What kind of kidney injury does Samarium-153 lexidronam cause?

Acute Tubular Necrosis — Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

How should kidney function be monitored during Samarium-153 lexidronam therapy?

CBC with platelets (weekly, through nadir and recovery); Renal function/eGFR before administration; Hydration and urinary output; Radiation-safety monitoring of excreta per protocol.

How can kidney injury from Samarium-153 lexidronam be prevented?

Ensure adequate hydration before and after administration to promote urinary clearance Encourage frequent voiding to limit bladder radiation; manage incontinence/retention Radiation-safety handling of urine per nuclear-medicine protocols

Who is at higher risk of kidney injury from Samarium-153 lexidronam?

Pre-existing renal impairment (delayed clearance, increased marrow exposure); Compromised bone marrow reserve / prior myelosuppressive therapy; Inadequate hydration at administration; Urinary retention/obstruction increasing tract radiation exposure.

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Printable monograph

Bone-seeking radiopharmaceutical (153Sm-EDTMP)

Samarium-153 lexidronam

Quadramet · Sm-153

Bone-seeking radiopharmaceutical (153Sm-EDTMP) · approved 1997 · 4 citations

Dated evidence· through 2014

Thinly sourced3/9 · 2 signals

Not met: 4 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Not met: Landmark reference
Not met: Current through 2014
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.

Bone-seeking radiopharmaceutical for painful osteoblastic metastases; renally excreted with dominant myelosuppression and caution in renal impairment.

Moderateestablished

Palliation of pain from osteoblastic skeletal metastases (e.g., prostate, breast, and other cancers) that are avid on bone scintigraphy

§01

Signature kidney injury

Signature lesion

Acute Tubular Necrosis

Clinically meaningful nephrotoxicity is uncommon; the dominant and dose-limiting toxicity is reversible myelosuppression. No reliable drug-specific AKI incidence is established. Renal caution stems from renal/urinary excretion of the unbound radiopharmaceutical.Source: Dolezal et al., Vnitr Lek 2003 (myelosuppression-dominant); renal events uncommon

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Myelosuppression reaches its nadir within weeks, with recovery over the subsequent weeks.

Distilled from: “Myelosuppression nadirs within weeks; recovery typically over the following weeks.”

§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.

Acute Tubular Necrosis#1 · Signaturequalitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

§03

Kidney injury

Mechanism of kidney injury

The agent and its non-bone-bound fraction are cleared by the kidneys and excreted in urine, so impaired renal function can prolong circulation, increase marrow radiation exposure, and theoretically deliver radiation to renal/urinary tract tissue. Direct renal injury is not a prominent clinical feature; the principal radiation toxicity is to bone marrow. Electrolyte shifts can accompany the underlying malignancy and supportive care.

Clinical presentation

Predominantly hematologic: transient leukopenia and thrombocytopenia nadiring around 3-4 weeks with subsequent recovery. Renal manifestations are uncommon; when renal function is impaired, expect heightened/prolonged myelosuppression rather than a distinct nephropathy.

Management

Largely supportive: monitor and manage cytopenias (transfusion, growth factors as indicated). For any AKI, ensure volume status, relieve urinary obstruction, and provide standard renal support; dialysis is supportive rather than a defined removal strategy.Lesion-level management framework

Risk factors

Pre-existing renal impairment (delayed clearance, increased marrow exposure)
Compromised bone marrow reserve / prior myelosuppressive therapy
Inadequate hydration at administration
Urinary retention/obstruction increasing tract radiation exposure

Prevention

Ensure adequate hydration before and after administration to promote urinary clearance
Encourage frequent voiding to limit bladder radiation; manage incontinence/retention
Radiation-safety handling of urine per nuclear-medicine protocols

Anticancer mechanism· how it treats cancer

Samarium-153 lexidronam (153Sm-EDTMP) couples the beta-/gamma-emitting radionuclide samarium-153 to the bone-avid chelator ethylenediaminetetramethylene phosphonic acid (EDTMP). It concentrates in regions of high osteoblastic activity at metastatic sites, delivering localized beta radiation for pain palliation rather than curative cytoreduction.

