What kind of kidney injury does Naxitamab cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Hypertension.

How should kidney function be monitored during Naxitamab therapy?

Continuous blood pressure and heart rate during the infusion and through the post-infusion observation window (capture both hypotensive and hypertensive swings); Cardiorespiratory/oxygen saturation monitoring for the broader infusion-reaction complex; Fluid balance, body weight, and edema (screen for capillary leak); Serum creatinine and electrolytes around each cycle, with closer checks after any significant hypotensive episode; Serum albumin if capillary-leak syndrome is suspected; Symptom review for pain, urticaria, bronchospasm to gauge premedication adequacy.

How can kidney injury from Naxitamab be prevented?

Protocolized premedication before every infusion (antihistamines, antipyretics, analgesia including opioids +/- ketamine, and corticosteroids per protocol) to blunt the infusion reaction Start at a slow infusion rate with stepwise escalation as tolerated Ensure adequate hydration and correct volume depletion before infusing Continuous blood-pressure and cardiorespiratory monitoring during and after the infusion, with IV fluids, vasopressors, and resuscitation equipment immediately available Educate patients/caregivers on premedication and post-infusion monitoring; treat in a setting equipped for rapid intervention Review and, where possible, hold agents that impair renal perfusion (NSAIDs, RAAS blockers, diuretics) around infusion days

Who is at higher risk of kidney injury from Naxitamab?

Early treatment cycles (infusion reactions and blood-pressure lability are most severe in the first 1-3 cycles); The high naxitamab dose itself (~270 mg/m2 per cycle, roughly 2.5x the dose of dinutuximab/dinutuximab beta); Pre-existing volume depletion from concurrent vomiting, diarrhea, or poor intake; Rapid infusion rate or inadequate premedication; Concomitant nephrotoxins or agents affecting renal perfusion (e.g., NSAIDs, ACE inhibitors/ARBs, diuretics); Underlying cardiac, renal, or hemodynamic compromise; Prior severe infusion reactions to an anti-GD2 antibody.

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Printable monograph

Anti-GD2 antibody

Naxitamab

Q: How does Naxitamab damage the kidney?

The kidney is an innocent bystander of the on-target infusion reaction rather than the site of a primary drug lesion. GD2 engagement triggers intense, largely complement-driven acute inflammation during each infusion, producing an infusion-related reaction spectrum that includes vasodilation, increased vascular permeability with capillary leak/third-spacing, bronchospasm, urticaria, and — most importantly for the kidney — abrupt hypotension. Effective circulating volume falls (from vasodilation, capillary leak, and any accompanying vomiting/diarrhea), renal perfusion pressure and glomerular filtration drop, and a hemodynamic/prerenal pattern of azotemia can result. Superimposed on this are swings toward hypertension: acute on-treatment hypertension is an expected naxitamab toxicity (partly pain- and catecholamine-mediated, partly from fluid resuscitation), so patients oscillate between hypo- and hypertension during and after the infusion. There is no evidence of direct tubular, interstitial, or glomerular immune injury; sustained or severe hypotension is what could tip a prerenal picture toward ischemic acute tubular necrosis.

Q: Is kidney injury from Naxitamab reversible?

Reversible. Typical onset: Acute and infusion-locked — hypotension, hypertension, and the rest of the infusion-reaction complex begin within minutes to a few hours of starting the infusion and are most pronounced during the early cycles; significant infusion-related events become rare after the first few treatment cycles..

Q: Does Naxitamab need a dose adjustment in kidney impairment?

No pharmacokinetic renal dose adjustment is defined: as a ~150 kDa IgG1 monoclonal antibody, naxitamab is cleared by reticuloendothelial catabolism, not renal excretion, so creatinine clearance does not drive dosing. Dose modifications are triggered by infusion reactions and hemodynamic toxicity — slowing the rate, interrupting, reducing the dose, or giving a half-dose for a given day (as has been done for infusion-associated hypotension), with subsequent full doses usually tolerated. There is no established creatinine- or eGFR-based dose reduction.

