Is kidney injury from Mitomycin C reversible?

Often irreversible. Typical onset: Delayed — after cumulative dosing, sometimes after therapy ends..

How should kidney function be monitored during Mitomycin C therapy?

Track cumulative lifetime mitomycin dose — nearly every case in the landmark C-HUS registry had passed a 60 mg total cumulative dose.; Before each cycle and during follow-up, check CBC with peripheral smear for schistocytes, platelet count, LDH, haptoglobin, and serum creatinine to detect early microangiopathic hemolysis.; Monitor for new or worsening hypertension and proteinuria, which often accompany or herald mitomycin TMA.; Continue surveillance after treatment ends — TMA characteristically presents weeks to months after the last dose, not only during active therapy.; If MAHA, thrombocytopenia, and rising creatinine co-occur, stop mitomycin immediately and send ADAMTS13 to exclude TTP before attributing the picture to the drug..

Who is at higher risk of kidney injury from Mitomycin C?

Cumulative dose >60 mg total; Concurrent 5-fluorouracil.

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Printable monograph

Antitumor antibiotic

Mitomycin C

Mutamycin · MMC

Antitumor antibiotic · approved 1974 · 13 citations

Up to date· through 2025

Deeply sourced8/9 · 7 signals

Met: 13 citations
Met: 12+ references
Met: Accrued over 10+ years (span: 41y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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.

The prototype dose-dependent TMA — risk climbs past a cumulative threshold.

SevereAntitumor antibiotic

GastrointestinalBladder (intravesical)Anal

§01

Signature kidney injury

Signature lesion

Thrombotic Microangiopathy

Representative incidence10%

4–15% range across studies

Dose-dependent, generally 4–15%; nearly every case in the landmark 85-patient registry had received a cumulative total dose above 60 mg. >50% historical mortality.Source: Lesesne et al., J Clin Oncol 1989

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

TMA appears after cumulative dosing, sometimes only after therapy has ended.

Distilled from: “Delayed — after cumulative dosing, sometimes after therapy ends.”

Long-term outlook & thresholds

Renal recoveryNot reported

The landmark registry reports DEATH, not renal trajectory: over half of the 85 patients died of or with the syndrome, most within 8 weeks of its onset, and conventional treatment was ineffective (10 of 21 given staphylococcal protein A immunopheresis responded). Because mortality that early forecloses renal follow-up, the registry cannot say how the surviving kidney fares — so this atlas states a recovery trajectory for neither direction. Entry criteria were creatinine >=1.6 mg/dL with hematocrit <=25% and platelets <100,000, so every case was renally involved at presentation.PMID 2497229 (opens PubMed in a new tab)

Outcome marker.: Over 50% of the 85 registry patients died of or with the syndrome, most within 8 weeks of its development; mitomycin was in the regimen of 84 of them.

Two different questions. Quick facts lists this agent's Reversibility as "Often irreversible" — this atlas's reading of the injury across its cited literature. The badge above is narrower: it reports only what the outcome study cited here measured, and that study does not follow renal recovery. The two are not in conflict, and the absence of a measured trajectory is not evidence that the kidney recovers.

Cumulative-dose threshold

>60 mg cumulative (total dose, not per m²)

In the 85-case national registry of cancer-associated hemolytic-uremic syndrome, mitomycin was part of the regimen in 84 patients and all but nine had received a cumulative dose greater than 60 mg. The registry put the risk of C-HUS after mitomycin at 4-15% overall and reported >50% mortality, most deaths within 8 weeks of syndrome onset. This is the exposure observed in reported cases, not a validated threshold below which the drug is safe.PMID 2497229 (opens PubMed in a new tab)

Early-detection biomarkers

Microangiopathic hemolysis panel (LDH, haptoglobin, schistocytes, platelet count) — Active microangiopathic hemolytic anemia / ongoing endothelial TMA injury. The defining early signal of mitomycin-C TMA - rising LDH, falling haptoglobin and platelets, and schistocytes on the peripheral smear; monitored before each cycle and during follow-up because onset is characteristically delayed and can appear after therapy ends.PMID 36706238 (opens PubMed in a new tab)
Terminal complement activation (soluble C5b-9 / sC5b-9) — Complement-mediated endothelial injury implicated in mitomycin-C TMA. Provides the mechanistic rationale for terminal complement blockade; eculizumab has produced renal recovery in mitomycin-C-induced TMA that was refractory to plasma exchange.PMID 30792638 (opens PubMed in a new tab)

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

§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.

