What kind of kidney injury does Cabazitaxel cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Hemorrhagic Cystitis.

How should kidney function be monitored during Cabazitaxel therapy?

Stool frequency and hydration status each cycle; CBC with differential (neutropenia) before each cycle; Creatinine/electrolytes with diarrhea or infection.

How can kidney injury from Cabazitaxel be prevented?

Antidiarrheal management and prompt oral/IV rehydration Primary G-CSF prophylaxis in high-risk patients to limit febrile neutropenia

Who is at higher risk of kidney injury from Cabazitaxel?

Severe diarrhea and dehydration; Neutropenic infection/sepsis (mitigated by G-CSF prophylaxis); Older age (>=75) and pre-existing renal impairment; Higher dose (25 vs 20 mg/m2).

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Printable monograph

Taxane

Cabazitaxel

Jevtana · CBZ

Taxane · approved 2010 · 9 citations · FAERS AKI reporting ROR 2.00 (95% CI 1.51–2.64, 50 AKI reports)

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 9 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2025
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 second-line taxane whose rare AKI is generally gastrointestinal and hemodynamic in origin.

MildTaxane

Metastatic castration-resistant prostate cancer

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Cabazitaxel has low direct nephrotoxicity; AKI is uncommon and usually mediated by gastrointestinal losses (diarrhea, occurring in a substantial minority), neutropenic sepsis, or hemodynamic instability rather than direct tubular toxicity. In real-world safety data, grade >=3 diarrhea and febrile neutropenia each occur in roughly 5% of patients. A drug-specific renal AKI rate is not well established.Source: Castellano et al., Expert Opin Drug Saf 2014

Onset & rechallenge

Time to injuryVariable / unpredictable

AKI arises when intercurrent GI or infectious complications occur during treatment cycles, without a fixed onset time.

Distilled from: “AKI follows intercurrent gastrointestinal or infectious complications during treatment cycles.”

§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.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Hemorrhagic CystitisRarequalitative — no citable incidence
Largely radiation recall of the previously irradiated bladder in mCRPC; at least one radiotherapy-naive case.

§03

Kidney injury

Mechanism of kidney injury

No characteristic intrinsic renal toxin effect. Severe diarrhea and dehydration or neutropenic sepsis reduce renal perfusion and can cause prerenal and ischemic injury; otherwise the kidney is generally spared.

Clinical presentation

Usually preserved renal function; in the setting of diarrhea or sepsis, prerenal azotemia with bland sediment, a high BUN:creatinine ratio, and volume-depletion signs.

Management

Volume repletion, control of diarrhea, and treatment of infection/neutropenic sepsis; prerenal AKI generally reverses with supportive care.Lesion-level management framework

Risk factors

Severe diarrhea and dehydration
Neutropenic infection/sepsis (mitigated by G-CSF prophylaxis)
Older age (>=75) and pre-existing renal impairment
Higher dose (25 vs 20 mg/m2)

Prevention

Antidiarrheal management and prompt oral/IV rehydration
Primary G-CSF prophylaxis in high-risk patients to limit febrile neutropenia

Anticancer mechanism· how it treats cancer

Semisynthetic taxane with poor affinity for P-glycoprotein, retaining activity in docetaxel-resistant disease; stabilizes microtubules to block mitosis. Used in metastatic castration-resistant prostate cancer (mCRPC) after docetaxel.

Note · Rare AKI, mostly GI- and sepsis-mediated; not a characteristic direct nephrotoxin and non-renally cleared.

§04

Clinical depth

Renal dose adjustment

Hepatically (CYP3A) metabolized with minimal renal excretion - no formal renal dose adjustment for mild-moderate impairment; use caution in severe impairment/ESKD given limited data. Reduce dose for hepatic impairment and with strong CYP3A inhibitors.

Dialyzability & ESKD dosing

Highly protein-bound and non-renally cleared; not dialyzable. No HD-timed dosing established.

Differential diagnosis

GI/sepsis-driven prerenal AKI (volume signs, bland urine) vs obstructive uropathy from prostate cancer vs concurrent nephrotoxin ATN. In mCRPC, also exclude post-renal obstruction.

Monitoring

Stool frequency and hydration status each cycle
CBC with differential (neutropenia) before each cycle
Creatinine/electrolytes with diarrhea or infection

Key trials & series

TROPIC (registrational survival benefit post-docetaxel)
Castellano Expert Opin Drug Saf 2014 Spanish expanded-access safety cohort

Clinical pearls

Cabazitaxel AKI is almost always downstream of diarrhea or neutropenic sepsis - treat the cause.
Primary G-CSF prophylaxis cuts the febrile-neutropenia (and resulting hemodynamic AKI) risk.
In a prostate-cancer patient with AKI, always exclude obstruction before blaming the taxane.
Cabazitaxel causes hemorrhagic cystitis largely as radiation recall of the previously irradiated bladder in mCRPC, though at least one radiotherapy-naive case exists.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Hemorrhagic Cystitis

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

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

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (taxanes, vinca)

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Hypersensitivity (taxane vehicles)

§05

References

7 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

7 references · 2014–2025 · 1 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· 2

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 · LimitedCabazitaxel Induced Thrombotic Microangiopathy in a Patient with Prostate Cancer.Nlandu Y et al. · Case Rep Nephrol 2019 · PMID 31827954Cabazitaxel-induced thrombotic microangiopathy with renal failure requiring dialysis and subsequent recovery of renal function in a man with metastatic prostate cancer.CaseC · LimitedTumor lysis syndrome following cabazitaxel administration for metastatic castration-resistant prostate cancer: A case report.Oshima M et al. · IJU Case Rep 2019 · PMID 32743405Acute tumor lysis syndrome after a single cabazitaxel dose, with the attendant metabolic/renal derangement managed by hydration and rasburicase.

