Mitomycin C
Mutamycin · Antitumor antibiotic
Prototype dose-dependent TMA.
TMAGLOMCYST
Severe#1 · 89% phenotype match
Doxorubicin
Adriamycin · Doxo
Anthracycline · approved 1974 · 12 citations · FAERS AKI reporting ROR 2.13 (95% CI 2.02–2.24, 1,454 AKI reports)
Up to date· through 2026
Deeply sourced9/9 · 8 signals
- Met: 12 citations
- Met: 12+ references
- Met: Accrued over 10+ years (span: 35y)
- Met: Beyond single case reports
- Met: High-impact journal
- Met: Landmark reference
- Met: Current through 2026
- 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.
The classic anthracycline whose podocyte-injury model defines experimental FSGS, though clinical proteinuria is rare.
MildAnthracycline
Breast cancerHodgkin and non-Hodgkin lymphomaSarcomasAcute leukemias
§01
Signature kidney injury
Signature lesion
Adriamycin nephropathy is the canonical rodent model of podocyte injury and focal segmental glomerulosclerosis (FSGS); clinically significant glomerular disease from therapeutic dosing in patients is rare and largely case-level. Separately, doxorubicin — especially the pegylated liposomal formulation — is an increasingly recognized but underreported cause of kidney-limited thrombotic microangiopathy (a vascular/endothelial lesion), described in biopsy-proven case reports and drug-induced-TMA series.Source: Lee & Harris, Nephrology (Carlton) 2011 (model review)
Onset & rechallenge
Time to injurySubacute (~1–6 weeks)
Glomerular injury develops subacutely over weeks in models, with clinical events rare and variable.
Distilled from: “Subacute in models (over weeks); clinical events rare and variable.”
§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.
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.
Intravesical instillation only - chemical cystitis in randomized instillation trials, not a systemic-route toxicity.
Toxicity fingerprint
Tap a signature to trace where it strikes the nephron.
Incidence not quantified
SeverityMild
ReversibilityVariable
Evidence12 citations
Nephron map
GlomerulusFiltration barrier (podocytes + endothelium)
Vasculature / Endothelium
Bladder / Urothelium
Glomerular Injury / Proteinuria
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
§03
Kidney injury
Also documented as kidney-sparing
Doxorubicin — Hepatobiliary clearance; clinically non-nephrotoxic. Cumulative cardiomyopathy (the real ceiling); a classic experimental podocyte model only.
Liposomal doxorubicin — Same renal-sparing profile with altered pharmacokinetics. Hand-foot syndrome.
The sparedMechanism of kidney injury
In the experimental model, doxorubicin directly injures the podocyte: reactive oxygen species and mitochondrial dysfunction disrupt the actin cytoskeleton and slit diaphragm, causing foot-process effacement, podocyte detachment/apoptosis and a loss of glomerular permselectivity that progresses to segmental sclerosis with secondary tubulointerstitial inflammation and fibrosis. Susceptibility is strain- and gene-dependent (e.g., loci on chromosome 16 in mice), underscoring a genetic component to podocyte vulnerability.
Clinical presentation
Heavy (nephrotic-range) proteinuria, hypoalbuminemia and edema in the experimental setting; in patients, overt glomerular disease is unusual and, when seen, presents as proteinuria with or without a fall in GFR.
Management
No specific renal therapy is established for the rare clinical glomerulopathy; supportive care with RAAS blockade (ACE inhibitor or ARB) to reduce proteinuria and management of any underlying glomerular disease. Liposomal formulations alter tissue distribution and are not associated with the podocytopathy signal clinically.Lesion-level management framework
Risk factors
- High cumulative exposure (experimental)
- Pre-existing glomerular disease or podocyte susceptibility
Prevention
- Adhere to cumulative dose limits (primarily for cardiotoxicity)
Anticancer mechanism· how it treats cancer
Anthracycline antitumor antibiotic that intercalates DNA, poisons topoisomerase II (trapping the cleavable complex and producing double-strand breaks), and generates reactive oxygen species via redox cycling of its quinone moiety, driving apoptosis. Broadly used across breast cancer, lymphomas, sarcomas and acute leukemias.
Note · Best known as an experimental podocyte-injury / FSGS model; clinical nephrotoxicity in patients is rare and largely case-level.
