Cetuximab & Panitumumab
Erbitux · Vectibix · Anti-EGFR antibody
TRPM6 magnesium wasting.
LYTE
MildOpen →
Anti-SLAMF7 mAb
Elotuzumab
Empliciti · Elotuz
A SLAMF7 antibody that is reassuringly kidney-neutral — usable across severe impairment and dialysis without adjustment.
MildAnti-SLAMF7 monoclonal antibody · approved 2015
Relapsed/refractory multiple myeloma (with lenalidomide or pomalidomide and dexamethasone)
Signature kidney injury
Electrolyte Wasting
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)
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 drug is, in effect, kidney-safe and is used to deepen 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.
Onset
Not applicable for direct renal injury; infusion reactions occur during/shortly after the first infusions.
Reversibility
Reversible
Anticancer mechanism
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.
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.
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
- Monitor and dose-adjust the renally-cleared partner (lenalidomide) for GFR
- Treat myeloma-related renal disease (hydration, anti-myeloma therapy, hypercalcemia management)
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.
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
- Elotuzumab needs no renal dose adjustment — including in dialysis patients — because its PK is unchanged in ESKD.
- 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.
- It is large-molecule and not dialyzed, so no special timing around hemodialysis sessions is required.
Where it strikes
Nephron segments
Glomerulus
Filtration barrier (podocytes + endothelium)
Injury signatures
Electrolyte Wasting
Evidence
3 peer-reviewed references. Citation metadata via PubMed / NLM.
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.PMIDElotuzumab 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.PMIDAcute 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.