FDA label — boxed warning & renal dosing· boxed warning · renal impairment

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

Boxed warning

WARNING: NEUTROPENIA AND HYPERSENSITIVITY WARNING: NEUTROPENIA AND HYPERSENSITIVITY See full prescribing information for complete boxed warning. Neutropenic deaths have been reported. Obtain frequent blood counts to monitor for neutropenia. JEVTANA is contraindicated in patients with neutrophil counts of ≤1,500 cells/mm 3 . Primary prophylaxis with G-CSF is recommended in patients with high-risk clinical features. Consider primary prophylaxis with G-CSF in all patients receiving a dose of 25 mg/m 2 ( 4 , 5.1 , 5.2 ) Severe hypersensitivity can occur and may include generalized rash/erythema, hypotension and bronchospasm. Discontinue JEVTANA immediately if severe reactions occur and administer appropriate therapy. ( 2.1 , 5.2 ) Contraindicated if history of severe hypersensitivity reactions to cabazitaxel or to drugs formulated with polysorbate 80. ( 4 ) Neutropenia : Neutropenic deaths have been reported. Monitor for neutropenia with frequent blood cell counts. JEVTANA is contraindicated in patients with neutrophil counts of ≤1,500 cells/mm 3 . Primary prophylaxis with G-CSF is recommended in patients with high-risk clinical features. Consider primary prophylaxis with G-CSF in all patients receiving a dose of 25 mg/m 2 [see Contraindications (4) and Warnings and Precautions (5.1 , 5.2) ] . Severe hypersensitivity : Severe hypersensitivity reactions can occur and may include…

Renal impairment — from the label

No dose adjustment is necessary in patients with renal impairment not requiring hemodialysis. Patients presenting with end-stage renal disease (creatinine clearance CL CR <15 mL/min/1.73 m 2 ), should be monitored carefully during treatment [see Clinical Pharmacology (12.3) ] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 3,469 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

Hemorrhagic Cystitiscorroborated · ROR 13.37 — on the terms that name the lesion (ROR 18.16)
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Hemorrhagic Cystitis

ROR 13.3795% CI 11.34–15.78· 147 reports

Crystal / Obstructive Nephropathy

ROR 9.9095% CI 8.02–12.22· 89 reports

Electrolyte Disturbance

ROR 3.4395% CI 2.83–4.16· 106 reports

SIADH / Hyponatremia

ROR 3.0395% CI 2.22–4.13· 40 reports

FAERS outcomes & reporting trend· 20% of reports w/ death · 38.3% w/ hospitalization

20%

Reported with a death outcome

693 of 3,469 reports

38.3%

Reported with hospitalization

1,329 of 3,469 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 3,469 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 2.0095% CI 1.51–2.64· 50 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Haematuria124

Blood & lymphatic

Febrile Neutropenia248Anaemia177Neutropenia170Thrombocytopenia109

General / constitutional

Fatigue208Pyrexia171Asthenia139Weight Decreased90

Gastrointestinal

Diarrhoea189Nausea118Vomiting84

Respiratory

Dyspnoea137Pulmonary Embolism93

Immune / infection

Sepsis105Pneumonia98

Metabolic & electrolyte

Decreased Appetite104

Musculoskeletal

Osteonecrosis Of Jaw88

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 Cabazitaxel 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

Docetaxel

Taxotere · Taxane

Profile

Fluid retention; low direct renal toxicity.

PRECYSTTMA

Mild#1 · 84% phenotype match

Paclitaxel

Taxol · Taxane

Profile

Low direct nephrotoxicity; vehicle reactions.

PRECYSTGLOM

Mild#2 · 84% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#3 · 76% phenotype match

Asparaginase

Elspar · Enzyme

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild#4 · 65% phenotype match

Belzutifan

Welireg · HIF-2α inhibitor

Profile

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

PRE

Mild#5 · 65% phenotype match

Dacarbazine

DTIC · Alkylator

Profile

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

PRE

Mild#6 · 65% phenotype match

Compare Cabazitaxel 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 Microtubule inhibitors

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.

1EribulinPRE — Prerenal / Hemodynamic AKIMild
2VinblastineSIADH — SIADH / HyponatremiaMild
3VinflunineLYTE — Electrolyte DisturbanceMild
4Cabazitaxel· this agentPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
5VincristineSIADH — SIADH / HyponatremiaFAERS AKIMild
6VinorelbineSIADH — SIADH / HyponatremiaFAERS AKIMild
7DocetaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
8PaclitaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild

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.