How should kidney function be monitored during Moxetumomab pasudotox therapy?

CBC/platelets and peripheral smear for schistocytes each cycle; LDH, haptoglobin and bilirubin (hemolysis screen); Daily weight, blood pressure, albumin and edema assessment (CLS surveillance).

How can kidney injury from Moxetumomab pasudotox be prevented?

Adequate IV/oral hydration before and after each infusion Do not initiate if CrCl <30 mL/min Consider low-dose aspirin thromboprophylaxis per label; antihistamine/antipyretic premedication

Who is at higher risk of kidney injury from Moxetumomab pasudotox?

Higher cumulative dose/exposure and repeat cycles; Pre-existing renal impairment (avoid initiating if CrCl <30 mL/min); Volume depletion.

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Printable monograph

Immunotoxin (anti-CD22 PE38)

Moxetumomab pasudotox

Lumoxiti · MOXE

Immunotoxin (anti-CD22 PE38) · approved 2018 · 8 citations

Aging evidence· through 2020

Fairly sourced5/9 · 4 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 14y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Not met: Current through 2020
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 anti-CD22 Pseudomonas-exotoxin immunotoxin with a boxed warning for capillary leak and hemolytic-uremic syndrome.

SevereAnti-CD22 immunotoxin (PE38)

Relapsed or refractory hairy-cell leukemia after at least two prior systemic therapies, including a purine nucleoside analog

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Signature kidney injury

Signature lesion

Thrombotic Microangiopathy

Representative incidence7.5%

Boxed warning for capillary-leak syndrome (CLS) and hemolytic-uremic syndrome (HUS)/TMA. In the pivotal phase 3 trial HUS occurred in ~7.5% and CLS in ~5%; reviews cite roughly 9% each. Fatal CLS has been reported (in a pediatric ALL case).Source: Kreitman et al., Leukemia 2018

Onset & rechallenge

Time to injuryVariable / unpredictable

Capillary-leak within the first days of a cycle; HUS often during/after cycles 2–3.

Distilled from: “Cycle-related: CLS within the first days of a cycle; HUS often during/after cycles 2-3.”

Long-term outlook & thresholds

Renal recoveryUsually reversible

In the pivotal hairy-cell-leukemia trial the two microvascular toxicities that define this agent's renal risk both reversed: treatment-related serious hemolytic uremic syndrome occurred in 7.5% and capillary leak syndrome in 5%, and both were reversible with supportive care and treatment discontinuation.PMID 30030507 (opens PubMed in a new tab)

Early-detection biomarkers

Platelet count paired with serum creatinine — Immunotoxin-associated HUS / thrombotic microangiopathy. This drug is unusual in that its registration programme caught HUS as a laboratory event: in the phase I hairy-cell trial the two HUS cases were transient laboratory abnormalities — peak creatinine 1.53–1.66 mg/dl with a platelet nadir of 106,000–120,000/µL — with no dose-limiting toxicity, which is exactly the pre-symptomatic window this layer exists to name. The ceiling is equally published: in the international paediatric phase 2 study (Shah 2020, PMID 31944549; CLS in 6 and HUS in 4 of the 30 children who received drug) no inflammatory marker differed between patients who did and did not develop capillary-leak syndrome or HUS, so nothing yet predicts the event before these two numbers move.PMID 22355053 (opens PubMed in a new tab)
Serum albumin with daily weight — Capillary leak → intravascular depletion and prerenal AKI — the drug's non-TMA renal pathway. Reversible weight gain, transaminase elevation and hypoalbuminaemia were the most common treatment-related events in the paediatric phase 1 study, where dose-limiting capillary-leak syndrome occurred and dexamethasone prophylaxis prevented further episodes; hypoalbuminaemia was likewise the single most frequent drug-related toxicity in the adult hairy-cell trial. Tracks the prerenal pathway, not the TMA lesion — and both are descriptive toxicity frequencies, not a validated monitoring threshold.PMID 28983018 (opens PubMed in a new tab)

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

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Renal toxicities, ranked

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

Thrombotic Microangiopathy#1 · Signature7.5%PMID 30030507 (opens PubMed in a new tab)
Hemolytic uremic syndrome 7.5% (treatment-related serious AE) in the pivotal relapsed/refractory HCL trial; boxed warning
Prerenal / Hemodynamic AKISecondaryno population incidence denominator
Capillary leak syndrome 5% causing intravascular volume depletion/hypoperfusion PMID 30030507 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

7.5%incidence

SeveritySevere

ReversibilityReversible

Evidence8 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Thrombotic Microangiopathy

Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

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Kidney injury

Mechanism of kidney injury

Two distinct vascular mechanisms. HUS/TMA: toxin-mediated endothelial injury produces glomerular microangiopathy with microthrombi, mechanical red-cell shearing (schistocytes) and platelet consumption, causing AKI. CLS: toxin- and cytokine-mediated capillary permeability leads to fluid/protein extravasation, intravascular volume depletion and prerenal/hypovolemic AKI.

Clinical presentation

HUS triad — microangiopathic hemolytic anemia (schistocytes, high LDH, low haptoglobin), thrombocytopenia and a rising creatinine. CLS — hypotension, edema, weight gain, hypoalbuminemia and hemoconcentration. HUS classically emerges during/after cycles 2-3 (anamnestic), CLS within the first days of a cycle.