Q: Is Naxitamab removed by dialysis?

Not dialyzable. Naxitamab is a large (~150 kDa) IgG1 monoclonal antibody with a large-molecule volume of distribution and reticuloendothelial clearance; it is not removed by hemodialysis or peritoneal dialysis, and dialysis has no role in enhancing its elimination.

Q: How is kidney injury from Naxitamab managed?

Manage the hemodynamics, not the kidney per se. For infusion-related hypotension, follow established stepwise algorithms: slow or interrupt the infusion, give an IV isotonic fluid bolus, position supine/Trendelenburg, and escalate to vasopressors for refractory or severe drops; resume at a reduced rate once stable. Treat acute hypertension with monitoring and antihypertensives per protocol, avoiding overcorrection given the coexisting hypotension risk. Bronchospasm/allergic features are treated with bronchodilators, antihistamines, and steroids. Restoring renal perfusion promptly is the key renal intervention; a transient creatinine bump usually resolves with hemodynamic stabilization. Most events are managed in the outpatient setting; dose is often reduced or a day's dose halved for significant reactions, with full dosing typically resumed at the next infusion. Persistent, severe, or life-threatening reactions warrant treatment interruption or discontinuation.

Danyelza · NAX

Anti-GD2 antibody · approved 2020 · 8 citations

Up to date· through 2025

Fairly sourced5/9 · 5 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
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.

Anti-GD2 antibody for relapsed/refractory neuroblastoma whose kidney risk is hemodynamic — infusion-driven capillary leak and blood-pressure swings (hypotension plus on-treatment hypertension), not intrinsic tubular injury.

ModerateAnti-GD2 immunotherapy era

Relapsed or refractory high-risk neuroblastoma in the bone or bone marrow that showed a partial response, minor response, or stable disease to prior therapy (in combination with GM-CSF) — U.S. accelerated approvalInvestigational / off-study use in chemo-immunotherapy regimens (e.g., with irinotecan, temozolomide, and GM-CSF) for primary refractory high-risk neuroblastoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Frank acute kidney injury is not a systematically reported endpoint for naxitamab and no validated AKI incidence figure exists; the renal-relevant risk is hemodynamic rather than a direct nephrotoxic lesion. The closest quantitative anchor comes from the pivotal single-arm phase 2 Trial 201 (NCT03363373), where naxitamab-related grade 3 adverse events were dominated by hypotension in 58% and pain in 54% of patients — the infusion-reaction physiology that can transiently compromise renal perfusion. Pharmacovigilance corroborates the signal: in an FDA Adverse Event Reporting System analysis of anti-GD2 antibodies, hypotension, hypertension, urticaria, and capillary-leakage syndrome were among the most frequent and strongest naxitamab-associated signals. Because these figures describe hemodynamic events (not measured creatinine-defined AKI), the numeric AKI rate is left unquantified.Source: 39952926

Onset & rechallenge

Time to injuryHyperacute (<24 h)

Infusion-locked — hypotension/hypertension and the infusion-reaction complex begin within minutes to a few hours of starting the infusion, most pronounced during the early cycles.

Distilled from: “Acute and infusion-locked — hypotension, hypertension, and the rest of the infusion-reaction complex begin within minutes to a few hours of starting the infusion and are most pronounced during the early cycles; significant infusion-related events become rare after the first few treatment cycles.” · PMID 39952926 (opens PubMed in a new tab)

§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.
HypertensionSecondaryqualitative — no citable incidence
On-target loss of endothelial nitric oxide from VEGF-pathway blockade — so characteristic it has been studied as a pharmacodynamic marker of drug exposure.

