Dasatinib
Sprycel · BCR-ABL TKI
Nephrotic-range proteinuria — a notable signal.
GLOM
Moderate#1 · 84% phenotype match
Antibody-drug conjugate (BCMA/MMAF)
Belantamab mafodotin
Blenrep · Bela
Antibody-drug conjugate (BCMA/MMAF) · approved 2020 · 6 citations · FAERS AKI reporting ROR 2.00 (95% CI 1.48–2.71, 42 AKI reports)
Up to date· through 2026
Fairly sourced6/9 · 6 signals
- Met: 6 citations
- Not met: 12+ references
- Not met: Accrued over 10+ years (span: 5y)
- 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 BCMA/MMAF conjugate for myeloma whose hallmark is ocular, not renal — kidney data are emerging.
MildAntibody-drug conjugate
Multiple myeloma
§01
Signature kidney injury
Signature lesion
Renal-specific data are emerging and sparse; direct nephrotoxicity is not an established signal. In myeloma, AKI more often reflects the underlying disease (cast nephropathy, hypercalcemia, volume status) than the ADC. A case of focal segmental glomerulosclerosis after belantamab mafodotin (confounded by severe COVID-19) has been reported. The defining toxicity is ocular keratopathy (71-77% in DREAMM-2).Source: Sabbah et al., Am J Case Rep 2024 (case); Baines et al., Clin Cancer Res 2022 (DREAMM-2)
Onset & rechallenge
Time to injuryVariable / unpredictable
Variable — renal events reported during prolonged therapy (ocular toxicity is the earlier, first-cycle signal).
Distilled from: “Variable; renal events reported during prolonged therapy. Ocular toxicity is often detectable within the first cycles.”
§02
Renal toxicities, ranked
This agent's defining kidney lesion — its #1 signature. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
§03
Kidney injury
Mechanism of kidney injury
No well-defined direct renal mechanism in humans; MMAF-based ADCs are dominated by corneal (keratopathy) toxicity from payload accumulation in proliferating epithelium. Reported renal events are case-level and often confounded by myeloma-related kidney disease (light-chain cast nephropathy, hypercalcemia) or intercurrent illness.
Clinical presentation
When present: proteinuria/nephrotic syndrome or AKI, typically requiring exclusion of myeloma-related causes; the hallmark drug toxicity is ocular (keratopathy with microcyst-like epithelial changes, blurred vision, dry eye, reduced visual acuity).
Management
Evaluate and treat myeloma-related renal causes first; supportive care; nephrology evaluation/biopsy for unexplained proteinuria or AKI. Ocular toxicity is managed by ophthalmology-guided dose modification, not by renal parameters.Lesion-level management framework
Risk factors
- Underlying myeloma kidney disease (cast nephropathy, MIDD)
- Hypercalcemia/volume depletion
- Pre-existing CKD
- Intercurrent infection
Prevention
- Treat myeloma-related renal drivers (light chains, calcium, volume)
- Mandatory baseline and pre-dose ophthalmologic exams under the REMS program (ocular toxicity is the dose-limiting issue)
Anticancer mechanism· how it treats cancer
Antibody-drug conjugate targeting B-cell maturation antigen (BCMA) and delivering the microtubule inhibitor monomethyl auristatin F (MMAF) via a non-cleavable linker; the charged, membrane-impermeable MMAF requires internalization, which limits bystander effect but concentrates payload in target and high-turnover tissues (notably corneal epithelium). Used in relapsed/refractory multiple myeloma.
Note · Renal data are emerging; the defining toxicity of belantamab mafodotin is ocular. Attribute renal findings cautiously given competing myeloma-related causes.
§04
Clinical depth
Renal dose adjustment
No renal dose adjustment defined; pharmacokinetics are not expected to depend on renal clearance for an IgG-MMAF conjugate. Dosing modifications are driven by ocular findings, not renal function.
Dialyzability & ESKD dosing
Not dialyzable (large ADC; non-cleavable linker, internalization-dependent MMAF). No supplemental dosing for HD/PD.
Differential diagnosis
In a myeloma patient on belantamab with AKI/proteinuria, prioritize myeloma-related causes (cast nephropathy, light-chain deposition, hypercalcemia, dehydration) before attributing injury to the ADC; biopsy may be needed for glomerular lesions. The ocular comorbidity (keratopathy) parallels mirvetuximab and shapes overall tolerability.
