What kind of kidney injury does Afamitresgene autoleucel (Afami-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 Afamitresgene autoleucel (Afami-cel) therapy?

Serum creatinine and urine output during and after the CRS window; Vital signs for hypotension/fever (CRS grading); Electrolytes, phosphate, uric acid, and LDH for tumor lysis; Volume status.

How can kidney injury from Afamitresgene autoleucel (Afami-cel) be prevented?

Pre-infusion optimization of volume status and renal function Early recognition and grading of CRS Prompt CRS-directed therapy (tocilizumab, supportive care) to limit hemodynamic insult Tumor lysis prophylaxis (hydration, urate-lowering therapy) in high-burden disease

Who is at higher risk of kidney injury from Afamitresgene autoleucel (Afami-cel)?

Higher-grade cytokine release syndrome; Pre-existing chronic kidney disease or reduced baseline GFR; Volume depletion and hypotension; High tumor burden predisposing to tumor lysis; Concomitant nephrotoxins.

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Printable monograph

MAGE-A4 TCR-T cell therapy

Afamitresgene autoleucel (Afami-cel)

Tecelra · MAGE-A4 TCR-T therapy

MAGE-A4 TCR-T cell therapy · approved 2024 · 4 citations

Up to date· through 2025

Fairly sourced4/9 · 4 signals

Not met: 4 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 2y)
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.

MAGE-A4-directed TCR T-cell therapy; renal risk is CRS-associated and hemodynamic, not a direct nephrotoxin.

ModerateMAGE-A4 TCR-engineered T-cell therapy

Unresectable or metastatic synovial sarcoma in HLA-A*02-eligible adults who have received prior chemotherapy and whose tumor expresses MAGE-A4 (accelerated approval)

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Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Drug-specific renal injury rates for afami-cel are not well defined; the SPEARHEAD-1 trial reported cytokine release syndrome (CRS) in most treated patients, predominantly low grade, as the dominant systemic toxicity. Acute kidney injury is best understood as a downstream, CRS-associated hemodynamic event rather than a measured signature toxicity. By analogy to CAR-T cellular therapy, AKI incidence in the broader engineered-T-cell setting spans roughly 5 to 33 percent depending on population and CRS severity. A precise afami-cel-specific incidence cannot be stated from current literature.Source: 38554725

Onset & rechallenge

Time to injuryAcute (~1–7 days)

During the acute CRS window, first days to ~2 weeks after infusion.

Distilled from: “AKI typically emerges during the acute CRS window in the first days to roughly two weeks after infusion, coinciding with peak cytokine activity.”

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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.
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).

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Kidney injury

Mechanism of kidney injury

The principal renal mechanism is hemodynamic (prerenal). CRS-driven systemic inflammation produces fever, vasodilation, capillary leak, and hypotension that reduce renal perfusion; superimposed tumor lysis can add an intratubular/metabolic insult. Afami-cel is not a direct tubular nephrotoxin; rather, the kidney is an innocent bystander to the inflammatory and hemodynamic storm, analogous to CRS-associated AKI described with CAR-T therapy.

Clinical presentation

Presentation typically tracks the CRS course: fever and hypotension with a rise in creatinine and reduced urine output. Sediment is usually bland, consistent with prerenal physiology or early ischemic tubular injury; electrolyte derangements may accompany concurrent tumor lysis.

Management

Management mirrors CRS-associated AKI care: restore renal perfusion with fluid resuscitation and vasopressors as needed, treat the underlying CRS (e.g., tocilizumab, corticosteroids per protocol), and manage tumor lysis with hydration and urate-lowering agents. Most cases are hemodynamic and improve as CRS resolves; renal replacement therapy is reserved for refractory or severe AKI.Lesion-level management framework

Risk factors

Higher-grade cytokine release syndrome
Pre-existing chronic kidney disease or reduced baseline GFR
Volume depletion and hypotension
High tumor burden predisposing to tumor lysis
Concomitant nephrotoxins

Prevention

Pre-infusion optimization of volume status and renal function
Early recognition and grading of CRS
Prompt CRS-directed therapy (tocilizumab, supportive care) to limit hemodynamic insult
Tumor lysis prophylaxis (hydration, urate-lowering therapy) in high-burden disease

Anticancer mechanism· how it treats cancer

Afamitresgene autoleucel is an autologous T-cell therapy engineered to express an affinity-enhanced T-cell receptor (TCR) recognizing a MAGE-A4 peptide presented on HLA-A*02. The modified T cells recognize and kill MAGE-A4-expressing tumor cells in HLA-A*02-positive patients. It received accelerated FDA approval in August 2024 for advanced synovial sarcoma, becoming the first engineered TCR T-cell therapy approved for a solid tumor.

