What kind of kidney injury does Dacarbazine cause?

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

Is kidney injury from Dacarbazine reversible?

Reversible. Typical onset: Variable; hepatic VOD typically days to weeks after exposure..

How should kidney function be monitored during Dacarbazine therapy?

Volume status and antiemetic adequacy each cycle; Liver function tests and clinical exam for veno-occlusive disease; Serum creatinine if volume-depleted or hepatically ill.

How can kidney injury from Dacarbazine be prevented?

Robust antiemesis and hydration

Who is at higher risk of kidney injury from Dacarbazine?

Volume depletion from severe emesis; Hepatic veno-occlusive disease / eosinophilia (reported association); Concurrent hepatotoxins/nephrotoxins.

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Printable monograph

Alkylator

Dacarbazine

DTIC · DTIC

Alkylator · approved 1975 · 2 citations

Dated evidence· through 2001

Thinly sourced2/9 · 1 signal

Not met: 2 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Not met: Beyond single case reports
Not met: Peer-reviewed sources
Not met: Landmark reference
Not met: Current through 2001
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 melanoma alkylator that menaces the hepatic endothelium far more than the nephron.

MildAlkylator

Metastatic melanomaHodgkin lymphoma (ABVD)Soft-tissue sarcoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is minimal and not well quantified; the notable vascular toxicity is hepatic veno-occlusive disease / sinusoidal obstruction (now recognized as not rare), with renal effects largely secondary to severe systemic illness, hepatic injury or volume loss.Source: Kintzel, Drug Saf 2001

Onset & rechallenge

Time to injuryVariable / unpredictable

Onset is variable, with hepatic veno-occlusive disease typically occurring days to weeks after exposure.

Distilled from: “Variable; hepatic VOD typically days to weeks after exposure.”

§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

Dacarbazine and its reactive metabolites are selectively toxic to hepatic sinusoidal endothelial cells through a glutathione-dependent mechanism (depletion of endothelial GSH precedes toxicity), the basis of hepatic veno-occlusive disease and, occasionally, fatal hepatic vein thrombotic occlusion. The kidney is not a primary target; any AKI is typically prerenal from vomiting/volume depletion or hepatorenal-type hypoperfusion accompanying severe hepatic injury.

Clinical presentation

When present, prerenal azotemia (elevated BUN:creatinine ratio, low urine sodium) in the setting of nausea/vomiting and volume depletion; in VOD, hepatomegaly, right-upper-quadrant pain, weight gain and hyperbilirubinemia with secondary renal hypoperfusion.

Management

Supportive: rehydration and antiemetics for prerenal AKI; supportive care for VOD. Prerenal injury reverses with restoration of perfusion; severe hepatic vascular toxicity can be fatal.Lesion-level management framework

Risk factors

Volume depletion from severe emesis
Hepatic veno-occlusive disease / eosinophilia (reported association)
Concurrent hepatotoxins/nephrotoxins

Prevention

Robust antiemesis and hydration

Anticancer mechanism· how it treats cancer

Imidazole-carboxamide prodrug activated in the liver (CYP-mediated N-demethylation) to a methylating diazonium species that alkylates DNA at O6-guanine. Used for metastatic melanoma, Hodgkin lymphoma (ABVD) and soft-tissue sarcoma.

§04

Clinical depth

Renal dose adjustment

No established renal CrCl dose modification; dacarbazine is partly renally excreted but dose adjustment is driven mainly by hematologic toxicity and hepatic function. Use general caution and maintain hydration in renal impairment.

Dialyzability & ESKD dosing

Short-lived parent prodrug undergoing hepatic activation; not a drug managed by dialysis. ESKD data are minimal.

Differential diagnosis

Renal injury here is almost always prerenal (low FeNa, volume-responsive) or hepatorenal in the setting of VOD - not intrinsic tubular or microangiopathic injury. Recognizing VOD (tender hepatomegaly, weight gain, hyperbilirubinemia) reframes the AKI as a hepatic, not renal, problem.

