Zolbetuximab
Vyloy · Anti-Claudin-18.2 monoclonal antibody
2024 gastric mAb; severe on-target nausea/vomiting → volume-depletion prerenal AKI.
Empliciti · Elotuz
Anti-SLAMF7 mAb · approved 2015 · 4 citations · FAERS AKI reporting ROR 2.58 (95% CI 2.10–3.16, 95 AKI reports)
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.
Signature lesion
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)
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.”
This agent's defining kidney lesion — its #1 signature. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
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.
Vasculature / Endothelium
Glomerular & peritubular capillaries
3 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.
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.
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.
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.
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
Reported with a death outcome
918 of 5,137 reports
Reported with hospitalization
2,010 of 5,137 reports
Reports per year
Yearly FAERS report volume · most recent year is partial.
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.
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
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.
Vyloy · Anti-Claudin-18.2 monoclonal antibody
2024 gastric mAb; severe on-target nausea/vomiting → volume-depletion prerenal AKI.
Xofigo · Radiopharmaceutical (alpha-emitter)
Bone-seeking alpha emitter; minimal direct renal toxicity.
Turalio · CSF1R inhibitor
Boxed hepatotoxicity; secondary renal effects.
Tivdak · Antibody-drug conjugate (tissue factor/MMAE)
Ocular/bleeding toxicity dominates; renal involvement essentially unreported.
Orserdu · Oral selective estrogen-receptor degrader (SERD)
2023 oral SERD; nausea-dominant, minimal intrinsic nephrotoxicity.
Ojemda · Type II pan-RAF (BRAF) inhibitor
2024 pediatric glioma RAF inhibitor; creatinine rise.
Nearest agents by kidney-injury phenotype (shared injuries, nephron target, severity, class) — a similarity approximation, not a claim of shared drug identity or mechanism.
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.