What kind of kidney injury does Imetelstat cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Electrolyte Disturbance.

How should kidney function be monitored during Imetelstat therapy?

CBC with platelets frequently (cytopenias are the dominant toxicity); Creatinine, uric acid, phosphate, potassium early in higher-burden patients (TLS screen); Volume status with transfusions and intercurrent illness.

How can kidney injury from Imetelstat be prevented?

Hydration in higher-burden disease Manage cytopenias and infections promptly

Who is at higher risk of kidney injury from Imetelstat?

Higher disease burden / rapid cytoreduction (TLS risk); Pre-existing CKD or hyperuricemia; Cytopenia-related infection or bleeding with volume depletion; Concurrent nephrotoxins.

Back to explorer

Printable monograph

Telomerase inhibitor

Imetelstat

Rytelo · IMET

Telomerase inhibitor · approved 2024 · 5 citations

Recent· through 2024

Fairly sourced4/9 · 4 signals

Not met: 5 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.

A first-in-class telomerase inhibitor for low-risk MDS — kidney concern is mainly tumor-lysis/cytopenia, not direct toxicity.

MildTelomerase inhibitor

Lower-risk myelodysplastic syndromes (transfusion-dependent anemia)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

No established direct nephrotoxicity. In IMerge the dominant toxicities were cytopenias (thrombocytopenia, neutropenia); renal injury was not a defining adverse event. Tumor-lysis-type metabolic risk is theoretical and most relevant with high disease burden, not a quantified rate in lower-risk MDS.Source: Platzbecker et al., Lancet 2023

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Any tumor-lysis-type risk arises early after initiation; otherwise no defined renal onset.

Distilled from: “Any tumor-lysis-type risk would be early after initiation; otherwise no defined renal onset.”

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. 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.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).

§03

Kidney injury

Mechanism of kidney injury

No characterized intrinsic tubular/glomerular injury. Potential renal stress is indirect: rapid cytoreduction could produce tumor-lysis metabolic derangements (hyperuricemia and hyperphosphatemia with intratubular urate/calcium-phosphate crystal deposition and AKI), and cytopenia-related complications (infection, bleeding, transfusion-related volume shifts) can drive prerenal AKI.

Clinical presentation

Generally bland renal picture; if tumor lysis occurs, rising uric acid/phosphate/potassium with creatinine elevation. Otherwise creatinine changes track intercurrent illness and volume status.

Management

Supportive; standard tumor-lysis prophylaxis/treatment (IV hydration, allopurinol or rasburicase for hyperuricemia) if metabolic derangements appear, and correction of prerenal factors. No drug-specific renal antidote; intrinsic nephrotoxicity has not been described.Lesion-level management framework

Risk factors

Higher disease burden / rapid cytoreduction (TLS risk)
Pre-existing CKD or hyperuricemia
Cytopenia-related infection or bleeding with volume depletion
Concurrent nephrotoxins

Prevention

Hydration in higher-burden disease
Manage cytopenias and infections promptly

Anticancer mechanism· how it treats cancer

13-mer lipid-conjugated oligonucleotide that binds the RNA template (hTR) of telomerase via Watson-Crick base pairing, competitively inhibiting telomerase enzymatic activity and shortening telomeres in malignant clones. Approved for transfusion-dependent anemia in lower-risk myelodysplastic syndromes (MDS) refractory to or ineligible for erythropoiesis-stimulating agents.

Note · 2024 first-in-class approval; renal literature is essentially absent. The tumor-lysis/prerenal framing is conservative class reasoning, supported by general onconephrology/TLS reviews rather than imetelstat-specific renal data.

§04

Clinical depth

Renal dose adjustment

No dedicated renal dose adjustment is established in lower-risk MDS labeling. As an oligonucleotide, elimination is largely via nuclease metabolism/tissue distribution rather than glomerular filtration; mild-moderate renal impairment is not expected to require change. No data in severe impairment or dialysis.

Dialyzability & ESKD dosing

Not characterized; large protein-bound oligonucleotides are generally not appreciably removed by hemodialysis. No ESKD dosing guidance.

Differential diagnosis

Distinguish tumor-lysis AKI (urate/phosphate elevation, early) from prerenal AKI of cytopenia-related infection/bleeding; structural drug nephrotoxicity is not a described entity for this agent.

Monitoring

CBC with platelets frequently (cytopenias are the dominant toxicity)
Creatinine, uric acid, phosphate, potassium early in higher-burden patients (TLS screen)
Volume status with transfusions and intercurrent illness

Key trials & series

IMerge phase 3 (Platzbecker, Lancet 2023) — registrational, cytopenia-dominant safety

Clinical pearls

The renal worry at initiation is tumor lysis, not a tubulopathy — screen labs early in higher-burden disease.
Cytopenias dominate the safety profile; renal events are incidental and indirect.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

§05

References

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

Evidence accrual

5 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 176 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.

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· 6.3% of reports w/ death · 19.9% w/ hospitalization

6.3%

Reported with a death outcome

11 of 176 reports

19.9%

Reported with hospitalization

35 of 176 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 176 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.

Blood & lymphatic

Platelet Count Decreased27Thrombocytopenia24Haemoglobin Decreased23Cytopenia20Neutropenia17

General / constitutional

Fatigue5Back Pain3Chills3Fall3Malaise3

Immune / infection

Infusion Related Reaction9

Respiratory

Dyspnoea7

Cardiac

Cardiac Failure Congestive4

Nervous system

Headache3

Gastrointestinal

Abdominal Discomfort2

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 Imetelstat 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

Afamitresgene autoleucel (Afami-cel)

Tecelra · MAGE-A4 TCR-T cell therapy

Profile

First TCR-T cell therapy for a solid tumor; CRS-associated hemodynamic AKI.

PRELYTE

Moderate#1 · 95% phenotype match

Ziftomenib

Komzifti · Menin inhibitor

Profile

2025 NPM1-mutated AML menin inhibitor; differentiation syndrome and tumor lysis.

PRELYTE

Moderate#2 · 94% phenotype match

Zanidatamab

Ziihera · HER2 bispecific antibody

Profile

2024 biliary-tract HER2 bispecific; renal data emerging.

PRELYTE

Mild#3 · 89% phenotype match

Zenocutuzumab

Bizengri · HER2×HER3 bispecific antibody

Profile

2024 NRG1-fusion bispecific; mostly grade 1-2 AEs — at most diarrhea-related prerenal risk, no CRS/TLS mechanism.

PRELYTE

Mild#4 · 89% phenotype match

Mirdametinib

Gomekli · MEK inhibitor

Profile

2025 NF1 MEK inhibitor; creatinine rise and edema.

PRELYTE

Mild#5 · 89% phenotype match

Quizartinib

Vanflyta · FLT3 inhibitor

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild#6 · 89% phenotype match

Compare Imetelstat 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 Other targeted agents

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.