§03

Kidney injury

Mechanism of kidney injury

The kidney is an innocent bystander of the on-target infusion reaction rather than the site of a primary drug lesion. GD2 engagement triggers intense, largely complement-driven acute inflammation during each infusion, producing an infusion-related reaction spectrum that includes vasodilation, increased vascular permeability with capillary leak/third-spacing, bronchospasm, urticaria, and — most importantly for the kidney — abrupt hypotension. Effective circulating volume falls (from vasodilation, capillary leak, and any accompanying vomiting/diarrhea), renal perfusion pressure and glomerular filtration drop, and a hemodynamic/prerenal pattern of azotemia can result. Superimposed on this are swings toward hypertension: acute on-treatment hypertension is an expected naxitamab toxicity (partly pain- and catecholamine-mediated, partly from fluid resuscitation), so patients oscillate between hypo- and hypertension during and after the infusion. There is no evidence of direct tubular, interstitial, or glomerular immune injury; sustained or severe hypotension is what could tip a prerenal picture toward ischemic acute tubular necrosis.

Clinical presentation

Manifestations cluster around the infusion (given on Days 1, 3, and 5 of each 4-week cycle). Patients develop pain, urticaria/rash, bronchospasm, cough, nausea/vomiting, tachycardia, and hypotension, sometimes with a compensatory or subsequent hypertensive phase. The renal correlate is a transient rise in serum creatinine and reduced urine output tracking the hypotensive episode, typically recovering as perfusion is restored. Overt capillary-leak syndrome (edema, hypoalbuminemia, hypoxia) is uncommon with the short outpatient infusions used for naxitamab but is the severe end of the spectrum. Electrolyte disturbances are generally minor and secondary to fluid shifts and resuscitation.

Management

Manage the hemodynamics, not the kidney per se. For infusion-related hypotension, follow established stepwise algorithms: slow or interrupt the infusion, give an IV isotonic fluid bolus, position supine/Trendelenburg, and escalate to vasopressors for refractory or severe drops; resume at a reduced rate once stable. Treat acute hypertension with monitoring and antihypertensives per protocol, avoiding overcorrection given the coexisting hypotension risk. Bronchospasm/allergic features are treated with bronchodilators, antihistamines, and steroids. Restoring renal perfusion promptly is the key renal intervention; a transient creatinine bump usually resolves with hemodynamic stabilization. Most events are managed in the outpatient setting; dose is often reduced or a day's dose halved for significant reactions, with full dosing typically resumed at the next infusion. Persistent, severe, or life-threatening reactions warrant treatment interruption or discontinuation.Lesion-level management framework

Risk factors

Early treatment cycles (infusion reactions and blood-pressure lability are most severe in the first 1-3 cycles)
The high naxitamab dose itself (~270 mg/m2 per cycle, roughly 2.5x the dose of dinutuximab/dinutuximab beta)
Pre-existing volume depletion from concurrent vomiting, diarrhea, or poor intake
Rapid infusion rate or inadequate premedication
Concomitant nephrotoxins or agents affecting renal perfusion (e.g., NSAIDs, ACE inhibitors/ARBs, diuretics)
Underlying cardiac, renal, or hemodynamic compromise
Prior severe infusion reactions to an anti-GD2 antibody

Prevention

Protocolized premedication before every infusion (antihistamines, antipyretics, analgesia including opioids +/- ketamine, and corticosteroids per protocol) to blunt the infusion reaction
Start at a slow infusion rate with stepwise escalation as tolerated
Ensure adequate hydration and correct volume depletion before infusing
Continuous blood-pressure and cardiorespiratory monitoring during and after the infusion, with IV fluids, vasopressors, and resuscitation equipment immediately available
Educate patients/caregivers on premedication and post-infusion monitoring; treat in a setting equipped for rapid intervention
Review and, where possible, hold agents that impair renal perfusion (NSAIDs, RAAS blockers, diuretics) around infusion days

Anticancer mechanism· how it treats cancer

Naxitamab (formerly hu3F8) is a humanized IgG1 monoclonal antibody targeting the disialoganglioside GD2, which is homogeneously and abundantly expressed on neuroblastoma and other neuroectodermal tumors. Binding GD2 on tumor cells drives antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity; it is given together with granulocyte-macrophage colony-stimulating factor (GM-CSF) to augment myeloid effector-cell killing.

