How should kidney function be monitored during Mogamulizumab therapy?

TLS labs in higher-burden responders (uric acid, phosphate, potassium, creatinine); Skin assessment for drug rash; Vital signs during infusions.

How can kidney injury from Mogamulizumab be prevented?

Tumor-lysis risk assessment with hydration +/- allopurinol or rasburicase in high-burden disease Infusion premedication; monitor for and manage drug rash

Who is at higher risk of kidney injury from Mogamulizumab?

High circulating tumor burden / Sezary syndrome (tumor-lysis risk); Pre-existing CKD and concurrent nephrotoxins; Volume depletion; Inadequate infusion premedication.

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Printable monograph

Anti-CCR4 antibody

Mogamulizumab

Poteligeo · MOG

Anti-CCR4 antibody · approved 2018 · 6 citations

Aging evidence· through 2021

Fairly sourced6/9 · 5 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2021
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.

Defucosylated anti-CCR4 antibody for cutaneous T-cell lymphoma — renal-relevant risks are treatment-related tumor lysis and rare AKI, not a direct nephropathy.

MildGlycoengineered antibody era

Relapsed/refractory mycosis fungoides and Sezary syndrome (cutaneous T-cell lymphoma) after >=1 prior systemic therapy

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Representative incidence2.5%

Drug rash and infusion reactions are characteristic; tumor lysis occurred in roughly 2-3% in some series. AKI is rare and largely secondary to tumor lysis or volume shifts; a discrete AKI incidence is not well quantified. Reported rate: tumor lysis syndrome in 2.5% — 484 patients (safety analysis population) with CCR4-positive relapsed or refractory adult T-cell leukemia-lymphoma in a… (Ishitsuka 2017, PMID 28597329).Source: Kim et al., Lancet Oncol 2018 (MAVORIC); Ishitsuka et al., Int J Hematol 2017

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor lysis early in responders.

Distilled from: “Infusion reactions early; rash over weeks; tumor lysis early in responders.”

§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).

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

2.5%incidence

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

Mogamulizumab has no characteristic direct renal lesion. Its renal relevance is indirect: (1) in patients with circulating tumor burden (Sezary syndrome), rapid CCR4-positive cell killing can cause tumor lysis with urate/phosphate intratubular crystal nephropathy and ATN; (2) infusion reactions and the characteristic skin toxicity with systemic inflammation can produce transient hemodynamic effects. Depletion of regulatory T cells underlies the autoimmune-flavored skin and immune adverse events but is not a defined renal mechanism.

Clinical presentation

Drug eruption/rash, infusion reactions; in responders with high tumor burden, TLS labs (hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia) and AKI early in treatment. Otherwise renal function is usually preserved.

Management

Treat tumor lysis with aggressive hydration, urate-lowering therapy and electrolyte correction (dialysis if refractory). Manage infusion reactions and drug rash (topical/systemic steroids; hold for severe rash). Restore volume for transient prerenal AKI; renal effects are generally reversible.Lesion-level management framework

Risk factors

High circulating tumor burden / Sezary syndrome (tumor-lysis risk)
Pre-existing CKD and concurrent nephrotoxins
Volume depletion
Inadequate infusion premedication

Prevention

Tumor-lysis risk assessment with hydration +/- allopurinol or rasburicase in high-burden disease
Infusion premedication; monitor for and manage drug rash

Anticancer mechanism· how it treats cancer

Defucosylated humanized monoclonal antibody against CC chemokine receptor 4 (CCR4), expressed on malignant T cells and regulatory T cells. Glycoengineering markedly enhances antibody-dependent cellular cytotoxicity, depleting CCR4-positive cells in mycosis fungoides and Sezary syndrome.

Note · The renal link is indirect — chiefly treatment-related tumor lysis in high-burden disease and rare transient AKI rather than a direct lesion.

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Clinical depth

Renal dose adjustment

No dose adjustment for renal impairment (a monoclonal antibody, not renally cleared); interruptions are driven by rash and infusion reactions.

Dialyzability & ESKD dosing

A monoclonal antibody; not dialyzable. Dialysis is used for TLS metabolic complications, not drug removal.

Differential diagnosis

Distinguish tumor-lysis crystalline nephropathy (early, in high-burden responders) from prerenal azotemia and other AKI causes. The drug rash is immune-mediated but not a renal lesion.

Monitoring

TLS labs in higher-burden responders (uric acid, phosphate, potassium, creatinine)
Skin assessment for drug rash
Vital signs during infusions

Key trials & series

MAVORIC (Kim, Lancet Oncol 2018) — registrational RCT vs vorinostat in CTCL
Ishitsuka et al. (Int J Hematol 2017) — tumor-lysis observations (~2-3%)

Clinical pearls

The kidney-relevant risk is tumor lysis in high-burden (Sezary) disease, not a direct mogamulizumab nephropathy.
Characteristic drug rash reflects regulatory T-cell depletion — manage with steroids, not as renal disease.
As an antibody it needs no renal dose adjustment and is not dialyzable.
Risk-stratify circulating tumor burden for TLS before the first infusions.

§05

References

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

Evidence accrual

6 references · 2010–2021 · 2 since 2019

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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,316 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· 2 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

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Electrolyte DisturbanceNo 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 4.1395% CI 1.55–11.01· 4 reports

Glomerular Injury / Proteinuria

ROR 2.7495% CI 1.14–6.61· 5 reports

FAERS outcomes & reporting trend· 14.4% of reports w/ death · 17.2% w/ hospitalization

14.4%

Reported with a death outcome

190 of 1,316 reports

17.2%

Reported with hospitalization

226 of 1,316 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 1,316 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 1.3695% CI 0.79–2.35· 13 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Skin

Rash188Drug Eruption77Pruritus67Erythema36Skin Disorder27

General / constitutional

Fatigue47Pyrexia45Chills40Malaise20

Immune / infection

Infusion Related Reaction57Sepsis27Infection24Graft Versus Host Disease22

Gastrointestinal

Diarrhoea27Nausea27

Blood & lymphatic

Lymphopenia26

Respiratory

Dyspnoea18

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 Mogamulizumab 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

Tafasitamab

Monjuvi · Anti-CD19 antibody

Profile

Tumor lysis and infusion reactions in lymphoma.

PRELYTE

Mild#1 · 100% phenotype match

Midostaurin

Rydapt · FLT3 / multikinase inhibitor

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild#2 · 89% phenotype match

Tazemetostat

Tazverik · EZH2 inhibitor

Profile

Tumor lysis; generally low direct renal toxicity.

PRELYTE

Mild#3 · 89% phenotype match

Zanidatamab

Ziihera · HER2 bispecific antibody

Profile

2024 biliary-tract HER2 bispecific; renal data emerging.

PRELYTE

Mild#4 · 88% phenotype match

Zenocutuzumab

Bizengri · HER2×HER3 bispecific antibody

Profile

2024 NRG1-fusion bispecific; mostly grade 1-2 AEs — at most diarrhea-related prerenal risk, no CRS/TLS mechanism.

PRELYTE

Mild#5 · 88% phenotype match

Daratumumab

Darzalex · Anti-CD38 antibody

Profile

Tumor lysis; usable in renal impairment.

PRELYTE

Mild#6 · 86% phenotype match

Compare Mogamulizumab 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.