Management

For CLS: hold the drug, give IV fluids and albumin, and add corticosteroids. For HUS/TMA: discontinue (do not retreat), provide supportive care with transfusion and dialysis as needed; plasma exchange and eculizumab are not established for this drug-induced TMA. Most hairy-cell-leukemia events are reversible with supportive care.Lesion-level management framework

Risk factors

Higher cumulative dose/exposure and repeat cycles
Pre-existing renal impairment (avoid initiating if CrCl <30 mL/min)
Volume depletion

Prevention

Adequate IV/oral hydration before and after each infusion
Do not initiate if CrCl <30 mL/min
Consider low-dose aspirin thromboprophylaxis per label; antihistamine/antipyretic premedication

Anticancer mechanism· how it treats cancer

Recombinant immunotoxin joining an anti-CD22 Fv fragment to PE38, a truncated Pseudomonas exotoxin A. Binding to CD22 on hairy-cell leukemia cells drives internalization; the toxin then ADP-ribosylates elongation factor 2 (eEF2), halting protein synthesis and triggering apoptosis. Hairy-cell leukemia is exquisitely sensitive owing to high CD22 density.

Note · Voluntarily withdrawn from the US market in 2023 for commercial (not safety) reasons; the renal mechanism and boxed-warning data remain reference-grade.

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Clinical depth

Renal dose adjustment

Do not initiate if CrCl <30 mL/min. Hold for serious CLS or HUS; permanently discontinue for HUS or recurrent serious CLS. No simple CrCl-based dose scaling otherwise.

Dialyzability & ESKD dosing

Not characterized — dialysis supports AKI/HUS rather than clearing the immunotoxin.

Differential diagnosis

Distinguish from other drug-induced TMA (gemcitabine, calcineurin inhibitors, mitomycin, VEGF inhibitors), atypical/typical HUS, TTP (check ADAMTS13), DIC, sepsis-related capillary leak, and tumor-related microangiopathy. The cycle timing and hemolysis labs anchor the diagnosis.

Monitoring

CBC/platelets and peripheral smear for schistocytes each cycle
LDH, haptoglobin and bilirubin (hemolysis screen)
Daily weight, blood pressure, albumin and edema assessment (CLS surveillance)

Key trials & series

Pivotal phase 3 in relapsed/refractory HCL (Kreitman, Leukemia 2018) — established reversible HUS (~7.5%) and CLS (~5%)
Phase 1 pediatric ALL study (Wayne, Blood 2017) — dose-dependent CLS and HUS/TMA

Clinical pearls

Anchor monitoring to hemolysis labs plus creatinine (HUS) and weight/BP/albumin (HUS vs CLS).
Hydration is the key prevention; do not initiate if CrCl <30 mL/min.
Do not retreat after HUS — anamnestic HUS classically appears at cycles 2-3.
Most hairy-cell-leukemia events are reversible, but fatal CLS exists — escalate early.

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References

7 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

7 references · 2006–2020 · 4 since 2018

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.

CaseB · ModerateClass II human leucocyte antigen DRB1*11 in hairy cell leukaemia patients with and without haemolytic uraemic syndrome.Arons E et al. · Br J Haematol 2014 · PMID 24931452Small case series identifying HLA-DRB1*11 as a susceptibility marker for anti-CD22 immunotoxin (moxetumomab pasudotox/BL22)-induced hemolytic uremic syndrome (thrombotic microangiopathy) in hairy cell leukemia patients.

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 Moxetumomab pasudotox 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

Tegafur-uracil (UFT)

UFT · Antimetabolite (oral 5-FU prodrug)

Profile

Oral tegafur+uracil; rare fluoropyrimidine-class TMA/HUS (often with mitomycin C), otherwise kidney-sparing.

TMALYTEPRE

Severe#1 · 70% phenotype match

Ixazomib

Ninlaro · Proteasome inhibitor

Profile

Rare TMA reports.

TMA

Moderate#2 · 68% phenotype match

Doxifluridine

Furtulon · Antimetabolite (oral 5-FU prodrug)

Profile

5'-DFUR prodrug; class-level TMA risk plus a real renal-clearance component warranting caution in renal impairment.

TMALYTEPRE

Moderate#3 · 65% phenotype match

Carmofur (HCFU)

Mifurol · Antimetabolite (oral 5-FU prodrug)

Profile

Lipophilic oral 5-FU prodrug (Japan); class-level renal risk; hallmark toxicity is leukoencephalopathy not nephropathy.

TMALYTEPRE

Moderate#4 · 64% phenotype match

Capecitabine

Xeloda · Pyrimidine analog (oral 5-FU)

Profile

Diarrhea-driven prerenal AKI; dose-adjust for CrCl.

PRETMA

Mild#5 · 64% phenotype match

5-Fluorouracil

Adrucil · Pyrimidine analog

Profile

Rare TMA, esp. with mitomycin; mostly renally safe.

TMAPRE

Mild#6 · 64% phenotype match

Compare Moxetumomab pasudotox 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.