What kind of kidney injury does Ibritumomab tiuxetan cause?

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

Is kidney injury from Ibritumomab tiuxetan reversible?

Reversible. Typical onset: TLS is early (hours to days); cytopenias are delayed (weeks)..

Does Ibritumomab tiuxetan need a dose adjustment in kidney impairment?

Administered activity is capped by platelet count (e.g. reduced to 0.3 mCi/kg if platelets 100,000-149,000/uL; contraindicated if platelets 25% lymphomatous marrow involvement) — a hematologic threshold. No renal CrCl-based dose adjustment is defined; the kidney does not drive dosing.

How should kidney function be monitored during Ibritumomab tiuxetan therapy?

CBC weekly for up to ~3 months (marrow nadir surveillance); Electrolytes, uric acid, phosphate and creatinine peri-treatment in TLS-risk patients; Volume status/urine output in bulky disease.

How can kidney injury from Ibritumomab tiuxetan be prevented?

TLS prophylaxis in at-risk/bulky patients: IV hydration plus allopurinol or rasburicase Activity capping by platelet count and marrow involvement (hematologic, not renal, threshold)

Who is at higher risk of kidney injury from Ibritumomab tiuxetan?

Bulky disease / high circulating tumor burden; High LDH and rapidly proliferative lymphoma; Pre-existing CKD and dehydration; High pre-treatment uric acid.

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Printable monograph

Radioimmunotherapy (Y-90 anti-CD20)

Ibritumomab tiuxetan

Zevalin · IBRI

Radioimmunotherapy (Y-90 anti-CD20) · approved 2002 · 6 citations

Dated evidence· through 2004

Fairly sourced4/9 · 4 signals

Met: 6 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 3y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2004
Not met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

A pure beta-emitting anti-CD20 radioimmunoconjugate whose kidney risk is not radiation but tumor lysis in bulky lymphoma.

MildRadioimmunotherapy (Y-90 anti-CD20)

Relapsed or refractory low-grade or follicular B-cell non-Hodgkin lymphomaConsolidation in previously untreated follicular lymphoma achieving response to first-line chemotherapy

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct renal radiation toxicity is essentially negligible — yttrium-90 is a pure beta-emitter and the kidney is not a critical organ on dosimetry; the dose-limiting toxicity is delayed myelosuppression. The renal hazard is indirect tumor lysis syndrome (TLS) in bulky/high-burden disease; a drug-specific TLS rate is not well quantified and is rare.Source: Witzig et al., J Clin Oncol 2002

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor-lysis AKI is early (hours to days); cytopenias are the delayed, non-renal effect.

Distilled from: “TLS is early (hours to days); cytopenias are delayed (weeks).”

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Crystal / Obstructive NephropathyRarequalitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.
Electrolyte DisturbanceRarequalitative — 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.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence6 citations

Nephron map

Vasculature / Endothelium

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

Mechanism of kidney injury

No meaningful direct radiation nephropathy: the pure beta-emitter clears with low renal absorbed dose. The kidney injury is metabolic — rapid lymphoma cell lysis releases uric acid and phosphate, producing crystal (urate/calcium-phosphate) nephropathy with intratubular obstruction and hemodynamic AKI. Myelosuppression (the true dose-limiting toxicity) is hematologic, not renal.

Clinical presentation

When TLS occurs: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia and a rising creatinine within days of therapy. Renal labs are otherwise typically unaffected; the dominant on-label toxicity is delayed cytopenias (nadir ~7-9 weeks).

Management

Standard TLS management: aggressive hydration, urate-lowering (rasburicase for established hyperuricemia), correct electrolytes, and dialysis for severe/refractory derangements. Support cytopenias with transfusion and growth factors. The radioconjugate is not removed by dialysis.Lesion-level management framework

Risk factors

Bulky disease / high circulating tumor burden
High LDH and rapidly proliferative lymphoma
Pre-existing CKD and dehydration
High pre-treatment uric acid

Prevention

TLS prophylaxis in at-risk/bulky patients: IV hydration plus allopurinol or rasburicase
Activity capping by platelet count and marrow involvement (hematologic, not renal, threshold)

Anticancer mechanism· how it treats cancer

Murine anti-CD20 monoclonal antibody chelated (tiuxetan) to yttrium-90, a pure high-energy beta-emitter. After a rituximab pre-dose to clear circulating B cells, the radioconjugate binds CD20 on B-cell non-Hodgkin lymphoma, delivering cross-fire beta radiation plus antibody-mediated cytotoxicity (radioimmunotherapy).

Note · Established (2002) agent; no dedicated renal cohort exists because direct renal toxicity is not a recognized effect. Renal framing rests on the pivotal dosimetry (kidney non-critical) plus the TLS literature for bulky lymphoma.

§04

Clinical depth

Renal dose adjustment

Administered activity is capped by platelet count (e.g. reduced to 0.3 mCi/kg if platelets 100,000-149,000/uL; contraindicated if platelets <100,000/uL or >25% lymphomatous marrow involvement) — a hematologic threshold. No renal CrCl-based dose adjustment is defined; the kidney does not drive dosing.

Dialyzability & ESKD dosing

The radioimmunoconjugate is not dialyzable. Dialysis is relevant only for managing TLS metabolic derangements, not for removing the drug.

Differential diagnosis

Distinguish TLS-driven AKI (urate/phosphate burden, early, post-treatment) from contrast/medication nephrotoxins, lymphomatous renal infiltration or obstruction, and sepsis. Radiation nephropathy is not part of the differential here.

