What kind of kidney injury does Catumaxomab 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 Catumaxomab therapy?

Electrolytes and volume status (especially around paracentesis); Temperature and cytokine-release symptoms; Liver function tests (transient rises expected).

How can kidney injury from Catumaxomab be prevented?

Premedicate and manage cytokine-release symptoms (antipyretics, antiemetics) Maintain euvolemia around paracentesis and infusions

Who is at higher risk of kidney injury from Catumaxomab?

Large-volume malignant ascites and frequent paracentesis; Pre-existing volume depletion or CKD; Severe cytokine-release reaction (high fever, vomiting); Concurrent nephrotoxins or diuretics.

Back to explorer

Printable monograph

Trifunctional bispecific (EpCAM×CD3)

Catumaxomab

Removab · Catux

Trifunctional bispecific (EpCAM×CD3) · approved 2009 · 4 citations

Dated evidence· through 2017

Thinly sourced3/9 · 3 signals

Not met: 4 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
Not met: Current through 2017
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.

An intraperitoneal trifunctional antibody whose cytokine-release storm threatens the kidney prerenally.

ModerateTrifunctional bispecific antibody (EpCAM x CD3)

Malignant ascites from EpCAM-positive carcinomas (intraperitoneal)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

No characteristic intrinsic nephrotoxicity. The dominant treatment-related toxicity is cytokine-release-related (pyrexia, nausea, vomiting, chills, fatigue) plus intraperitoneal-administration effects (abdominal pain); transient transaminase rises and lymphopenia are common but usually clinically minor. Cytokine release with fever, GI losses, and large-volume ascites/paracentesis creates a setting for prerenal/hemodynamic AKI rather than a direct renal lesion. Drug-specific renal incidence is not quantified.Source: Berek et al., Int J Gynecol Cancer 2014 (phase II); Frampton, Drugs 2012 (pivotal II/III review)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Cytokine-release symptoms within hours of each intraperitoneal infusion; prerenal AKI follows the inflammatory/volume insult.

Distilled from: “Cytokine-release symptoms within hours of each intraperitoneal infusion; any prerenal AKI follows the inflammatory/volume insult.”

§02

Renal toxicities, ranked

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

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

§03

Kidney injury

Mechanism of kidney injury

Catumaxomab's renal risk is hemodynamic and indirect. By cross-linking tumor cells, T cells, and Fc-receptor-bearing accessory cells, it triggers a brisk cytokine release (TNF-alpha, IL-6, IFN-gamma), producing fever, vomiting, and a systemic inflammatory/vasodilatory state; combined with the fluid shifts of malignant ascites and therapeutic paracentesis, this can cause volume depletion and renal hypoperfusion — a prerenal acute kidney injury pattern — and contribute to electrolyte disturbance. There is no described direct tubular, glomerular, or crystal toxicity from the antibody itself. Management is supportive and hemodynamic.

Clinical presentation

Cytokine-release symptoms (fever, chills, nausea, vomiting) and abdominal pain after intraperitoneal dosing; if AKI develops it is typically prerenal — oliguria with a bland sediment, responsive to volume — in the context of fever, GI losses, and ascites management. Transient transaminitis and lymphopenia are expected and usually benign.

Management

Supportive: treat fever and GI losses, restore volume for prerenal AKI, and correct electrolytes. The antibody requires no renal dose adjustment; manage the hemodynamic/inflammatory insult and the underlying ascites.Lesion-level management framework

Risk factors

Large-volume malignant ascites and frequent paracentesis
Pre-existing volume depletion or CKD
Severe cytokine-release reaction (high fever, vomiting)
Concurrent nephrotoxins or diuretics

Prevention

Premedicate and manage cytokine-release symptoms (antipyretics, antiemetics)
Maintain euvolemia around paracentesis and infusions

Anticancer mechanism· how it treats cancer

Trifunctional rat/mouse hybrid bispecific antibody binding EpCAM on tumor cells and CD3 on T cells, while its intact Fc region engages Fc-gamma-receptor-positive accessory immune cells (macrophages, NK cells, dendritic cells). This tri-cell complex drives potent T-cell- and accessory-cell-mediated tumor killing. Administered intraperitoneally for malignant ascites due to EpCAM-positive tumors.

Note · Renal injury is indirect (cytokine-release- and ascites/paracentesis-driven prerenal AKI), not a direct antibody nephrotoxin. Catumaxomab was withdrawn from the EU market in 2017 for commercial reasons; profile retained for onconephrology completeness. Drug-specific renal data are sparse and conservative.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment defined; the agent is given intraperitoneally as an antibody and is not renally cleared. The actionable interventions are hemodynamic/supportive rather than renal dosing.

Dialyzability & ESKD dosing

A large trifunctional antibody — not dialyzable and cleared by proteolysis; no ESKD dosing guidance. Renal management is volume- and electrolyte-focused.

Differential diagnosis

Distinguish cytokine-release-/ascites-driven prerenal AKI (bland sediment, volume-responsive, fever and GI losses) from intrinsic renal disease or obstruction; a fixed, non-volume-responsive creatinine rise should prompt search for an alternative cause.

Monitoring

Electrolytes and volume status (especially around paracentesis)
Temperature and cytokine-release symptoms
Liver function tests (transient rises expected)

Key trials & series

Pivotal phase II/III malignant-ascites trial (Frampton Drugs 2012 review)
Berek Int J Gynecol Cancer 2014 phase II in chemotherapy-refractory ovarian cancer

Clinical pearls

Expect transient transaminitis and lymphopenia — usually benign and not a renal warning.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

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

Class-level context for the major non-renal toxicities of the Trifunctional bispecific (EpCAM×CD3) 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

3 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

3 references · 2012–2017 · 1 since 2015

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· 1

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.

CaseC · LimitedTreatment of malignant ascites with a second cycle of catumaxomab in gastric signet cell carcinoma--a report of 2 cases.Thomaidis T et al. · Oncol Res Treat 2014 · PMID 25427585One patient developed an inflammatory response with acute deterioration of kidney function during the first catumaxomab cycle, consistent with prerenal/hemodynamic AKI, with quick recovery.

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.

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 Catumaxomab 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

Loncastuximab tesirine

Zynlonta · Antibody-drug conjugate (CD19/PBD)

Profile

Capillary-leak-type edema, effusions and AKI.

PRELYTE

Moderate#1 · 88% phenotype match

Capivasertib

Truqap · AKT inhibitor

Profile

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

PRELYTE

Moderate#2 · 88% phenotype match

Afamitresgene autoleucel (Afami-cel)

Tecelra · MAGE-A4 TCR-T cell therapy

Profile

First TCR-T cell therapy for a solid tumor; CRS-associated hemodynamic AKI.

PRELYTE

Moderate#3 · 88% phenotype match

Ziftomenib

Komzifti · Menin inhibitor

Profile

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

PRELYTE

Moderate#4 · 88% phenotype match

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#5 · 83% phenotype match

Quizartinib

Vanflyta · FLT3 inhibitor

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild#6 · 82% phenotype match

Compare Catumaxomab 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 Bispecifics / T-cell engagers

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.