Skip to content
Back to explorer
Printable monograph

Anti-SLAMF7 mAb

Elotuzumab

Empliciti · Elotuz

Anti-SLAMF7 mAb · approved 2015 · 4 citations · FAERS AKI reporting ROR 2.58 (95% CI 2.10–3.16, 95 AKI reports)

Dated evidence· through 2017
Fairly sourced4/9 · 4 signals
  • Not met: 4 citations
  • Not met: 12+ references
  • Not met: Accrued over 10+ years (span: 2y)
  • Met: Beyond single case reports
  • Met: High-impact journal
  • Met: Landmark reference
  • Not met: Current through 2017
  • 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 SLAMF7 antibody that is reassuringly kidney-neutral — usable across severe impairment and dialysis without adjustment.

MildAnti-SLAMF7 monoclonal antibody
Relapsed/refractory multiple myeloma (with lenalidomide or pomalidomide and dexamethasone)
§01

Signature kidney injury

Elotuzumab itself has no characteristic direct nephrotoxicity. A dedicated phase Ib study in myeloma patients with normal renal function, severe renal impairment (CrCl < 30 mL/min, not on dialysis), and end-stage renal disease on dialysis found comparable elotuzumab pharmacokinetics across all groups, with grade 3-4 adverse events of similar frequency and no need for dose adjustment. The relevant renal context is the underlying myeloma kidney disease the regimen treats, plus the partner-drug toxicities (lenalidomide is renally cleared).Source: Berdeja et al., Clin Lymphoma Myeloma Leuk 2015 (phase Ib renal-impairment study)

Onset & rechallenge

Time to injuryHyperacute (<24 h)

No direct renal injury; infusion reactions occur during or shortly after the first infusions.

Distilled from: “Not applicable for direct renal injury; infusion reactions occur during/shortly after the first infusions.”

§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.

  1. Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence

    Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

As a large IgG1 antibody, elotuzumab is cleared by reticuloendothelial proteolysis, not renal filtration, and does not concentrate in or injure the nephron; its serum exposure is unchanged in severe renal impairment and dialysis. It carries no intrinsic tubular, glomerular, or crystal toxicity. Electrolyte or renal abnormalities seen during therapy are attributable to the underlying plasma-cell disorder (light-chain cast nephropathy, hypercalcemia), to the renally-cleared immunomodulatory partner (lenalidomide), or to infusion reactions — not to elotuzumab. The only elotuzumab-attributable renal risk is therefore indirect and prerenal: a transient, hemodynamic effect if a severe infusion reaction drops blood pressure, which is why it sits — like the anti-CD38 myeloma antibodies (daratumumab, isatuximab) — in the prerenal/kidney-neutral category rather than carrying any direct nephrotoxic lesion. It deepens disease control that can itself improve myeloma-related renal function.

Clinical presentation

No drug-specific renal syndrome. Infusion reactions are the main acute toxicity (largely grade 1-2, mitigated by premedication). Any creatinine rise or electrolyte disturbance should be traced to myeloma activity, the partner immunomodulator, or intercurrent causes rather than to elotuzumab.

Management

No elotuzumab-specific renal dose change is required, including in dialysis. Manage infusion reactions per protocol; address renal events through the underlying myeloma and the renally-cleared partner agents.Lesion-level management framework

Risk factors

  • Underlying myeloma cast nephropathy / hypercalcemia (disease-related)
  • Concurrent lenalidomide in renal impairment (partner-drug accumulation)
  • Pre-existing CKD

Prevention

  • Standard infusion-reaction premedication
  • Dose-adjust the renally-cleared partner (lenalidomide) for GFR
  • Treat myeloma-related renal disease (hydration, anti-myeloma therapy, hypercalcemia management)
Anticancer mechanism· how it treats cancer

Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1), expressed on myeloma cells and NK cells. It kills myeloma cells through antibody-dependent cellular cytotoxicity and direct NK-cell activation. Given with lenalidomide/dexamethasone or pomalidomide/dexamethasone for relapsed/refractory multiple myeloma.

Note · Among myeloma antibodies, elotuzumab is notably kidney-neutral: a dedicated study supports use without dose adjustment across severe impairment and ESKD. Renal vigilance should focus on the disease and on lenalidomide rather than on this antibody.
§04

Clinical depth

Renal dose adjustment

No dose adjustment for any degree of renal impairment, including severe impairment and end-stage renal disease on dialysis (Berdeja 2015). The actionable renal adjustment is to the partner immunomodulator, not to elotuzumab.

Dialyzability & ESKD dosing

A ~150 kDa IgG1 antibody — not removed by hemodialysis and cleared by proteolysis; pharmacokinetics are unchanged in dialysis patients, so no peri-dialysis timing change is needed.

Differential diagnosis

A creatinine rise on an elotuzumab regimen is far more likely myeloma cast nephropathy, hypercalcemia, or lenalidomide effect than antibody toxicity; serum free light chains, calcium, and urinalysis help distinguish disease relapse from drug effect.