Note · The renal angle is the renal/urinary excretion route warranting caution, not a frequent direct nephrotoxic lesion; the dominant toxicity is mild, temporary myelosuppression.

§04

Clinical depth

Renal dose adjustment

Renal impairment reduces clearance and increases marrow radiation exposure; administer with caution and assess renal function before dosing. Follow product labeling/nuclear-medicine guidance for impaired renal function.

Dialyzability & ESKD dosing

Not established as a removal modality; clinical role of dialysis is supportive only.

Differential diagnosis

Differentiate transient radiopharmaceutical myelosuppression from disease- or other-therapy-related cytopenias; distinguish any AKI from tumor-related obstructive uropathy, hypercalcemia of malignancy, or volume depletion rather than a primary radiopharmaceutical nephropathy.

Monitoring

CBC with platelets (weekly, through nadir and recovery)
Renal function/eGFR before administration
Hydration and urinary output
Radiation-safety monitoring of excreta per protocol

Key trials & series

Pain-palliation efficacy and tolerability shown in 153Sm-EDTMP series (e.g., PMID 24681187, PMID 12728593), with myelosuppression as the dominant, reversible toxicity and no significant hematologic worsening signal in reported cohorts.

Clinical pearls

Renal impairment chiefly matters because delayed clearance increases marrow radiation exposure.

Where it strikes· nephron segments & injury signatures

Nephron segments

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Tubular Lumen

The urine flow path

Interstitium

Supporting tissue around the tubules

Injury signatures

Acute Tubular Necrosis

§05

References

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

Evidence accrual

4 references · 2003–2014 · 2 since 2012

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.

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 Samarium-153 lexidronam 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

Sonidegib

Odomzo · Hedgehog (SMO) inhibitor

Profile

Elevated CK / rhabdomyolysis → pigment nephropathy.

ATN

Mild#1 · 74% phenotype match

Raltitrexed

Tomudex · Antifolate (TS inhibitor)

Profile

Renally cleared antifolate; exposure ~doubles in renal impairment; forerunner CB3717 withdrawn for crystal nephrotoxicity.

ATNXTAL

Moderate#2 · 57% phenotype match

Methotrexate (high-dose)

Trexall · Antifolate

Profile

Crystal nephropathy; glucarpidase rescue.

XTALATN

Moderate#3 · 57% phenotype match

Trabectedin

Yondelis · Marine alkylating agent

Profile

Rhabdomyolysis → pigment nephropathy; hepatotoxicity.

ATNLYTE

Moderate#4 · 56% phenotype match

Procarbazine

Matulane · Hydrazine alkylating agent

Profile

Classic cytotoxic with recognized renal/urological complications; AKI usually multifactorial; hypersensitivity AIN possible.

ATNAIN

Moderate#5 · 55% phenotype match

Cobimetinib

Cotellic · MEK inhibitor

Profile

Real-world AKI signal with BRAF partners.

ATNAIN

Mild#6 · 51% phenotype match

Compare Samarium-153 lexidronam 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 Radiopharmaceuticals

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.

1Radium-223 dichloridePRE — Prerenal / Hemodynamic AKIMild
2Ibritumomab tiuxetanPRE — Prerenal / Hemodynamic AKIMild
3Iobenguane I-131ATN — Acute Tubular NecrosisMild
4Samarium-153 lexidronam· this agentATN — Acute Tubular NecrosisModerate
5Lutetium-177 DotatateCIN — Chronic Interstitial NephropathyModerate
6Lutetium-177 PSMA-617 (vipivotide)CIN — Chronic Interstitial NephropathyModerate
7Strontium-89 chlorideLYTE — Electrolyte DisturbanceModerate

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.