Monitoring

CBC weekly for up to ~3 months (marrow nadir surveillance)
Electrolytes, uric acid, phosphate and creatinine peri-treatment in TLS-risk patients
Volume status/urine output in bulky disease

Key trials & series

Pivotal randomized trial of Y-90 ibritumomab vs rituximab (Witzig, J Clin Oncol 2002)
Pivotal-trial dosimetry (Wiseman, Crit Rev Oncol Hematol 2001) — kidneys not a critical organ

Clinical pearls

Direct renal radiation toxicity is negligible — the renal story is tumor lysis, not the radioisotope.
Dosing is limited by platelets and marrow involvement, not by kidney function.
Bulky lymphoma is the red flag for TLS prophylaxis with hydration and rasburicase/allopurinol.
The dose-limiting toxicity overall is delayed myelosuppression (nadir ~7-9 weeks).

§05

References

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

Evidence accrual

6 references · 2001–2004 · 5 since 2002

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 (Apr 2023) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: SERIOUS INFUSION REACTIONS, PROLONGED AND SEVERE CYTOPENIAS, and SEVERE CUTANEOUS AND MUCOCUTANEOUS REACTIONS Serious Infusion Reactions: Deaths have occurred within 24 hours of rituximab infusion, an essential component of the Zevalin therapeutic regimen. These fatalities were associated with hypoxia, pulmonary infiltrates, acute respiratory distress syndrome, myocardial infarction, ventricular fibrillation, or cardiogenic shock. Most (80%) fatalities occurred with the first rituximab infusion [ see Warnings and Precautions ( 5.1 ) and Adverse Reactions ( 6.1 ) ] . Discontinue rituximab and Y-90 Zevalin infusions in patients who develop severe infusion reactions. Prolonged and Severe Cytopenias: Y-90 Zevalin administration results in severe and prolonged cytopenias in most patients. Do not administer Y-90 Zevalin to patients with ≥ 25% lymphoma marrow involvement and/or impaired bone marrow reserve [ see Warnings and Precautions ( 5.2 ) and Adverse Reactions ( 6.1 ) ]. Severe Cutaneous and Mucocutaneous Reactions: Severe cutaneous and mucocutaneous reactions, some fatal, can occur with the Zevalin therapeutic regimen. Discontinue rituximab and Y-90 Zevalin infusions in patients experiencing severe cutaneous or mucocutaneous reactions [ see Warnings and Precautions ( 5.3 ) and Adverse Reactions ( 6.2 ) ]. Dosing: The dose of Y-90 Zevalin should not exceed 32 mCi (1184…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,521 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.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
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 reported renal phenotypes· 3 signals

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Electrolyte Disturbancecorroborated · ROR 2.49 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Crystal / Obstructive NephropathyNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

Thrombotic Microangiopathy

ROR 7.1695% CI 3.57–14.35· 8 reports

SIADH / Hyponatremia

ROR 2.5895% CI 1.55–4.30· 15 reports

Electrolyte Disturbance

ROR 2.4995% CI 1.77–3.49· 34 reports

FAERS outcomes & reporting trend· 36.2% of reports w/ death · 40% w/ hospitalization

36.2%

Reported with a death outcome

551 of 1,521 reports

40%

Reported with hospitalization

609 of 1,521 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 1,521 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 0.2795% CI 0.09–0.84· 3 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Blood & lymphatic

Thrombocytopenia174Neutropenia141Febrile Neutropenia94Anaemia84Platelet Count Decreased84

Immune / infection

Sepsis172Pneumonia73Cytomegalovirus Infection35Septic Shock35

Gastrointestinal

Mucosal Inflammation72Diarrhoea60Nausea40

Nervous system

Progressive Multifocal Leukoencephalopathy90

General / constitutional

Pyrexia67

Respiratory

Respiratory Failure62

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 Ibritumomab tiuxetan 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

Cladribine

Leustatin · Purine analog

Profile

Tumor lysis; high-dose nephrotoxicity.

XTALPRELYTE

Mild#1 · 88% phenotype match

Etoposide

Etopophos · Topoisomerase II inhibitor

Profile

Tumor lysis; renally cleared.

XTALPRELYTE

Mild#2 · 88% phenotype match

Hydroxyurea

Hydrea · Ribonucleotide reductase inhibitor

Profile

Tumor lysis in myeloproliferative disease.

XTALPRELYTE

Mild#3 · 88% phenotype match

Nelarabine

Arranon · Purine analog

Profile

Tumor lysis in T-ALL.

XTALPRELYTE

Mild#4 · 88% phenotype match

Pomalidomide

Pomalyst · Immunomodulatory drug (IMiD)

Profile

Tumor lysis; usable in renal impairment.

PRELYTEXTAL

Mild#5 · 88% phenotype match

Thalidomide

Thalomid · Immunomodulatory drug (IMiD)

Profile

Tumor lysis and bradycardia.

PRELYTEXTAL

Mild#6 · 88% phenotype match

Compare Ibritumomab tiuxetan 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 Radiopharmaceuticals

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.

1Radium-223 dichloridePRE — Prerenal / Hemodynamic AKIMild
2Ibritumomab tiuxetan· this agentPRE — Prerenal / Hemodynamic AKIMild
3Iobenguane I-131ATN — Acute Tubular NecrosisMild
4Samarium-153 lexidronamATN — Acute Tubular NecrosisModerate
5Lutetium-177 DotatateCIN — Chronic Interstitial NephropathyModerate
6Lutetium-177 PSMA-617 (vipivotide)CIN — Chronic Interstitial NephropathyModerate
7Strontium-89 chlorideLYTE — Electrolyte DisturbanceModerate

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.