What kind of kidney injury does Tagraxofusp cause?

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

How should kidney function be monitored during Tagraxofusp therapy?

Serum albumin before each dose (hold if <3.2 g/dL); Daily weight and blood pressure during cycle 1; Edema, oxygen saturation, and signs of pulmonary edema; Daily serum albumin during cycle 1 inpatient observation.

How can kidney injury from Tagraxofusp be prevented?

Require serum albumin >= 3.2 g/dL before the first dose and before each subsequent dose Premedicate (corticosteroids, antihistamines, antipyretics) and give prompt corticosteroids and albumin at the first CLS signs; hold dosing per protocol

Who is at higher risk of kidney injury from Tagraxofusp?

Low baseline serum albumin (<3.2 g/dL); Pre-existing cardiac or volume-overload states; First cycle of therapy; Pre-existing low platelet count / bleeding risk amplifying hemodynamic instability.

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Printable monograph

IL-3 immunotoxin

Tagraxofusp

Elzonris · Tagrax

IL-3 immunotoxin · approved 2018 · 7 citations · FAERS AKI reporting ROR 6.33 (95% CI 4.16–9.61, 23 AKI reports)

Up to date· through 2026

Fairly sourced6/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 6y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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 CD123-directed diphtheria-toxin fusion whose capillary leak can collapse the circulation and the kidneys.

ModerateIL-3 / CD123-directed immunotoxin

Blastic plasmacytoid dendritic cell neoplasm (BPDCN)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Capillary leak syndrome (CLS) is a boxed-warning toxicity occurring in ~19-21% of treated patients in the registrational trial (mostly grade 2; grade >=3 in ~4% — 2% grade 3 plus 2% grade 4 — with two deaths); the resulting hypotension, hypoalbuminemia, and fluid shifts can precipitate prerenal AKI and, with prolonged hypoperfusion, ischemic ATN. Renal-specific AKI incidence is not separately quantified.Source: Pemmaraju et al., J Clin Oncol 2022

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Usually during the first cycle, often within days of the first doses.

Distilled from: “Typically during the first treatment cycle, often within days of the first doses; recurrence in later cycles is uncommon with proactive monitoring.”

RechallengeOften tolerated

Recurrence in later cycles is uncommon with proactive monitoring.

§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 · Signature19%PMID 31018069 (opens PubMed in a new tab)
Capillary leak syndrome in 19% of patients in the pivotal BPDCN trial (fatal in one patient per dose subgroup); CLS drives intravascular volume depletion / prerenal physiology
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

§03

Kidney injury

Mechanism of kidney injury

Endothelial injury from the diphtheria-toxin immunotoxin (CD123 is also expressed on endothelium) produces a systemic capillary-leak state: intravascular fluid and albumin extravasate into the interstitium, causing hypoalbuminemia, edema, weight gain, and hypotension. The fall in effective circulating volume drives prerenal azotemia and, when severe or prolonged, ischemic acute tubular necrosis.

Clinical presentation

Weight gain, peripheral and pulmonary edema, hypoalbuminemia (often <3.0 g/dL), hypotension, and rising creatinine, usually in cycle 1. Falling serum albumin and rising weight are the earliest CLS signals; severe cases progress to shock and pulmonary edema.

Management

Treat CLS aggressively: corticosteroids, IV albumin to support oncotic pressure, judicious fluid management, and interruption of tagraxofusp. Support blood pressure and renal perfusion (vasopressors if needed). Most AKI is prerenal and improves with CLS resolution; established ATN requires standard supportive care and occasionally renal replacement therapy.Lesion-level management framework

Risk factors

Low baseline serum albumin (<3.2 g/dL)
Pre-existing cardiac or volume-overload states
First cycle of therapy
Pre-existing low platelet count / bleeding risk amplifying hemodynamic instability

Prevention

Require serum albumin >= 3.2 g/dL before the first dose and before each subsequent dose
Premedicate (corticosteroids, antihistamines, antipyretics) and give prompt corticosteroids and albumin at the first CLS signs; hold dosing per protocol

Anticancer mechanism· how it treats cancer

Recombinant fusion of interleukin-3 (IL-3) and truncated diphtheria toxin that binds the IL-3 receptor alpha chain (CD123) overexpressed on malignant cells, internalizes, and the diphtheria-toxin payload ADP-ribosylates elongation factor 2 to halt protein synthesis and trigger apoptosis. First approved therapy for blastic plasmacytoid dendritic cell neoplasm (BPDCN).

Note · Capillary-leak syndrome carries a boxed warning; renal injury is a downstream consequence of endothelial leak and hemodynamic collapse rather than direct tubular toxicity.