§04
Clinical depth
Renal dose adjustment
No renal dose adjustment is required — doxorubicin is hepatically metabolized and biliary-excreted, so dosing is guided by hepatic function and bilirubin rather than renal function. Renal impairment does not mandate dose reduction.
Dialyzability & ESKD dosing
Not dialyzable to any clinically meaningful extent; doxorubicin is large, highly protein- and tissue-bound, with a very large volume of distribution, so hemodialysis does not remove it and no supplemental dosing is needed in ESKD.
Differential diagnosis
In a patient on doxorubicin with proteinuria, the differential is dominated by other causes of FSGS/podocytopathy (primary FSGS, viral, obesity-related, secondary maladaptive) and paraneoplastic glomerulonephritis; a kidney biopsy distinguishes drug-attributable podocyte injury from these far more common etiologies.
Monitoring
- Cumulative anthracycline dose and cardiac function (LVEF) — the principal dose-limiting toxicity
- Urinalysis/UPCR in patients who develop edema or proteinuria
- Urine protein in susceptible patients
Key trials & series
- No clinical trial carries a renal signal; the evidence base is the experimental adriamycin nephropathy literature
Clinical pearls
- Adriamycin nephropathy is a workhorse research model of FSGS, not a common clinical nephrotoxicity — keep the distinction clear.
- Doxorubicin is dosed by hepatic/bilirubin status, not renal function, and is not dialyzable.
- Real-world proteinuria in a doxorubicin-treated patient is more likely another glomerulopathy; biopsy before attributing it to the drug.
- Chemical cystitis is an intravesical-route doxorubicin toxicity documented in randomized instillation trials (irritative symptoms, occasionally contracted bladder); systemic doxorubicin is almost always cyclophosphamide-paired, so systemic hemorrhagic-cystitis reports mostly belong to the partner drug.
Beyond the kidney — non-renal toxicities· 2 organ systems
Class-level context for the major non-renal toxicities of the Anthracycline class.
Cardiac
Cardiomyopathy, QT, ischemia, myocarditis
- Dose-dependent cardiomyopathy and heart failure
Hematologic
Cytopenias, thrombosis, TMA
- Myelosuppression
§05
References
9 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
9 references · 1991–2026 · 1 since 2024Primary (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.
- 1.Renoprotective approaches against anthracycline nephrotoxicity.Weldemichael T, Hye Khan MA, Imig JD · Biochem Pharmacol · 2026 · PMID 41621691Review characterizing doxorubicin-induced nephrotoxicity as multifactorial (oxidative stress, inflammation, apoptosis) presenting as proteinuria, hypertension, electrolyte imbalance, glomerulopathy, interstitial nephritis, and AKI with progression to CKD; catalogs investigational nephroprotective strategies including natural compounds and pharmacologic agents targeting oxidative/inflammatory pathways.
- 2.LandmarkAdriamycin nephropathy: a model of focal segmental glomerulosclerosis.Lee VW et al. · Nephrology (Carlton) · 2011 · PMID 21175974Definitive review of the adriamycin nephropathy FSGS model: pharmacology, podocyte injury, genetics and pathogenesis.
- 3.Sirt6 deficiency exacerbates podocyte injury and proteinuria through targeting Notch signaling.Liu M et al. · Nat Commun · 2017 · PMID 28871079Uses adriamycin-induced nephropathy as the experimental podocyte-injury/proteinuria model.
- 4.New drug toxicities in the onco-nephrology world.Perazella MA et al. · Kidney Int · 2015 · PMID 25671763Onco-nephrology review of glomerular and other chemotherapy-associated renal injury.
- 5.Anticancer Drug-Induced Acute Kidney Injury.Izzedine H et al. · Kidney Int Rep · 2017 · PMID 29318217Review covering glomerular mechanisms of drug-induced kidney injury.
- 6.Onconephrology: The intersections between the kidney and cancer.Rosner MH et al. · CA Cancer J Clin · 2020 · PMID 32853404Reviews chemotherapy-associated glomerular disease and paraneoplastic glomerulopathy in the differential.
- 7.A randomized trial of intravesical doxorubicin and immunotherapy with bacille Calmette-Guérin for transitional-cell carcinoma of the bladder.Lamm DL et al. · N Engl J Med · 1991 · PMID 1922207Randomized SWOG trial recording local irritative bladder symptoms in the intravesical doxorubicin arm.
