic microangiopathy following chimeric antigen receptor T-cell therapy.Wu MS et al. · Clin Nephrol Case Stud 2023 · PMID 36844260Two patients developed kidney injury with thrombocytopenia and hemolytic anemia consistent with thrombotic microangiopathy 2-3 months after CAR-T infusion.

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 CAR-T Cell Therapy sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

Blinatumomab

Blincyto · BiTE (CD19×CD3)

Profile

CRS and tumor lysis → AKI.

PREATNXTAL

Moderate#1 · 81% phenotype match

Elranatamab

Elrexfio · Bispecific (BCMA×CD3)

Profile

CRS and tumor lysis — emerging.

PREATNXTAL

Moderate#2 · 81% 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#3 · 79% phenotype match

Idecabtagene vicleucel

Abecma · BCMA CAR-T cell therapy

Profile

CRS-driven AKI and tumor lysis in myeloma.

PREATNLYTE

Moderate#4 · 77% phenotype match

Ciltacabtagene autoleucel

Carvykti · BCMA CAR-T cell therapy

Profile

CRS-driven AKI; delayed neurotoxicity.

PREATNLYTE

Moderate#5 · 77% phenotype match

Obinutuzumab

Gazyva · Anti-CD20 antibody

Profile

High tumor-lysis risk in CLL.

XTALATNPRE

Moderate#6 · 77% phenotype match

Compare CAR-T Cell Therapy 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 Therapy· this agentPRE — 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.

Who studies this

The leading contributors to CAR-T Cell Therapy’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on CAR-T Cell Therapy; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 58 clinical records among all 74 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.