How should kidney function be monitored during Dactinomycin (actinomycin D) therapy?

Serum creatinine and electrolytes (K, phosphate, calcium, uric acid) during cytoreduction; Liver function tests, weight and abdominal exam for VOD.

How can kidney injury from Dactinomycin (actinomycin D) be prevented?

Risk-stratify for TLS before cytoreductive therapy Aggressive IV hydration Allopurinol or rasburicase per TLS risk

Who is at higher risk of kidney injury from Dactinomycin (actinomycin D)?

Bulky or rapidly proliferating chemosensitive tumor (e.g., advanced Wilms tumor); Pre-existing volume depletion or reduced kidney function; Young age and right-sided/large unilateral renal tumors (VOD risk); Inadequate hydration or uric-acid prophylaxis.

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Printable monograph

Antitumor antibiotic

Dactinomycin (actinomycin D)

Cosmegen · DACT

Antitumor antibiotic · approved 1964 · 4 citations

Dated evidence· through 2017

Fairly sourced5/9 · 4 signals

Not met: 4 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 21y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Not met: Current through 2017
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.

Actinomycin antibiotic whose renal risk is indirect: tumor lysis in chemosensitive pediatric tumors, with hepatic veno-occlusive disease as the signature organ toxicity.

Moderateearly-cytotoxic

Wilms tumorRhabdomyosarcoma and other soft-tissue sarcomasEwing sarcomaGestational trophoblastic neoplasiaTesticular germ-cell tumors (regimen component)

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

Direct nephrotoxicity is not an established feature of dactinomycin. The clinically relevant renal risk is tumor lysis syndrome (TLS) when used against bulky, chemosensitive pediatric tumors; precise incidence attributable to dactinomycin alone is not quantified, as it is given in multi-agent regimens.Source: Carmichael et al., case report 2013 (TLS); not quantified as a single agent

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor-lysis AKI within hours to days of starting effective chemotherapy.

Distilled from: “TLS within hours to days of initiating effective chemotherapy; VOD typically within the first weeks of treatment.”

§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.

Electrolyte Disturbance#1 · Signaturequalitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Prerenal / Hemodynamic AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Crystal / Obstructive NephropathySecondaryqualitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityReversible

Evidence4 citations

Nephron map

Vasculature / Endothelium

Distal Tubule / Collecting DuctFine-tuning of Na, K, Mg, acid & water

Tubular Lumen

Electrolyte Disturbance

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 characteristic direct tubular or glomerular toxin. Renal involvement is secondary: rapid lysis of treatment-sensitive tumor cells releases uric acid, potassium and phosphate, producing uric-acid and calcium-phosphate intratubular precipitation and AKI; volume depletion from chemotherapy-associated nausea/vomiting can add a prerenal component. The classic dactinomycin organ toxicity is hepatic sinusoidal obstruction syndrome (veno-occlusive disease), not nephrotoxicity.

Clinical presentation

When TLS occurs, hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia and rising creatinine within days of starting therapy in a child with a large tumor burden. Hepatic VOD presents separately with painful hepatomegaly, weight gain, ascites and thrombocytopenia and can secondarily threaten renal perfusion.

Management

Manage TLS with hydration, uric-acid lowering (allopurinol/rasburicase), correction of electrolytes, and renal replacement therapy if refractory. VOD is managed supportively with attention to preserving renal and respiratory function; consider defibrotide in severe hepatic VOD. There is no dactinomycin-specific tubular antidote.Lesion-level management framework

Risk factors

Bulky or rapidly proliferating chemosensitive tumor (e.g., advanced Wilms tumor)
Pre-existing volume depletion or reduced kidney function
Young age and right-sided/large unilateral renal tumors (VOD risk)
Inadequate hydration or uric-acid prophylaxis

Prevention

Risk-stratify for TLS before cytoreductive therapy
Aggressive IV hydration
Allopurinol or rasburicase per TLS risk

Anticancer mechanism· how it treats cancer

Chromopeptide antitumor antibiotic that intercalates into double-stranded DNA at GC-rich sequences, blocking RNA polymerase-dependent transcription and, at higher concentrations, DNA synthesis, leading to apoptosis.

Note · The single-kidney state common in Wilms tumor survivors (post-nephrectomy) heightens the importance of nephron preservation, making any superimposed insult clinically significant.

§04

Clinical depth

Renal dose adjustment

No well-established renal dose-adjustment scheme; dactinomycin is largely excreted in bile/feces with minor renal elimination. Dose modification is generally driven by hepatic toxicity and myelosuppression rather than kidney function.