Monitoring

Volume status and antiemetic adequacy each cycle
Liver function tests and clinical exam for veno-occlusive disease
Serum creatinine if volume-depleted or hepatically ill

Key trials & series

ABVD lymphoma and dacarbazine-based melanoma regimens as the principal exposure context
Hepatic vascular toxicity (veno-occlusive disease / Budd-Chiari) is the characteristic severe event; renal involvement is secondary

Clinical pearls

Dacarbazine's dangerous vascular toxicity is hepatic (VOD), not renal - the kidney suffers only secondarily.
Most dacarbazine-associated AKI is simple prerenal azotemia from emesis - hydrate and the creatinine follows.
New hepatomegaly, weight gain and jaundice after dacarbazine should trigger a VOD work-up, not a renal biopsy.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI

Beyond the kidney — non-renal toxicities· 3 organ systems

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

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression; secondary malignancy risk

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Ifosfamide encephalopathy (chloroacetaldehyde)

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

High-dose cyclophosphamide cardiotoxicity

§05

References

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

Evidence accrual

2 references · 1990–2001 · 1 since 1999

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.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Sep 2025) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING It is recommended that dacarbazine be administered under the supervision of a qualified physician experienced in the use of cancer chemotherapeutic agents. 1.Hemopoietic depression is the most common toxicity with dacarbazine (see WARNINGS ). 2.Hepatic necrosis has been reported (see WARNINGS ). 3.Studies have demonstrated this agent to have a carcinogenic and teratogenic effect when used in animals. 4.In treatment of each patient, the physician must weigh carefully the possibility of achieving therapeutic benefit against the risk of toxicity.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 7,411 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· 3 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

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

SIADH / Hyponatremia

ROR 2.6995% CI 2.15–3.37· 76 reports

Thrombotic Microangiopathy

ROR 2.2095% CI 1.25–3.87· 12 reports

Electrolyte Disturbance

ROR 2.0095% CI 1.69–2.38· 134 reports

FAERS outcomes & reporting trend· 17.6% of reports w/ death · 37.8% w/ hospitalization

17.6%

Reported with a death outcome

1,301 of 7,411 reports

37.8%

Reported with hospitalization

2,802 of 7,411 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 7,411 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 1.2595% CI 0.98–1.59· 67 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Febrile Neutropenia643Neutropenia504Anaemia254Thrombocytopenia223Leukopenia134

Gastrointestinal

Nausea280Vomiting237Diarrhoea227Abdominal Pain182

General / constitutional

Pyrexia387Fatigue186

Respiratory

Pulmonary Toxicity200Dyspnoea191Respiratory Failure146

Immune / infection

Sepsis212Pneumonia207

Nervous system

Neuropathy Peripheral300

Guidelines & consensus· 14

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.

ADQIConventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupKidney Int 2026 · PMID 41881107Cisplatin is identified as a leading cytotoxic nephrotoxin; the workgroup details preventive measures (adequate isotonic hydration, correction of volume depletion, avoidance of concurrent nephrotoxins, attention to electrolyte/magnesium wasting) and management of cisplatin-associated AKI, with a research agenda for knowledge gaps.

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 Dacarbazine 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

Estramustine

Emcyt · Hormonal–alkylating conjugate

Profile

Fluid retention, edema and thromboembolism.

PRE

Mild#1 · 99% phenotype match

Asparaginase

Elspar · Enzyme

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild#2 · 89% phenotype match

Belzutifan

Welireg · HIF-2α inhibitor

Profile

Anemia/hypoxia; emerging renal profile in VHL/RCC.

PRE

Mild#3 · 89% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#4 · 89% phenotype match

Irinotecan

Camptosar · Topoisomerase I inhibitor

Profile

Diarrhea-driven prerenal AKI.

PRE

Mild#5 · 89% phenotype match

Mirvetuximab soravtansine

Elahere · Antibody-drug conjugate (FRα/DM4)

Profile

Ocular toxicity dominates; renal involvement indirect/case-level (GI volume loss).

PRE

Mild#6 · 89% phenotype match

Compare Dacarbazine 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 Alkylating 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.