- 8.Intravesical epirubicin versus doxorubicin for superficial bladder tumors (stages pTa and pT1): a randomized prospective study.Ali-el-Dein B et al. · J Urol · 1997 · PMID 9186325Randomized intravesical epirubicin-vs-doxorubicin comparison: 41.7% toxicity in the doxorubicin arm; contracted bladder also reported with doxorubicin.
- 9.Epirubicin: a review of its intravesical use in superficial bladder cancer.Onrust SV et al. · Drugs Aging · 1999 · PMID 10582777Review noting intravesical doxorubicin causes more chemical cystitis than epirubicin.
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.
CaseA · StrongPegylated Liposomal Doxorubicin and Kidney-Limited Thrombotic Microangiopathy in a Kidney Transplant Recipient: A Case Report.Rodriguez-Ramirez S et al. · Kidney Med 2022 · PMID 35509676Kidney transplant recipient on pegylated liposomal doxorubicin developed biopsy-proven kidney-limited thrombotic microangiopathy with subnephrotic proteinuria that recurred on drug re-challenge.CaseB · ModeratePegylated Liposomal Doxorubicin Causes Kidney-limited Thrombotic Microangiopathy.Glezerman I et al. · Am J Kidney Dis 2024 · PMID 37839689Two cases of pegylated liposomal doxorubicin-induced kidney-limited thrombotic microangiopathy presenting with rising creatinine and proteinuria, confirmed on biopsy and resolving after drug cessation.CaseC · LimitedPegylated-liposomal Doxorubicin-induced Glomerular Thrombotic Microangiopathy.Yokoyama S et al. · Intern Med 2024 · PMID 38462521Patient on prolonged pegylated liposomal doxorubicin developed glomerular thrombotic microangiopathy with hypertension, proteinuria, and renal impairment.
Conference abstracts & journal reports· 1 non-PubMed
Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.
FDA label — boxed warning & renal dosing· boxed warning
Quoted verbatim from this agent's current FDA label (May 2026) — not paraphrased or interpreted. Full label on DailyMed .
Boxed warning
WARNING: CARDIOMYOPATHY, SECONDARY MALIGNANCIES, EXTRAVASATION AND TISSUE NECROSIS, and SEVERE MYELOSUPPRESSION • Cardiomyopathy: Myocardial damage, including acute left ventricular failure, can occur with doxorubicin hydrochloride. The risk of cardiomyopathy is proportional to the cumulative exposure with incidence rates from 1%–20% for cumulative doses ranging from 300 mg/m 2 to 500 mg/m 2 when doxorubicin hydrochloride is administered every 3 weeks. The risk of cardiomyopathy is further increased with concomitant cardiotoxic therapy. Assess left ventricular ejection fraction (LVEF) before and regularly during and after treatment with doxorubicin hydrochloride [see Warnings and Precautions (5.1) ] . • Secondary Malignancies: Secondary acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) occur at a higher incidence in patients treated with anthracyclines, including doxorubicin hydrochloride [see Warnings and Precautions (5.2) ] . • Extravasation and Tissue Necrosis: Extravasation of doxorubicin hydrochloride can result in severe local tissue injury and necrosis requiring wide excision of the affected area and skin grafting. Immediately terminate the drug and apply ice to the affected area [see Warnings and Precautions (5.3) ] . • Severe myelosuppression resulting in serious infection, septic shock, requirement for transfusions, hospitalization, and death may…
What gets reported — FAERS
Everything below is FAERS — adverse events someone chose to report, about 95,403 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· 8 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
- Thrombotic Microangiopathycorroborated · ROR 3.42
- Hemorrhagic Cystitiscorroborated · ROR 1.69 — on the terms that name the lesion (ROR 12.64)
- Glomerular Injury / Proteinuriacorroborated · ROR 1.49 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Fanconi Syndrome
ROR 4.4095% CI 3.62–5.36· 101 reports
Thrombotic Microangiopathy
ROR 3.4295% CI 3.01–3.89· 238 reports
Electrolyte Disturbance
ROR 2.4595% CI 2.35–2.56· 2,089 reports
SIADH / Hyponatremia
ROR 2.2695% CI 2.11–2.42· 820 reports
Hemorrhagic Cystitis
ROR 1.6995% CI 1.55–1.84· 530 reports
Acute Interstitial Nephritis
ROR 1.6695% CI 1.41–1.96· 141 reports
Glomerular Injury / Proteinuria
ROR 1.4995% CI 1.30–1.72· 197 reports
Acute Tubular Necrosis
ROR 1.3095% CI 1.00–1.68· 58 reports
FAERS outcomes & reporting trend· 18.7% of reports w/ death · 34.2% w/ hospitalization
18.7%
Reported with a death outcome
17,873 of 95,403 reports
34.2%
Reported with hospitalization
32,623 of 95,403 reports
Reports per year
- 2015: 4,458 reports
- 2016: 3,899 reports
- 2017: 5,141 reports
- 2018: 7,418 reports
- 2019: 6,608 reports
- 2020: 7,985 reports
- 2021: 6,342 reports
- 2022: 8,395 reports
- 2023: 10,106 reports
- 2024: 9,628 reports
- 2025: 8,109 reports
- 2026: 3,899 reports
Yearly FAERS report volume · most recent year is partial.
