What kind of kidney injury does Elacestrant cause?

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

How should kidney function be monitored during Elacestrant therapy?

Nausea/vomiting severity and volume/intake status; Liver function and CYP3A4-interacting comedications.

How can kidney injury from Elacestrant be prevented?

Antiemetic prophylaxis and adequate hydration/intake Review CYP3A4 drug interactions

Who is at higher risk of kidney injury from Elacestrant?

Volume depletion from nausea/vomiting/poor intake; Pre-existing CKD; Concurrent nephrotoxins; Strong CYP3A4 interactions affecting exposure (pharmacologic, not directly renal).

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Printable monograph

Oral selective estrogen-receptor degrader (SERD)

Elacestrant

Orserdu · Elac

Oral selective estrogen-receptor degrader (SERD) · approved 2023 · 4 citations

Recent· through 2024

Fairly sourced4/9 · 4 signals

Not met: 4 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 3y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2024
Not 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.

An oral SERD with a nausea-dominant profile and minimal intrinsic nephrotoxicity.

MildOral selective estrogen-receptor degrader (SERD)

ER-positive HER2-negative ESR1-mutated advanced/metastatic breast cancer

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is not a recognized feature. In the pivotal phase 3 EMERALD trial the dominant toxicities were nausea, fatigue, vomiting and decreased appetite; a discrete renal-injury rate was not reported. Any renal involvement is best understood as indirect/case-level (e.g., volume depletion from GI toxicity).Source: Bidard et al., J Clin Oncol 2022 (EMERALD)

Onset & rechallenge

Time to injuryVariable / unpredictable

Renal events are uncharacterized; any prerenal AKI would track GI toxicity.

Distilled from: “Not characterized for renal events; any prerenal AKI would track GI toxicity.”

§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.

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

No characteristic intrinsic renal lesion is established. Elacestrant is hepatically metabolized (predominantly CYP3A4) and not primarily renally cleared, so direct tubular toxicity is not expected. The plausible, indirect pathway is prerenal/hemodynamic AKI from nausea, vomiting or decreased intake causing volume depletion. Any creatinine change is more likely hemodynamic than a drug-specific tubular effect.

Clinical presentation

If renal injury occurs, a prerenal creatinine rise during GI toxicity with clinical volume depletion; there is no signature proteinuric or tubular syndrome. Nausea, vomiting, fatigue and decreased appetite are the dominant non-renal findings.

Management

Supportive: antiemetics, hydration and dose modification per label for GI toxicity; volume resuscitation for prerenal AKI. There is no drug-specific renal therapy; injury is generally reversible with volume repletion.Lesion-level management framework

Risk factors

Volume depletion from nausea/vomiting/poor intake
Pre-existing CKD
Concurrent nephrotoxins
Strong CYP3A4 interactions affecting exposure (pharmacologic, not directly renal)

Prevention

Antiemetic prophylaxis and adequate hydration/intake
Review CYP3A4 drug interactions

Anticancer mechanism· how it treats cancer

Oral selective estrogen-receptor degrader (SERD) that binds the estrogen receptor and promotes its degradation, antagonizing ER signaling including in ESR1-mutant tumors. Approved for ER-positive, HER2-negative, ESR1-mutated advanced or metastatic breast cancer after progression on endocrine therapy.

Note · Renal literature is genuinely thin/absent — no elacestrant nephrotoxicity or creatinine-specific publication exists. Direct nephrotoxicity is minimal; nausea is the dominant adverse event. Any creatinine mention should be framed conservatively from PK and trial-safety data, not a dedicated renal study.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment is established for mild–moderate impairment; severe impairment/ESKD are not well studied. Dose reductions per label are driven by hepatic impairment and CYP3A4 interactions, not renal function.

Dialyzability & ESKD dosing

Highly protein-bound and hepatically metabolized; not expected to be dialyzable. No ESKD dosing guidance exists.

Differential diagnosis

Prerenal AKI from GI volume loss (fluid-responsive) vs unrelated intrinsic renal disease; elacestrant has no characteristic tubular or glomerular lesion, so significant AKI warrants a search for an alternative cause.

Monitoring

Nausea/vomiting severity and volume/intake status
Liver function and CYP3A4-interacting comedications

Key trials & series

EMERALD (Bidard JCO 2022) — pivotal phase 3
EMERALD ESR1-mutant subgroup analyses (Bardia Clin Cancer Res 2024)

Clinical pearls

GI, not renal: elacestrant's defining toxicity is nausea — any AKI is most likely prerenal from volume loss.
Renal literature is absent; keep claims qualitative and conservative.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI

§05

References

4 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

4 references · 2021–2024 · 3 since 2022

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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 7,117 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.
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 outcomes & reporting trend· 7.7% of reports w/ death · 12.5% w/ hospitalization

7.7%

Reported with a death outcome

548 of 7,117 reports

12.5%

Reported with hospitalization

891 of 7,117 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 7,117 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 0.1095% CI 0.04–0.23· 5 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Gastrointestinal

Nausea1,501Vomiting685Diarrhoea563Constipation407Dyspepsia236

General / constitutional

Fatigue1,122Pain373Asthenia245Malaise152Back Pain149

Musculoskeletal

Arthralgia336Myalgia212Bone Pain163Pain In Extremity134

Nervous system

Headache228Dizziness164

Metabolic & electrolyte

Decreased Appetite373

Vascular

Hot Flush194

Skin

Rash141

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 Elacestrant 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

Vepdegestrant

Veppanu · PROTAC estrogen-receptor degrader

Profile

2026 first PROTAC ER degrader; no meaningful intrinsic renal signal.

PRE

Mild#1 · 100% phenotype match

Tovorafenib

Ojemda · Type II pan-RAF (BRAF) inhibitor

Profile

2024 pediatric glioma RAF inhibitor; creatinine rise.

PRE

Mild#2 · 89% phenotype match

Dordaviprone

Modeyso · Imipridone (ONC201; DRD2/ClpP)

Profile

2025 imipridone for H3 K27M glioma; renally well tolerated — QT prolongation, not nephrotoxicity, is the safety focus.

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

Iberdomide

Zenbexus · Cereblon E3 ligase modulator (CELMoD)

Profile

2026 first-in-class CELMoD; no attributable lesion (renal impairment 11% vs 8% on the comparator arm) but exposure rises 1.8x below eGFR 30 off dialysis.

PRE

Mild#5 · 89% phenotype match

Zidesamtinib

Jideytro · ROS1-selective TKI

Profile

2026 TRK-sparing ROS1 TKI; no creatinine abnormality reached the label's >=20% lab-table cutoff — unlike the class's benign pseudo-AKI rise. Renally quiet so far.

PRE

Mild#6 · 89% phenotype match

Compare Elacestrant 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 Hormonal / endocrine

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.