§04

Clinical depth

Renal dose adjustment

No pharmacokinetic renal dose adjustment is defined: as a ~150 kDa IgG1 monoclonal antibody, naxitamab is cleared by reticuloendothelial catabolism, not renal excretion, so creatinine clearance does not drive dosing. Dose modifications are triggered by infusion reactions and hemodynamic toxicity — slowing the rate, interrupting, reducing the dose, or giving a half-dose for a given day (as has been done for infusion-associated hypotension), with subsequent full doses usually tolerated. There is no established creatinine- or eGFR-based dose reduction.

Dialyzability & ESKD dosing

Not dialyzable. Naxitamab is a large (~150 kDa) IgG1 monoclonal antibody with a large-molecule volume of distribution and reticuloendothelial clearance; it is not removed by hemodialysis or peritoneal dialysis, and dialysis has no role in enhancing its elimination.

Differential diagnosis

The transient creatinine rise should be read as hemodynamic/prerenal from the infusion reaction, but consider: (1) volume depletion from concurrent vomiting/diarrhea or poor intake; (2) prolonged or severe hypotension tipping into ischemic acute tubular necrosis; (3) full anti-GD2 capillary-leak syndrome (well documented in the class — e.g., fatal capillary leak with dinutuximab beta plus IL-2), which causes intravascular volume loss and hypoperfusion; (4) nephrotoxicity from co-administered agents or supportive drugs (though partner cytotoxics like irinotecan/temozolomide are not classically nephrotoxic); (5) contrast- or sepsis-associated AKI in a heavily pretreated child; and (6) hypertension-related processes (e.g., PRES), which are uncommon with short outpatient naxitamab infusions.

Monitoring

Continuous blood pressure and heart rate during the infusion and through the post-infusion observation window (capture both hypotensive and hypertensive swings)
Cardiorespiratory/oxygen saturation monitoring for the broader infusion-reaction complex
Fluid balance, body weight, and edema (screen for capillary leak)
Serum creatinine and electrolytes around each cycle, with closer checks after any significant hypotensive episode
Serum albumin if capillary-leak syndrome is suspected
Symptom review for pain, urticaria, bronchospasm to gauge premedication adequacy

Key trials & series

Trial 201 (NCT03363373) — pivotal single-arm, multicenter phase 2 of naxitamab + GM-CSF in relapsed/refractory high-risk neuroblastoma in bone/bone marrow; supported U.S. accelerated approval and defined the safety profile (grade 3 hypotension 58%, pain 54%)
Study 201/12750 outpatient AE-management experience — protocolized algorithms for infusion-related hypotension and bronchospasm
HITS regimen study (irinotecan, temozolomide, naxitamab + GM-CSF) — chemo-immunotherapy for primary refractory disease, with pain and hypertension noted as expected naxitamab toxicities

Clinical pearls

The kidney is a bystander: naxitamab has no intrinsic tubular/glomerular lesion — renal injury, when it occurs, is prerenal/hemodynamic from infusion-reaction blood-pressure swings and capillary leak.
Expect blood-pressure lability in BOTH directions — hypotension is the dominant grade 3 event, but on-treatment hypertension is also an expected naxitamab toxicity.
Naxitamab is dosed roughly 2.5x higher (~270 mg/m2/cycle) than dinutuximab/dinutuximab beta, yet hemodynamic events concentrate in the first few cycles and are largely outpatient-manageable.
Overt capillary-leak syndrome and PRES are uncommon with the short (30-90 minute) outpatient infusions used for naxitamab.
Rate reduction, an IV fluid bolus, or a half-dose for the day rescues most hypotensive episodes; full dosing usually resumes at the next infusion.
Not renally cleared and not dialyzable — there is no creatinine-based dose adjustment; manage the hemodynamics, not a clearance number.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Glomerulus

Filtration barrier (podocytes + endothelium)

