What kind of kidney injury does Bleomycin 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 Bleomycin therapy?

Pulmonary function tests and symptoms (the key exposure-driven toxicity); Cumulative bleomycin dose tracking; Electrolytes (in context of platinum co-therapy).

How can kidney injury from Bleomycin be prevented?

Accurate GFR assessment before and during therapy (note eGFR equations are unreliable during platinum chemotherapy) Dose reduction in renal impairment Limit cumulative dose; monitor for pulmonary toxicity which exposure rise potentiates

Who is at higher risk of kidney injury from Bleomycin?

Pre-existing renal impairment (CrCl <35 mL/min); Concurrent cisplatin (reduces bleomycin clearance and is itself nephrotoxic); High cumulative bleomycin dose; Older age; Volume depletion from chemotherapy-induced vomiting.

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Printable monograph

Antitumor antibiotic

Bleomycin

Blenoxane · Bleo

Antitumor antibiotic · approved 1973 · 7 citations · FAERS AKI reporting ROR 1.30 (95% CI 1.07–1.59, 97 AKI reports)

Aging evidence· through 2021

Fairly sourced6/9 · 5 signals

Met: 7 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 44y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Not met: Current through 2021
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 glycopeptide antibiotic prized for marrow-sparing cancer kill, whose renal excretion makes the failing kidney a setup for runaway exposure and lethal lung toxicity, not a direct nephron target.

Mild1970s antibiotic

Testicular and other germ-cell tumors (BEP/EP)Hodgkin lymphoma (ABVD)Squamous-cell carcinoma of head/neck, cervix, skinMalignant pleural effusion (sclerotherapy)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Bleomycin is not a classic direct nephrotoxin; the actionable renal issue is exposure-driven. Roughly two-thirds of a dose is cleared renally, and terminal half-life rises exponentially once creatinine clearance falls below ~25-35 mL/min, magnifying systemic (especially pulmonary) toxicity. Direct kidney injury is not well quantified and is largely confounded by co-administered cisplatin.Source: Crooke et al., Cancer Treat Rep 1977

Onset & rechallenge

Time to injuryVariable / unpredictable

Pharmacokinetic accumulation is immediate in renal impairment, whereas clinical (pulmonary) toxicity accrues cumulatively over weeks to months.

Distilled from: “Pharmacokinetic accumulation is immediate in renal impairment; clinical (pulmonary) toxicity is cumulative over weeks to months.”

§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

Also documented as kidney-sparing

Bleomycin — Renal effect minimal; dose-adjust for clearance. Pulmonary fibrosis is the dose-limiting toxicity.

The spared

Mechanism of kidney injury

No well-characterized direct tubular toxin mechanism. The dominant renal concern is pharmacokinetic: bleomycin is predominantly renally eliminated, so declining GFR causes drug accumulation and exponentially prolonged half-life, increasing the risk of dose-dependent toxicities (notably pulmonary fibrosis). Any AKI seen in BEP regimens is generally attributable to concurrent cisplatin (tubular injury) or prerenal insults, with bleomycin contributing chiefly by exposure amplification.

Clinical presentation

Renal presentation is usually that of the regimen rather than the drug: declining GFR, electrolyte wasting and prerenal physiology from cisplatin and vomiting. Bleomycin's own exposure-driven toxicity manifests as pulmonary (cough, dyspnea, infiltrates) rather than renal signs. Rising serum creatinine should prompt dose/exposure review because it predicts heightened systemic toxicity.

Management

Manage the underlying cause of declining renal function (hold/adjust cisplatin, restore volume). Reduce bleomycin exposure in renal impairment and monitor closely for pulmonary toxicity, which is the clinically dangerous consequence of accumulation. There is no specific antidote; supportive care and discontinuation if toxicity emerges.Lesion-level management framework

Risk factors

Pre-existing renal impairment (CrCl <35 mL/min)
Concurrent cisplatin (reduces bleomycin clearance and is itself nephrotoxic)
High cumulative bleomycin dose
Older age
Volume depletion from chemotherapy-induced vomiting

Prevention

Accurate GFR assessment before and during therapy (note eGFR equations are unreliable during platinum chemotherapy)
Dose reduction in renal impairment
Limit cumulative dose; monitor for pulmonary toxicity which exposure rise potentiates

Anticancer mechanism· how it treats cancer

Bleomycin is a Streptomyces-derived glycopeptide antitumor antibiotic that chelates iron and oxygen to generate reactive oxygen species, producing single- and double-strand DNA breaks; it is cell-cycle phase-specific (G2/M). Because it causes minimal myelosuppression, it anchors curative combinations such as BEP (bleomycin, etoposide, cisplatin) for germ-cell tumors and ABVD for Hodgkin lymphoma, and is also used in squamous-cell carcinomas and as a sclerosant for malignant effusions.

Note · The renal story for bleomycin is one of clearance and exposure, not a signature nephron lesion. In germ-cell survivors, long-term nephrotoxicity is driven mainly by cisplatin, with bleomycin contributing to pulmonary morbidity.

§04

Clinical depth

Renal dose adjustment

Reduce dose in renal impairment; common guidance reduces by ~25% for CrCl 40-50 mL/min and progressively more (up to ~50-60%) for CrCl 10-40 mL/min, reflecting the exponential rise in half-life below ~25-35 mL/min. Verify against local protocol.

Dialyzability & ESKD dosing

Low-molecular-weight and water-soluble, so some dialytic removal is plausible and case-level reports suggest it, but it has not been formally characterized and is not relied upon clinically. Dosing in dialysis patients should be conservative and individualized.

Differential diagnosis

Distinguish exposure-driven systemic toxicity from cisplatin-induced ATN and electrolyte wasting (the usual cause of AKI in BEP), prerenal azotemia from vomiting, and tumor-related obstruction. Bleomycin itself rarely produces an isolated nephron lesion.