§04

Clinical depth

Renal dose adjustment

No established renal dose adjustment (clearance is proteolytic, not renal). Dosing decisions hinge on albumin, weight, and CLS status rather than eGFR.

Dialyzability & ESKD dosing

Large fusion protein cleared by proteolysis; not dialyzable. Hemodialysis/CRRT is used to support AKI/volume overload, not to remove the drug.

Differential diagnosis

Tagraxofusp CLS-driven prerenal AKI/ATN (hypoalbuminemia, weight gain, edema in cycle 1) vs sepsis/neutropenic shock vs cardiogenic edema vs tumor-related fluid overload. Hypoalbuminemia with weight gain and hemoconcentration points to CLS.

Monitoring

Serum albumin before each dose (hold if <3.2 g/dL)
Daily weight and blood pressure during cycle 1
Edema, oxygen saturation, and signs of pulmonary edema
Daily serum albumin during cycle 1 inpatient observation

Key trials & series

Pemmaraju phase 1/2 pivotal BPDCN trial (NEJM 2019) and JCO 2022 long-term follow-up
Pemmaraju & Konopleva Blood Adv 2020 approval review

Clinical pearls

Albumin is the vital sign for tagraxofusp - do not dose if <3.2 g/dL.
CLS clusters in cycle 1; intensive monitoring then prevents most severe events.
The AKI is a hemodynamic consequence of capillary leak, not a direct tubular toxin - fix the circulation and the kidney follows.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Injury signatures

Prerenal / Hemodynamic AKI Acute Tubular Necrosis

§05

References

6 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

6 references · 2020–2025 · 3 since 2023

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Case reports — ranked by strength· 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 · LimitedSustained response to minimal-dose tagraxofusp in a patient with BPDCN and advanced chronic kidney disease.Brummer C et al. · Ann Hematol 2026 · PMID 41535617Case report of a 79-year-old with BPDCN and advanced CKD who developed acute-on-chronic renal failure after three doses of dose-reduced tagraxofusp, fully reversible after drug discontinuation, consistent with hemodynamic/prerenal AKI.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Dec 2024) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: CAPILLARY LEAK SYNDROME Capillary Leak Syndrome (CLS) which may be life-threatening or fatal, can occur in patients receiving ELZONRIS. Monitor for signs and symptoms of CLS and take actions as recommended [see Warnings and Precautions ( 5.1 )] . WARNING: CAPILLARY LEAK SYNDROME See full prescribing information for complete boxed warning. Capillary Leak Syndrome (CLS), which may be life-threatening or fatal if not properly managed, can occur in patients receiving ELZONRIS. ( 5.1 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 520 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· 30% of reports w/ death · 25.4% w/ hospitalization

30%

Reported with a death outcome

156 of 520 reports

25.4%

Reported with hospitalization

132 of 520 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 520 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 6.3395% CI 4.16–9.61· 23 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury23

Hepatobiliary

Transaminases Increased22Liver Function Test Increased19Aspartate Aminotransferase Increased17Alanine Aminotransferase Increased16Hepatic Enzyme Increased15

General / constitutional

Pyrexia46Weight Increased28Fatigue16

Metabolic & electrolyte

Tumour Lysis Syndrome26Hypoalbuminaemia25

Blood & lymphatic

Thrombocytopenia35Platelet Count Decreased13

Immune / infection

Sepsis23Pneumonia17

Respiratory

Dyspnoea15Hypoxia13

Vascular

Hypotension20

Psychiatric

Confusional State13

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 Tagraxofusp 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

Tretinoin (ATRA)

Vesanoid · Retinoid (differentiating agent)

Profile

Differentiation syndrome → capillary leak and AKI.

PREATN

Moderate#1 · 100% phenotype match

Sotorasib

Lumakras · KRAS G12C inhibitor

Profile

Newer agent; renal data emerging.

PREATN

Mild#2 · 95% phenotype match

Talquetamab

Talvey · Bispecific (GPRC5D×CD3)

Profile

CRS-related AKI — emerging.

PREATN

Moderate#3 · 89% phenotype match

Teclistamab

Tecvayli · Bispecific (BCMA×CD3)

Profile

CRS-associated AKI in myeloma — emerging signal.

PREATN

Moderate#4 · 89% phenotype match

Tasonermin

Beromun · Recombinant TNF-α (cytokine)

Profile

Isolated-limb-perfusion agent; systemic leakage → SIRS/hypotension → prerenal AKI.

PREATN

Moderate#5 · 88% phenotype match

Arsenic trioxide

Trisenox · Differentiating agent

Profile

Differentiation syndrome; QT prolongation.

PREATNLYTE

Moderate#6 · 84% phenotype match

Compare Tagraxofusp 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.