Dialyzability & ESKD dosing

Not meaningfully dialyzable; high tissue binding and predominantly biliary/fecal elimination. Dialysis is used only for TLS-related metabolic derangements, not drug removal.

Differential diagnosis

Distinguish TLS-related AKI from prerenal AKI due to vomiting/poor intake, from obstructive uropathy by tumor mass, and from VOD-associated hepatorenal physiology. Direct dactinomycin tubular toxicity is a diagnosis of exclusion and is not well supported.

Monitoring

Serum creatinine and electrolytes (K, phosphate, calcium, uric acid) during cytoreduction
Liver function tests, weight and abdominal exam for VOD

Key trials & series

NWTS/COG and SIOP Wilms tumor protocols establishing vincristine/dactinomycin-based regimens (regimen-level evidence; renal events reported as TLS and VOD in associated literature)

Clinical pearls

Think electrolytes and tumor lysis, not direct tubular toxicity, when a child on dactinomycin develops AKI.

Beyond the kidney — non-renal toxicities· 2 organ systems

Class-level context for the major non-renal toxicities of the Antitumor antibiotic class.

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Mitomycin / bleomycin pulmonary toxicity

Hematologic

Cytopenias, thrombosis, TMA

Cumulative myelosuppression

§05

References

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

Evidence accrual

4 references · 1996–2017 · 1 since 2015

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 2,188 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.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
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 reported renal phenotypes· 5 signals

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

Electrolyte DisturbanceNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Crystal / Obstructive NephropathyNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

Fanconi Syndrome

ROR 18.8195% CI 10.10–35.04· 10 reports

Acute Interstitial Nephritis

ROR 11.9095% CI 7.89–17.95· 23 reports

Thrombotic Microangiopathy

ROR 9.3595% CI 5.63–15.54· 15 reports

Glomerular Injury / Proteinuria

ROR 3.9795% CI 2.25–7.00· 12 reports

Hemorrhagic Cystitis

ROR 3.3595% CI 2.24–5.00· 24 reports

FAERS outcomes & reporting trend· 17.6% of reports w/ death · 31% w/ hospitalization

17.6%

Reported with a death outcome

386 of 2,188 reports

31%

Reported with hospitalization

679 of 2,188 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 2,188 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 0.8895% CI 0.52–1.49· 14 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Febrile Neutropenia192Neutropenia126Thrombocytopenia103Anaemia86Myelosuppression51

Gastrointestinal

Vomiting104Stomatitis73Nausea72Mucosal Inflammation67Diarrhoea48

Hepatobiliary

Venoocclusive Liver Disease75Venoocclusive Disease73

General / constitutional

Pyrexia90

Metabolic & electrolyte

Dehydration42

Nervous system

Neuropathy Peripheral41

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 Dactinomycin (actinomycin D) 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

Fludarabine

Fludara · Purine analog

Profile

Tumor lysis; accumulates in renal impairment.

XTALPRELYTE

Moderate#1 · 87% phenotype match

Idarubicin

Idamycin · Anthracycline

Profile

Tumor lysis in acute leukemia.

XTALLYTEPRE

Mild#2 · 85% phenotype match

Etoposide

Etopophos · Topoisomerase II inhibitor

Profile

Tumor lysis; renally cleared.

XTALPRELYTE

Mild#3 · 81% phenotype match

Hydroxyurea

Hydrea · Ribonucleotide reductase inhibitor

Profile

Tumor lysis in myeloproliferative disease.

XTALPRELYTE

Mild#4 · 81% phenotype match

Nelarabine

Arranon · Purine analog

Profile

Tumor lysis in T-ALL.

XTALPRELYTE

Mild#5 · 81% phenotype match

Pomalidomide

Pomalyst · Immunomodulatory drug (IMiD)

Profile

Tumor lysis; usable in renal impairment.

PRELYTEXTAL

Mild#6 · 81% phenotype match

Compare Dactinomycin (actinomycin D) 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 Antitumor antibiotics

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.

1IdarubicinXTAL — Crystal / Obstructive NephropathyMild
2BleomycinPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
3DoxorubicinGLOM — Glomerular Injury / ProteinuriaFAERS AKIMild
4MitoxantroneXTAL — Crystal / Obstructive NephropathyFAERS AKIMild
5Plicamycin (mithramycin)ATN — Acute Tubular NecrosisModerate
6Dactinomycin (actinomycin D)· this agentLYTE — Electrolyte DisturbanceModerate
7Mitomycin CTMA — Thrombotic MicroangiopathySevere

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.