Monitoring

Pulmonary function tests and symptoms (the key exposure-driven toxicity)
Cumulative bleomycin dose tracking
Electrolytes (in context of platinum co-therapy)

Key trials & series

Crooke et al. 1977 — renal-function-dependent bleomycin pharmacokinetics (half-life rises exponentially below CrCl 25-35 mL/min)
Broughton et al. 1977 — renal clearance correlates with creatinine clearance; markedly elevated steady-state levels and 33-h half-life in renal impairment
Lauritsen et al. 2014 — unreliability of eGFR during BEP chemotherapy

Clinical pearls

A rising creatinine on BEP is a red flag for dose adjustment, not primarily because of bleomycin nephrotoxicity but because accumulation worsens lung injury.
eGFR equations are unreliable during platinum-based chemotherapy because creatinine and true GFR fall together — consider measured GFR.
Cisplatin co-administration further reduces bleomycin clearance, compounding exposure.

Where it strikes· nephron segments & injury signatures

Nephron segments

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Glomerulus

Filtration barrier (podocytes + endothelium)

Injury signatures

Prerenal / Hemodynamic 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. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

4 references · 1977–2017 · 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.

Case reports — ranked by strength· 3

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseC · LimitedComplement C5 inhibition reverses bleomycin-induced thrombotic microangiopathy.Salhi S et al. · Clin Kidney J 2021 · PMID 33841872Case of bleomycin-induced renal thrombotic microangiopathy (with cisplatin/etoposide) that achieved complete renal remission with eculizumab C5 blockade.CaseC · LimitedHemolytic uremic syndrome following cisplatin, bleomycin, and vincristine chemotherapy: a report of a case and a review of the literature.Gardner G et al. · Ren Fail 1989 · PMID 2482985Fatal hemolytic uremic syndrome with renal failure in a patient on a bleomycin-containing regimen, with endothelial injury attributed to bleomycin combination chemotherapy.CaseC · LimitedThrombotic microangiopathy associated with chemotherapy: case report and review of the literature.Fields SM et al. · DICP 1989 · PMID 2669373Case of probable cisplatin- and bleomycin-induced thrombotic microangiopathy presenting with microangiopathic hemolytic anemia, thrombocytopenia, and renal impairment.

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Apr 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING It is recommended that Bleomycin for Injection, USP be administered under the supervision of a qualified physician experienced in the use of cancer chemotherapeutic agents. Appropriate management of therapy and complications is possible only when adequate diagnostic and treatment facilities are readily available. Pulmonary fibrosis is the most severe toxicity associated with bleomycin. The most frequent presentation is pneumonitis occasionally progressing to pulmonary fibrosis. Its occurrence is higher in elderly patients and in those receiving greater than 400 units total dose, but pulmonary toxicity has been observed in young patients and those treated with low doses. A severe idiosyncratic reaction consisting of hypotension, mental confusion, fever, chills, and wheezing has been reported in approximately 1% of lymphoma patients treated with bleomycin.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 10,270 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· 4 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.

Thrombotic Microangiopathy

ROR 5.9795% CI 4.45–8.01· 45 reports

Acute Tubular Necrosis

ROR 4.1795% CI 2.69–6.46· 20 reports

SIADH / Hyponatremia

ROR 1.7595% CI 1.39–2.22· 69 reports

Electrolyte Disturbance

ROR 1.3695% CI 1.14–1.62· 127 reports

FAERS outcomes & reporting trend· 23.1% of reports w/ death · 32.1% w/ hospitalization

23.1%

Reported with a death outcome

2,370 of 10,270 reports

32.1%

Reported with hospitalization

3,292 of 10,270 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 10,270 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 1.3095% CI 1.07–1.59· 97 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Blood & lymphatic

Febrile Neutropenia826Neutropenia599Anaemia356Thrombocytopenia354Pancytopenia214

Respiratory

Pulmonary Toxicity415Respiratory Failure322Dyspnoea286Interstitial Lung Disease227Pneumonitis206

Gastrointestinal

Vomiting370Nausea367Mucosal Inflammation213

Immune / infection

Sepsis321Pneumonia257Infection194

General / constitutional

Pyrexia463Fatigue223

Nervous system

Neuropathy Peripheral197

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 Bleomycin 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

Altretamine (hexamethylmelamine)

Hexalen · Alkylating agent (methylmelamine)

Profile

Mild reversible creatinine rises only; dose-limiting toxicities are neurologic and GI; renal data confounded by cisplatin.

PRE

Mild#1 · 76% phenotype match

Estramustine

Emcyt · Hormonal–alkylating conjugate

Profile

Fluid retention, edema and thromboembolism.

PRE

Mild#2 · 65% phenotype match

Asparaginase

Elspar · Enzyme

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild#3 · 65% phenotype match

Belzutifan

Welireg · HIF-2α inhibitor

Profile

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

PRE

Mild#4 · 65% phenotype match

Dacarbazine

DTIC · Alkylator

Profile

Rare hepatic veno-occlusive disease; minimal direct renal injury.

PRE

Mild#5 · 65% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#6 · 65% phenotype match

Compare Bleomycin 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
2Bleomycin· this agentPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
3DoxorubicinGLOM — Glomerular Injury / ProteinuriaFAERS AKIMild
4MitoxantroneXTAL — Crystal / Obstructive NephropathyFAERS AKIMild
5Plicamycin (mithramycin)ATN — Acute Tubular NecrosisModerate
6Dactinomycin (actinomycin D)LYTE — 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.

Who studies this

The leading contributors to Bleomycin’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Bleomycin; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 55 clinical records among all 214 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.