Thrombotic Microangiopathy#1 · Signature10%PMID 2497229 (opens PubMed in a new tab)
Mitomycin-associated (cancer-associated) HUS/TMA occurs in roughly 4-15% of treated patients; risk is cumulative-dose related, most cases after total dose >60 mg.
Glomerular Injury / ProteinuriaSecondaryqualitative — no citable incidence
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Hemorrhagic CystitisRarequalitative — no citable incidence
Intravesical instillation only - direct chemical urothelial injury, not a systemic-route toxicity.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

10%incidence

SeveritySevere

ReversibilityOften irreversible

Evidence13 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Bladder / Urothelium

Thrombotic Microangiopathy

Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

§03

Kidney injury

Deep diveGemcitabine and mitomycin thrombotic microangiopathyTwo old cytotoxics — mitomycin and gemcitabine — injure the microvascular endothelium directly and in proportion to the cumulative dose, so months into therapy the small vessels clot, red cells shear, platelets fall, and the kidney fails: a dose-dependent thrombotic microangiopathy that is not TTP, does not respond to plasma exchange, and is answered first by stopping the drug.Appears in 1 documented synergy combination

Mechanism of kidney injury

Direct cumulative endothelial toxicity drives a systemic thrombotic microangiopathy — the classic dose-related drug-induced TTP/HUS.

Clinical presentation

Microangiopathic hemolytic anemia, thrombocytopenia and AKI, often with pulmonary edema; high historical mortality.

Management

Discontinue, supportive care, dialysis; eculizumab in selected cases. Plasma exchange has limited benefit.Lesion-level management framework

Risk factors

Cumulative dose >60 mg total
Concurrent 5-fluorouracil

Prevention

Cumulative-dose limits

Anticancer mechanism· how it treats cancer

Antitumor antibiotic that cross-links DNA after bioreductive activation. GI, intravesical bladder and anal cancers.

§04

Clinical depth

Renal dose adjustment

No validated CrCl-based renal dosing algorithm exists; the FDA label gives no creatinine-clearance thresholds, but mitomycin is generally avoided or used cautiously when serum creatinine exceeds roughly 1.7 mg/dL. The dominant renal hazard is cumulative-exposure-dependent thrombotic microangiopathy (TMA): in the 85-case national C-HUS registry all but nine mitomycin-treated patients had received a cumulative total dose above 60 mg, so capping total lifetime exposure is the key protective measure rather than per-cycle renal adjustment.

Dialyzability & ESKD dosing

Mitomycin undergoes rapid hepatic/tissue metabolism with a short plasma half-life (~10-20 min), so hemodialysis is not expected to meaningfully remove parent drug and is not a strategy to mitigate acute exposure (limited formal PK data in HD). Dialysis is relevant chiefly as renal-replacement support for the ESKD that frequently follows mitomycin-induced TMA.

Differential diagnosis

Distinguish mitomycin TMA from TTP (severely deficient ADAMTS13, more CNS-predominant) and from Shiga-toxin/atypical HUS by the cumulative-dose history and characteristic delayed, dose-related onset. It also mimics other chemo/cancer-associated TMA (gemcitabine, VEGF inhibitors, calcineurin inhibitors) and the underlying malignancy itself, so exposure timeline and ruling out alternative drugs are essential; blood-transfusion-triggered exacerbations are a recognized clue.

Monitoring

Track cumulative lifetime mitomycin dose — nearly every case in the landmark C-HUS registry had passed a 60 mg total cumulative dose.
Before each cycle and during follow-up, check CBC with peripheral smear for schistocytes, platelet count, LDH, haptoglobin, and serum creatinine to detect early microangiopathic hemolysis.
Monitor for new or worsening hypertension and proteinuria, which often accompany or herald mitomycin TMA.
Continue surveillance after treatment ends — TMA characteristically presents weeks to months after the last dose, not only during active therapy.
If MAHA, thrombocytopenia, and rising creatinine co-occur, stop mitomycin immediately and send ADAMTS13 to exclude TTP before attributing the picture to the drug.

Key trials & series

Lesesne et al. (J Clin Oncol 1989) — landmark cancer-associated HUS series that established mitomycin as a leading cause of chemotherapy-induced TMA and documented its dose dependence and high mortality.
Cantrell et al. (Cancer 1985) — early systematic report characterizing mitomycin-induced microangiopathic hemolytic anemia with renal failure as a distinct, frequently fatal syndrome.
Contemporary case reports/series of mitomycin-associated TMA treated with eculizumab — describe complement-pathway involvement and renal recovery in selected patients, informing modern off-label management.

Clinical pearls

Mitomycin TMA is the prototypic cumulative-dose-dependent chemotherapy-induced microangiopathy.
Onset is characteristically delayed, often appearing weeks to months after the last dose and even after treatment has stopped, so a normal creatinine during therapy is falsely reassuring.
Blood transfusion can acutely precipitate or worsen the microangiopathic hemolysis and renal failure — transfuse cautiously and watch closely in affected patients.
Plasma exchange is generally disappointing for mitomycin TMA (unlike TTP); drug discontinuation plus supportive care is the mainstay, and the renal injury is often irreversible.
Non-cardiogenic pulmonary edema/ARDS can accompany the renal-hematologic syndrome and markedly worsens prognosis, a feature that helps separate it from idiopathic TTP-HUS.
Chemical/hemorrhagic cystitis — occasionally with bladder contracture and calcification — is a quantified toxicity of intravesical mitomycin for bladder cancer; a route-specific lesion, not a systemic-IV toxicity.

