Bendamustine
Treanda · Alkylator
Tumor lysis-mediated AKI is the principal risk; TMA is rare.
PRETMALYTE
ModerateOpen →
Anti-CCR4 antibody
Mogamulizumab
Poteligeo · MOG
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 · approved 2018
Relapsed/refractory mycosis fungoides and Sezary syndrome (cutaneous T-cell lymphoma) after >=1 prior systemic therapy
Signature kidney injury
Prerenal / Hemodynamic AKI
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.
Source: Kim et al., Lancet Oncol 2018 (MAVORIC); Ishitsuka et al., Int J Hematol 2017
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.
Onset
Infusion reactions early; rash over weeks; tumor lysis early in responders.
Reversibility
Reversible
Anticancer mechanism
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.
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.
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
- Maintain hydration; monitor renal function and electrolytes early
- Avoid additive nephrotoxins
Note · The renal link is indirect — chiefly treatment-related tumor lysis in high-burden disease and rare transient AKI rather than a direct lesion.
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
- Renal function and CBC periodically
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.
Where it strikes
Nephron segments
Vasculature / Endothelium
Glomerular & peritubular capillaries
Tubular Lumen
The urine flow path
Injury signatures
Prerenal / Hemodynamic AKIElectrolyte Wasting
Evidence
6 peer-reviewed references. Citation metadata via PubMed / NLM.
LandmarkMogamulizumab versus vorinostat in previously treated cutaneous T-cell lymphoma (MAVORIC): an international, open-label, randomised, controlled phase 3 trial.Kim YH et al. · Lancet Oncol 2018 · PMID 30100375Registrational RCT establishing efficacy and the rash/infusion safety profile.PMIDPhase 1/2 study of mogamulizumab in patients with relapsed/refractory cutaneous T-cell lymphoma.Duvic M et al. · Blood 2015 · PMID 25605368Early efficacy/safety including tumor-lysis observations.PMIDTumor lysis syndrome associated with mogamulizumab in adult T-cell leukemia/lymphoma.Ishitsuka K et al. · Int J Hematol 2017 · PMID 28597329Documents tumor lysis (~2-3%) as the key renal-relevant complication.PMIDMogamulizumab-associated cutaneous adverse reactions.Hirotsu KE et al. · JAMA Dermatol 2021 · PMID 33881447Characterizes the immune-mediated drug rash distinct from renal injury.PMIDMogamulizumab in cutaneous T-cell lymphoma: clinical experience and management.Trager MH et al. · Clin Lymphoma Myeloma Leuk 2020 · PMID 32449779Practical management of mogamulizumab toxicities.PMIDGuidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review.Cairo MS et al. · J Clin Oncol 2010 · PMID 20331465Consensus TLS prophylaxis/management applicable to high-burden CTCL.
Related agents
Other agents sharing the same signature kidney injury.