Monitoring
- Ophthalmologic exam (including slit-lamp/visual acuity) at baseline and before each dose per REMS - the defining monitoring requirement
- Serum creatinine, calcium and urine protein, interpreted against myeloma disease activity
- Serum free light chains as the relevant driver of myeloma kidney disease
Key trials & series
- DREAMM-2 (Baines Clin Cancer Res 2022 FDA summary; keratopathy 71-77%)
- Sabbah Am J Case Rep 2024 (FSGS case, COVID-confounded)
Clinical pearls
- Belantamab and mirvetuximab share the ADC ocular-toxicity story (keratopathy/visual changes) - the eye, not the kidney, is the dose-limiting organ.
- Most AKI in these patients is myeloma, not drug - work up light chains, calcium and volume before blaming belantamab.
- REMS-mandated eye exams, not renal labs, govern dosing.
Where it strikes· nephron segments & injury signatures
Nephron segments
Glomerulus
Filtration barrier (podocytes + endothelium)
Injury signatures
Beyond the kidney — non-renal toxicities· 4 organ systems
Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (BCMA/MMAF) class.
Hematologic
Cytopenias, thrombosis, TMA
- Myelosuppression (payload-dependent)
Ophthalmic
Keratopathy, uveitis, retinopathy
- Keratopathy (belantamab, mirvetuximab, tisotumab)
Pulmonary
Pneumonitis, ILD, effusions, hypertension
- Interstitial lung disease (deruxtecan ADCs)
Neurologic
Neuropathy, encephalopathy, ICANS, PRES
- Peripheral neuropathy (MMAE payloads)
§05
References
6 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.
Evidence accrual
6 references · 2021–2026 · 4 since 2024Primary (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.
- 1.Pharmacokinetics and Safety of Belantamab Mafodotin Monotherapy in Patients With Relapsed/Refractory Multiple Myeloma Who Have Normal and Varying Degrees of Impaired Renal Function.Chen X, Hakim S, Lien YTK, Dimopoulos MA, et al · Clin Lymphoma Myeloma Leuk · 2026 · PMID 42297668Phase 1 DREAMM-12 dedicated renal-impairment PK study (n=36) shows renal elimination is a minor route for the cys-mcMMAF payload (<20% of dose), with belantamab mafodotin and payload exposures similar across normal/mild, severe renal impairment, and ESRD (including dialysis-dependent) patients and a consistent safety profile.
- 2.Mechanism of uptake and toxicity of a BCMA antibody drug conjugate with a MMAF payload by nonantigen expressing cells.Newman C et al · Cell Biol Toxicol · 2026 · PMID 41951857In vitro, belantamab mafodotin is internalized by non-BCMA-expressing primary human renal proximal tubule cells (RPTEC) via a BCMA-independent endocytic route, where the ADC is cleaved to release cys-mcMMAF, breaking down the microtubule network and triggering apoptosis — though uptake and cytotoxicity are lower in renal cells than in corneal epithelial cells (the study's primary focus).
- 3.LandmarkFocal and Segmental Glomerulosclerosis in a Multiple Myeloma Patient After Belantamab Mafodotin Therapy and Severe COVID-19 Infection: A Case Report.Sabbah M et al. · Am J Case Rep · 2024 · PMID 39482831Rare FSGS after belantamab mafodotin, with COVID-19 as a confounder - illustrates case-level renal data.
- 4.FDA Approval Summary: Belantamab Mafodotin for Patients with Relapsed or Refractory Multiple Myeloma.Baines AC et al. · Clin Cancer Res · 2022 · PMID 35736811DREAMM-2 summary: keratopathy in 71-77% with a boxed ocular-toxicity warning and REMS - defines the ocular-dominant profile.
- 5.Advances in the Treatment of Relapsed and Refractory Multiple Myeloma in Patients with Renal Insufficiency: Novel Agents, Immunotherapies and Beyond.Bozic B et al. · Cancers (Basel) · 2021 · PMID 34680184Reviews novel myeloma agents (including BCMA-directed therapy) in patients with renal insufficiency.
- 6.Antibody-Drug Conjugates: The Toxicities and Adverse Effects That Emergency Physicians Must Know.Markides DM et al. · Ann Emerg Med · 2024 · PMID 39641680Class review of ADC toxicities, including ocular-dominant MMAF agents.
FDA label — boxed warning & renal dosing· boxed warning
Quoted verbatim from this agent's current FDA label (Oct 2025) — not paraphrased or interpreted. Full label on DailyMed .