Monitoring

  • Serum creatinine/eGFR (largely to guide the renally-cleared partner drug)
  • Serum calcium and free light chains (disease activity)
  • Infusion-reaction monitoring during administration

Key trials & series

  • ELOQUENT-2 (Lonial NEJM 2015) pivotal phase III with lenalidomide/dexamethasone
  • Berdeja Clin Lymphoma Myeloma Leuk 2015 phase Ib renal-impairment/ESKD PK study

Clinical pearls

  • When the kidney function worsens on an elotuzumab regimen, suspect the myeloma or the lenalidomide, not the antibody.
  • Infusion reactions, not nephrotoxicity, are the toxicity to premedicate for.
Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

§05

References

3 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

3 references · 2015–2017 · 3 since 2015
202015: 2 citations2017: 1 citation20152017

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.

  1. 1.LandmarkPharmacokinetics and Safety of Elotuzumab Combined With Lenalidomide and Dexamethasone in Patients With Multiple Myeloma and Various Levels of Renal Impairment: Results of a Phase Ib Study.Berdeja J et al. · Clin Lymphoma Myeloma Leuk · 2015 · PMID 26795075Phase Ib across normal function, severe impairment, and ESKD on dialysis: comparable PK and safety, supporting use without dose adjustment.
  2. 2.Elotuzumab Therapy for Relapsed or Refractory Multiple Myeloma.Lonial S et al. · N Engl J Med · 2015 · PMID 26035255Pivotal ELOQUENT-2 trial establishing efficacy and the infusion-reaction-dominant safety profile.
  3. 3.Acute Kidney Injury in Patients with Cancer.Rosner MH et al. · N Engl J Med · 2017 · PMID 28467867Onconephrology reference framing myeloma-related kidney disease versus drug toxicity in plasma-cell disorders.
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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 5,137 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 Disturbance
ROR 2.6595% CI 2.21–3.17· 122 reports
Thrombotic Microangiopathy
ROR 2.3895% CI 1.24–4.57· 9 reports
FAERS outcomes & reporting trend· 17.9% of reports w/ death · 39.1% w/ hospitalization
17.9%

Reported with a death outcome

918 of 5,137 reports

39.1%

Reported with hospitalization

2,010 of 5,137 reports

Reports per year

  • 2015: 120 reports
  • 2016: 495 reports
  • 2017: 691 reports
  • 2018: 598 reports
  • 2019: 622 reports
  • 2020: 629 reports
  • 2021: 566 reports
  • 2022: 392 reports
  • 2023: 283 reports
  • 2024: 190 reports
  • 2025: 207 reports
  • 2026: 81 reports

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 10 systems · 5,137 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 2.5895% CI 2.10–3.16· 95 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 Injury95
Blood & lymphatic
Neutropenia192Anaemia173Thrombocytopenia147Platelet Count Decreased134White Blood Cell Count Decreased98
General / constitutional
Fatigue236Pyrexia221Asthenia93Fall81
Immune / infection
Pneumonia304Sepsis124Infection85Covid-1976
Gastrointestinal
Diarrhoea231Nausea110Constipation88
Nervous system
Neuropathy Peripheral114
Skin
Rash101
Respiratory
Dyspnoea83
Cardiac
Atrial Fibrillation79
Metabolic & electrolyte
Decreased Appetite77
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 Elotuzumab 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

Zolbetuximab

Vyloy · Anti-Claudin-18.2 monoclonal antibody

Profile

2024 gastric mAb; severe on-target nausea/vomiting → volume-depletion prerenal AKI.

PRE
Moderate#1 · 94% phenotype match

Radium-223 dichloride

Xofigo · Radiopharmaceutical (alpha-emitter)

Profile

Bone-seeking alpha emitter; minimal direct renal toxicity.

PRE
Mild#2 · 89% phenotype match

Pexidartinib

Turalio · CSF1R inhibitor

Profile

Boxed hepatotoxicity; secondary renal effects.

PRE
Mild#3 · 89% phenotype match

Tisotumab vedotin

Tivdak · Antibody-drug conjugate (tissue factor/MMAE)

Profile

Ocular/bleeding toxicity dominates; renal involvement essentially unreported.

PRE
Mild#4 · 89% phenotype match

Elacestrant

Orserdu · Oral selective estrogen-receptor degrader (SERD)

Profile

2023 oral SERD; nausea-dominant, minimal intrinsic nephrotoxicity.

PRE
Mild#5 · 88% phenotype match

Tovorafenib

Ojemda · Type II pan-RAF (BRAF) inhibitor

Profile

2024 pediatric glioma RAF inhibitor; creatinine rise.

PRE
Mild#6 · 88% phenotype match
Compare Elotuzumab 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.

  1. 1DaratumumabMild
  2. 2MogamulizumabMild
  3. 3ZenocutuzumabMild
  4. 4Elotuzumab· this agentFAERS AKIMild
  5. 5CetuximabFAERS AKIMild
  6. 6IsatuximabFAERS AKIMild
  7. 7PanitumumabFAERS AKIMild
  8. 8TafasitamabFAERS AKIMild
  9. 9ZanidatamabFAERS AKIMild
  10. 10NecitumumabModerate
  11. 11ZolbetuximabModerate
  12. 12AmivantamabModerate
  13. 13NaxitamabModerate
  14. 14DinutuximabFAERS AKIModerate
  15. 15ObinutuzumabFAERS AKIModerate
  16. 16RituximabFAERS 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.