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

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 · 1985–2025 · 3 since 2023

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· 4

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.

CaseB · ModerateMitomycin-induced hemolytic-uremic syndrome.Proia AD et al. · Arch Pathol Lab Med 1984 · PMID 6210069Four-patient autopsy series describing mitomycin-induced hemolytic-uremic syndrome with renal failure and glomerular/arteriolar thrombotic microangiopathy.CaseB · ModerateDrug-Induced Thrombotic Microangiopathy Arising During the Treatment of Anal Carcinoma After the Use of Mitomycin C.Sheth K et al. · Cureus 2025 · PMID 4033038257-year-old woman on capecitabine/mitomycin C plus radiation for anal carcinoma developed AKI; renal biopsy confirmed thrombotic microangiopathy diagnosed as mitomycin-C-induced TMA, treated successfully with eculizumab. Biopsy-proven, recent.CaseC · LimitedErythropoietin is beneficial in mitomycin-induced hemolytic-uremic syndrome.Catalano C et al. · Nephron 2002 · PMID 12053072Case of mitomycin C-induced hemolytic-uremic syndrome with progressive renal failure eventually requiring chronic hemodialysis.CaseC · LimitedMitomycin-Induced Thrombotic Thrombocytopenic Purpura Treated Successfully With Plasmapheresis and Steroid: A Case Report.Khaja M et al. · Cureus 2022 · PMID 35494991Case of worsening kidney function with thrombotic microangiopathy (TTP) following mitomycin therapy for anal squamous cell carcinoma.

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

WARNINGS Mitomycin should 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. Bone marrow suppression, notably thrombocytopenia and leukopenia, which may contribute to overwhelming infections in an already compromised patient, is the most common and severe of the toxic effects of mitomycin (see “ WARNINGS ” and “ ADVERSE REACTIONS ” Sections). Hemolytic Uremic Syndrome (HUS) a serious complication of chemotherapy, consisting primarily of microangiopathic hemolytic anemia, thrombocytopenia, and irreversible renal failure, has been reported in patients receiving systemic mitomycin. The syndrome may occur at any time during systemic therapy with mitomycin as a single agent or in combination with other cytotoxic drugs; however, most cases occur at doses ≥ 60 mg of mitomycin. Blood product transfusion may exacerbate the symptoms associated with this syndrome. The incidence of the syndrome has not been defined.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 3,418 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

Thrombotic Microangiopathycorroborated · ROR 21.8
Hemorrhagic Cystitiscorroborated · ROR 8.82 — on the terms that name the lesion (ROR 6.12)
Glomerular Injury / Proteinuriacorroborated · ROR 2.96 — on the terms that name the lesion (ROR 3.11)

Thrombotic Microangiopathy

ROR 21.8095% CI 16.65–28.54· 54 reports

Hemorrhagic Cystitis

ROR 8.8295% CI 7.21–10.80· 97 reports

Glomerular Injury / Proteinuria

ROR 2.9695% CI 1.75–5.00· 14 reports

Crystal / Obstructive Nephropathy

ROR 2.8895% CI 1.96–4.23· 26 reports

FAERS outcomes & reporting trend· 11.5% of reports w/ death · 28.7% w/ hospitalization

11.5%

Reported with a death outcome

392 of 3,418 reports

28.7%

Reported with hospitalization

982 of 3,418 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 3,418 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 1.0595% CI 0.71–1.54· 26 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Renal & urinary

Dysuria100Urinary Tract Infection85Haematuria69Renal Failure55

Blood & lymphatic

Thrombocytopenia110Neutropenia108Pancytopenia103Leukopenia77Febrile Neutropenia72

Gastrointestinal

Nausea170Diarrhoea158Vomiting109Mucosal Inflammation58

General / constitutional

Fatigue121Pyrexia102Pain90Asthenia55

Skin

Rash122

Respiratory

Dyspnoea66

Immune / infection

Sepsis57

Metabolic & electrolyte

Decreased Appetite55

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 Mitomycin C 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

Doxorubicin

Adriamycin · Anthracycline

Profile

Experimental podocyte model; clinical proteinuria rare.

GLOMTMACYST

Mild#1 · 89% phenotype match

Gemcitabine

Gemzar · Nucleoside analog

Profile

Dose-cumulative thrombotic microangiopathy.

TMAHTNGLOM

Severe#2 · 77% phenotype match

Interferon-α

Intron A · Cytokine

Profile

Collapsing FSGS in APOL1 carriers.

GLOMTMA

Severe#3 · 62% phenotype match

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate#4 · 60% phenotype match

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#5 · 60% phenotype match

Ramucirumab

Cyramza · Anti-VEGFR2 antibody

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#6 · 60% phenotype match

Compare Mitomycin C 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)LYTE — Electrolyte DisturbanceModerate
7Mitomycin C· this agentTMA — 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 Mitomycin C’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 Mitomycin C; 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 37 clinical records among all 166 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.