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Clinical depth

Renal dose adjustment

Not applicable in the conventional sense - this is a one-time autologous cell product, not a renally cleared small molecule, so there are no CrCl-based dose thresholds. No renal dose adjustment is established; lymphodepleting chemotherapy given before infusion may itself require attention to renal function.

Dialyzability & ESKD dosing

Not applicable. As a living-cell therapy, afami-cel is not dialyzable; dialysis is used only to support severe AKI, not to clear the product.

Differential diagnosis

In a treated patient with rising creatinine, separate CRS-driven prerenal/ischemic AKI from tumor lysis syndrome (hyperuricemia, hyperphosphatemia, hyperkalemia) and from lymphodepletion-related or concomitant nephrotoxin injury. The temporal link to fever and hypotension points to CRS-associated hemodynamic AKI.

Monitoring

Serum creatinine and urine output during and after the CRS window
Vital signs for hypotension/fever (CRS grading)
Electrolytes, phosphate, uric acid, and LDH for tumor lysis
Volume status

Key trials & series

SPEARHEAD-1 (NCT04044768): international open-label phase 2 of afami-cel in advanced synovial sarcoma and myxoid round cell liposarcoma; supported accelerated approval. CRS was common but predominantly low grade, framing renal risk as CRS-associated and hemodynamic.

Clinical pearls

AKI clusters with the CRS window in the first days to ~2 weeks; controlling CRS is the main renal-protective lever.
Tumor lysis is a co-traveler in high-burden disease and adds an intratubular/metabolic insult.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

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References

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

Evidence accrual

4 references · 2023–2025 · 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 (Jul 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: CYTOKINE RELEASE SYNDROME Cytokine Release Syndrome (CRS), which may be severe or life-threatening, occurred in patients receiving TECELRA. At the first sign of CRS, immediately evaluate patient for hospitalization and institute treatment with supportive care. Ensure that healthcare providers administering TECELRA have immediate access to medications and resuscitative equipment to manage CRS [see Preparation and Administration (2.2) , and Warnings and Precautions (5.1) ] . WARNING: CYTOKINE RELEASE SYNDROME See full prescribing information for complete boxed warning. Cytokine Release Syndrome (CRS), which may be severe or life-threatening, occurred in patients receiving TECELRA. At the first sign of CRS, immediately evaluate patient for hospitalization and institute treatment with supportive care. Ensure that healthcare providers administering TECELRA have immediate access to medications and resuscitative equipment to manage CRS ( 2.2 , 5.1 ).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 6 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.

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· 1 of 6 reports w/ death · 2 w/ hospitalization

6 reports is below the 50 this atlas requires before quoting a percentage, so the counts are shown instead of shares.

1 of 6

Reported with a death outcome

too few reports to express as a share

2 of 6

Reported with hospitalization

too few reports to express as a share

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 5 systems · 6 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.

General / constitutional

Pyrexia2Fatigue1Pain1

Immune / infection

Cytokine Release Syndrome2

Skin

Rash1Urticaria1

Respiratory

Dyspnoea1

Psychiatric

Hallucination1

Guidelines & consensus· 13

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.

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 Afamitresgene autoleucel (Afami-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

Ziftomenib

Komzifti · Menin inhibitor

Profile

2025 NPM1-mutated AML menin inhibitor; differentiation syndrome and tumor lysis.

PRELYTE

Moderate#1 · 100% phenotype match

Imetelstat

Rytelo · Telomerase inhibitor

Profile

2024 MDS agent; tumor lysis risk.

PRELYTE

Mild#2 · 95% phenotype match

Capivasertib

Truqap · AKT inhibitor

Profile

2023 breast-cancer AKT inhibitor; AKI with diarrhea/hyperglycemia.

PRELYTE

Moderate#3 · 89% phenotype match

Loncastuximab tesirine

Zynlonta · Antibody-drug conjugate (CD19/PBD)

Profile

Capillary-leak-type edema, effusions and AKI.

PRELYTE

Moderate#4 · 89% phenotype match

Olutasidenib

Rezlidhi · IDH1 inhibitor

Profile

Differentiation syndrome and tumor lysis in AML.

PRELYTE

Moderate#5 · 88% phenotype match

Catumaxomab

Removab · Trifunctional bispecific (EpCAM×CD3)

Profile

Intraperitoneal; cytokine-release- and ascites/paracentesis-driven prerenal AKI; withdrawn (EU) 2017.

PRELYTE

Moderate#6 · 88% phenotype match

Compare Afamitresgene autoleucel (Afami-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 Other targeted agents

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.

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.