FAERS adverse-event signal — all organ systems· 7 systems · 95,403 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 2.1395% CI 2.02–2.24· 1,454 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 Neutropenia9,530Neutropenia6,687Anaemia4,096Thrombocytopenia3,987Pancytopenia2,393
Gastrointestinal
Nausea3,568Diarrhoea2,918Vomiting2,877Mucosal Inflammation2,150
Immune / infection
Pneumonia3,095Sepsis2,982Infection2,229Septic Shock1,649
General / constitutional
Pyrexia4,361Fatigue2,565Asthenia1,678
Skin
Alopecia2,831
Nervous system
Neuropathy Peripheral2,298
Respiratory
Dyspnoea2,139
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 Doxorubicin 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.
Phenotype-similar agents· the numbered markers on the map above
Profile
Gemcitabine
Gemzar · Nucleoside analog
Dose-cumulative thrombotic microangiopathy.
TMAHTNGLOM
Severe#2 · 66% phenotype match
Nintedanib
Ofev · VEGFR/FGFR/PDGFR TKI
Proteinuria and rare TMA.
HTNTMAGLOM
Mild#3 · 65% phenotype match
Ziv-aflibercept
Zaltrap · VEGF trap
Hypertension and proteinuria like bevacizumab.
HTNGLOMTMA
Moderate#4 · 60% phenotype match
Bevacizumab
Avastin · Anti-VEGF antibody
Proteinuria, hypertension, glomerular TMA.
GLOMHTNTMA
Moderate#5 · 60% phenotype match
Ramucirumab
Cyramza · Anti-VEGFR2 antibody
Hypertension and proteinuria, class effect.
HTNGLOMTMA
Moderate#6 · 60% phenotype match
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
- 3Doxorubicin· this agentGLOM — 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 Doxorubicin’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 Doxorubicin; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.
- Artunc, Ferruh — their work on Doxorubicin, on PubMed (opens in a new tab)4 papers · 92 citesPMID 35569011 (opens PubMed in a new tab)PMID 34537228 (opens PubMed in a new tab)PMID 34423816 (opens PubMed in a new tab)
- Bohnert, Bernhard N — their work on Doxorubicin, on PubMed (opens in a new tab)4 papers · 92 citesPMID 35569011 (opens PubMed in a new tab)PMID 34537228 (opens PubMed in a new tab)PMID 34423816 (opens PubMed in a new tab)
- Devarajan, Padma V — their work on Doxorubicin, on PubMed (opens in a new tab)2 papers · 145 citesPMID 28155331 (opens PubMed in a new tab)PMID 18540835 (opens PubMed in a new tab)
- Xiao, Mengyun — their work on Doxorubicin, on PubMed (opens in a new tab)3 papers · 78 citesPMID 35569011 (opens PubMed in a new tab)PMID 34537228 (opens PubMed in a new tab)PMID 34423816 (opens PubMed in a new tab)
- Grahammer, Florian — their work on Doxorubicin, on PubMed (opens in a new tab)3 papers · 78 citesPMID 35569011 (opens PubMed in a new tab)PMID 34537228 (opens PubMed in a new tab)PMID 34423816 (opens PubMed in a new tab)
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 106 clinical records among the 300 most-relevant of 939 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.