Injury signatures

Prerenal / Hemodynamic AKI Hypertension

§05

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 · 2018–2025 · 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 (May 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: SERIOUS INFUSION-RELATED REACTIONS and NEUROTOXICITY WARNING: SERIOUS INFUSION-RELATED REACTIONS and NEUROTOXICITY See full prescribing information for complete boxed warning Serious Infusion-Related Reactions: DANYELZA can cause serious infusion reactions, including cardiac arrest, anaphylaxis, hypotension, bronchospasm, and stridor. Premedicate prior to each DANYELZA infusion as recommended. Reduce the rate, interrupt infusion, or permanently discontinue DANYELZA based on severity ( 2.2 , 2.3 , 4 , 5.1 ). Neurotoxicity: DANYELZA can cause severe neurotoxicity, including severe neuropathic pain, transverse myelitis, and reversible posterior leukoencephalopathy syndrome (RPLS). Premedicate to treat neuropathic pain as recommended. Permanently discontinue DANYELZA based on the adverse reaction and severity ( 2.2 , 2.3 , 5.2 ). Serious Infusion-Related Reactions DANYELZA can cause serious infusion reactions, including cardiac arrest, anaphylaxis, hypotension, bronchospasm, and stridor. Infusion reactions of any Grade occurred in 94-100% of patients. Severe infusion reactions occurred in 32-68% and serious infusion reactions occurred in 4 - 18% of patients in DANYELZA clinical studies [see Warnings and Precautions (5.1) ]. Premedicate prior to each DANYELZA infusion as recommended and monitor patients for at least 2 hours following completion of each infusion. Reduce the…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 241 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· 4.6% of reports w/ death · 34.9% w/ hospitalization

4.6%

Reported with a death outcome

11 of 241 reports

34.9%

Reported with hospitalization

84 of 241 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 241 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 1.1495% CI 0.28–4.60· 2 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Vascular

Hypotension65Hypertension33Blood Pressure Decreased6

General / constitutional

Pain63Pyrexia23Fatigue6

Skin

Urticaria29Rash26

Respiratory

Oxygen Saturation Decreased17Hypoxia15Cough12Dyspnoea10

Gastrointestinal

Abdominal Pain14Vomiting13Nausea7

Immune / infection

Anaphylactic Reaction11Hypersensitivity10Anaphylactic Shock8

Blood & lymphatic

Febrile Neutropenia11Myelosuppression9

Cardiac

Tachycardia15

Nervous system

Posterior Reversible Encephalopathy Syndrome9

Guidelines & consensus· 12

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 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 Naxitamab 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

Dinutuximab

Unituxin · Anti-GD2 antibody

Profile

Capillary-leak syndrome, hypertension and severe pain in neuroblastoma.

PREHTNTMA

Moderate#1 · 72% phenotype match

Asciminib

Scemblix · BCR-ABL STAMP inhibitor

Profile

Hypertension and pancreatitis; allosteric BCR-ABL inhibitor.

HTNPRE

Mild#2 · 72% phenotype match

Zolbetuximab

Vyloy · Anti-Claudin-18.2 monoclonal antibody

Profile

2024 gastric mAb; severe on-target nausea/vomiting → volume-depletion prerenal AKI.

PRE

Moderate#3 · 64% phenotype match

Sunitinib

Sutent · VEGFR TKI

Profile

VEGFR-TKI; hypertension and proteinuria, TMA reported.

HTNGLOMTMA

Moderate#4 · 64% phenotype match

Olverembatinib

Olverembatinib (HQP1351) · BCR-ABL1 tyrosine kinase inhibitor (3rd generation)

Profile

Potent T315I-active TKI with a largely renal-sparing profile

GLOMPREHTN

Mild#5 · 59% phenotype match

Ponatinib

Iclusig · BCR-ABL TKI

Profile

Vascular toxicity and hypertension.

HTNPRETMA

Moderate#6 · 59% phenotype match

Compare Naxitamab 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 Monoclonal antibodies (other)

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.