Boxed warning
WARNING: OCULAR TOXICITY • BLENREP causes changes in the corneal epithelium resulting in changes in vision, including severe visual impairment, and symptoms such as blurred vision and dry eyes. In the clinical study, corneal ulcers, including cases with infection, also occurred [see Warnings and Precautions ( 5.1 )] . • Conduct ophthalmic exams at baseline, before each dose, promptly for new or worsening symptoms, and as clinically indicated. In the clinical study, 83% of patients required a dosage modification due to ocular toxicity. Withhold BLENREP until improvement and resume or permanently discontinue, based on severity [see Dosage and Administration ( 2.3 ), Warnings and Precautions ( 5.1 )] . • Because of the risk of ocular toxicity, BLENREP is available only through a restricted program called the BLENREP Risk Evaluation and Mitigation Strategy (REMS) [see Warnings and Precautions ( 5.2 )] . WARNING: OCULAR TOXICITY See full prescribing information for complete boxed warning. • BLENREP causes changes in the corneal epithelium resulting in changes in vision, including severe visual impairment, and symptoms such as blurred vision and dry eyes. In the clinical study, corneal ulcers, including cases with infection, also occurred. ( 5.1 ) • Conduct ophthalmic exams at baseline, before each dose, promptly for new or worsening symptoms, and as clinically indicated. In the…
What gets reported — FAERS
Everything below is FAERS — adverse events someone chose to report, about 2,911 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· 1 signal
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
- Glomerular Injury / ProteinuriaNo 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.
Electrolyte Disturbance
ROR 1.7595% CI 1.30–2.34· 46 reports
FAERS outcomes & reporting trend· 34.1% of reports w/ death · 25.5% w/ hospitalization
34.1%
Reported with a death outcome
993 of 2,911 reports
25.5%
Reported with hospitalization
742 of 2,911 reports
Reports per year
- 2015: 0 reports
- 2016: 0 reports
- 2017: 0 reports
- 2018: 0 reports
- 2019: 3 reports
- 2020: 185 reports
- 2021: 776 reports
- 2022: 1,149 reports
- 2023: 270 reports
- 2024: 82 reports
- 2025: 160 reports
- 2026: 286 reports
Yearly FAERS report volume · most recent year is partial.
FAERS adverse-event signal — all organ systems· 4 systems · 2,911 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 2.0095% CI 1.48–2.71· 42 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.
Eye
Keratopathy845Visual Acuity Reduced773Dry Eye393Night Blindness317Vision Blurred186
General / constitutional
Fatigue107Pyrexia86Asthenia66
Blood & lymphatic
Thrombocytopenia118
Immune / infection
Pneumonia109
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 Belantamab mafodotin 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.
Phenotype-similar agents· the numbered markers on the map above
Profile
Pamidronate
Aredia · Bisphosphonate
Collapsing FSGS — first drug ever linked.
GLOM
Severe#2 · 78% phenotype match
Gefitinib
Iressa · EGFR TKI
Rare nephrotic syndrome.
GLOMAINCYST
Mild#3 · 57% phenotype match
Interferon-α
Intron A · Cytokine
Collapsing FSGS in APOL1 carriers.
GLOMTMA
Severe#4 · 54% phenotype match
Temsirolimus
Torisel · mTOR inhibitor
Proteinuria and glomerular effects; less firmly quantified than everolimus.
GLOMLYTE
Mild#5 · 52% phenotype match
Fruquintinib
Fruzaqla · VEGFR TKI
2023 colorectal VEGFR-TKI; hypertension and proteinuria, class effect.
HTNGLOMTMA
Moderate#6 · 48% phenotype match
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 Antibody-drug conjugates
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.
- 1Mirvetuximab soravtansinePRE — Prerenal / Hemodynamic AKIMild
- 2Belantamab mafodotin· this agentGLOM — Glomerular Injury / ProteinuriaFAERS AKIMild
- 3Tisotumab vedotinPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
- 4Brentuximab vedotinPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
- 5Polatuzumab vedotinPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
- 6Datopotamab deruxtecan (Dato-DXd)ATN — Acute Tubular NecrosisModerate
- 7Loncastuximab tesirinePRE — Prerenal / Hemodynamic AKIModerate
- 8Telisotuzumab vedotin (Teliso-V)ATN — Acute Tubular NecrosisModerate
- 9Sacituzumab govitecanPRE — Prerenal / Hemodynamic AKIModerate
- 10Trastuzumab deruxtecanATN — Acute Tubular NecrosisModerate
- 11Trastuzumab emtansine (T-DM1)TMA — Thrombotic MicroangiopathyModerate
- 12Pivekimab sunirinePRE — Prerenal / Hemodynamic AKIModerate
- 13Enfortumab vedotinATN — Acute Tubular NecrosisFAERS AKIModerate
- 14Gemtuzumab ozogamicinPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate
- 15Inotuzumab ozogamicinPRE — Prerenal / Hemodynamic AKIFAERS AKIModerate
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.