How should kidney function be monitored during Paclitaxel therapy?

Vital signs during infusion (especially first 1-2 cycles) for hypersensitivity; Volume status and creatinine if a reaction occurs; CBC and peripheral neuropathy assessment per cycle.

How can kidney injury from Paclitaxel be prevented?

Standard premedication: corticosteroid, H1-antihistamine, and H2-blocker before infusion Slow, monitored infusion with prompt management of reactions; consider nab-paclitaxel or desensitization in prior reactors Maintain euvolemia and minimize additive nephrotoxins

Who is at higher risk of kidney injury from Paclitaxel?

Severe infusion/hypersensitivity reactions; Cremophor-EL-containing (solvent-based) formulation; Volume depletion and concurrent nephrotoxins; Pre-existing renal impairment.

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Printable monograph

Taxane

Paclitaxel

Taxol · PTX

Taxane · approved 1992 · 9 citations · FAERS AKI reporting ROR 1.94 (95% CI 1.84–2.05, 1,372 AKI reports)

Recent· through 2024

Fairly sourced5/9 · 5 signals

Met: 9 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 9y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2024
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 taxane that mostly spares the kidney, with reactions tied to its vehicle rather than the tubule.

MildTaxane

Breast cancerOvarian cancerNon-small-cell lung cancer

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Paclitaxel has low direct nephrotoxicity. Hypersensitivity/infusion reactions - historically attributed to the Cremophor EL (polyoxyethylated castor oil) vehicle via complement activation, with newer evidence for IgE-mediated reactions - and associated fluid shifts can transiently compromise renal perfusion, but structural kidney injury is uncommon and not well quantified.Source: Picard & Castells, Clin Rev Allergy Immunol 2015

Onset & rechallenge

Time to injuryHyperacute (<24 h)

Any prerenal AKI follows infusion-reaction hemodynamic instability (during or shortly after administration).

Distilled from: “Infusion reactions occur during or shortly after administration (typically first/second exposure); any prerenal AKI follows the hemodynamic instability.”

§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
Case-level reports, specifically with nab-paclitaxel given without oxazaphosphorines.
Glomerular Injury / ProteinuriaRarequalitative — no citable incidence
A single biopsy-documented immune-complex GN case; proteinuria in paclitaxel regimens usually belongs to the anti-VEGF partner.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence9 citations

Nephron map

Glomerulus

Vasculature / Endothelium

Bladder / Urothelium

Prerenal / Hemodynamic AKI

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

§03

Kidney injury

Also documented as kidney-sparing

Paclitaxel — Hepatic (CYP) metabolism and biliary excretion; no renal dose adjustment. Vehicle (Cremophor) hypersensitivity; neuropathy.

Nab-paclitaxel — Albumin-bound paclitaxel; no renal clearance dependence. Neuropathy, myelosuppression.

The spared

Mechanism of kidney injury

No characteristic intrinsic tubular or glomerular toxin effect. Renal compromise, when it occurs, is hemodynamic: a hypersensitivity reaction with hypotension or large fluid shifts reduces renal perfusion (prerenal). The Cremophor EL solvent (absent in nab-paclitaxel) drives many infusion reactions through complement activation and possible IgE mechanisms.

Clinical presentation

Usually normal renal function; during a hypersensitivity reaction, flushing, dyspnea, back pain, and transient hypotension with a prerenal creatinine bump and bland urinalysis. Reactions cluster within minutes of the first or second infusion.

Management

Stop the infusion and treat hypersensitivity (epinephrine for anaphylaxis, fluids, antihistamines, steroids); restore hemodynamics. Prerenal AKI reverses with perfusion. Rapid drug desensitization allows safe re-treatment after reactions. No drug-specific renal antidote is needed.Lesion-level management framework

Risk factors

Severe infusion/hypersensitivity reactions
Cremophor-EL-containing (solvent-based) formulation
Volume depletion and concurrent nephrotoxins
Pre-existing renal impairment

Prevention

Standard premedication: corticosteroid, H1-antihistamine, and H2-blocker before infusion
Slow, monitored infusion with prompt management of reactions; consider nab-paclitaxel or desensitization in prior reactors
Maintain euvolemia and minimize additive nephrotoxins

Anticancer mechanism· how it treats cancer

Binds beta-tubulin and stabilizes microtubules, preventing depolymerization, freezing the mitotic spindle, and triggering apoptosis. Broadly used in breast, ovarian, lung, and other solid tumors.

Note · Low direct nephrotoxicity; renal events are vehicle/hypersensitivity- and hemodynamics-driven and reversible.

§04

Clinical depth

Renal dose adjustment

Hepatically (CYP2C8/CYP3A4) metabolized and biliary excreted - no renal dose adjustment; reduce dose for significant hepatic impairment. Renal impairment does not require dose change.

Dialyzability & ESKD dosing

Highly protein-bound, large volume of distribution, and non-renally cleared; not dialyzable. Can be given without regard to dialysis timing.

Differential diagnosis

Hypersensitivity-driven prerenal AKI (infusion-timed hypotension, bland urine) vs concurrent nephrotoxin ATN vs tumor- or sepsis-related AKI. The temporal link to the infusion reaction is the clue.

Monitoring

Vital signs during infusion (especially first 1-2 cycles) for hypersensitivity
Volume status and creatinine if a reaction occurs
CBC and peripheral neuropathy assessment per cycle

Key trials & series

Picard & Castells Clin Rev Allergy Immunol 2015 taxane hypersensitivity/desensitization review

Clinical pearls

The kidney risk with paclitaxel is the vehicle and the reaction, not the molecule - premedicate and it is rare.
Switching to nab-paclitaxel removes Cremophor EL and most solvent-related reactions.
After a hypersensitivity reaction, desensitization allows safe continuation of an effective drug.
The rare hemorrhagic-cystitis case reports are specifically for nab-paclitaxel given without oxazaphosphorines.
A single biopsy-documented immune-complex proliferative glomerulonephritis is attributed to paclitaxel; most proteinuria in paclitaxel regimens belongs to the anti-VEGF partner (bevacizumab, ramucirumab).

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 · 2015–2024 · 2 since 2022

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 · LimitedPaclitaxel-induced diffuse scleroderma with possible scleroderma-renal crisis: a case report and literature review of taxanes-induced scleroderma.Ketpueak T et al. · Clin Rheumatol 2022 · PMID 36085204Paclitaxel therapy followed by diffuse scleroderma with possible scleroderma renal crisis (acute kidney injury).CaseC · LimitedSevere hyponatremia caused by nab-paclitaxel-induced syndrome of inappropriate antidiuretic hormone secretion: A case report in a patient with metastatic pancreatic adenocarcinoma.Neuzillet C et al. · Medicine (Baltimore) 2016 · PMID 27368013Grade 4 hyponatremia from nab-paclitaxel-induced SIADH, attributed to the drug by imputability analysis and dose-reduced rechallenge.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING Paclitaxel injection should be administered under the supervision of a physician experienced in the use of cancer chemotherapeutic agents. Appropriate management of complications is possible only when adequate diagnostic and treatment facilities are readily available. Anaphylaxis and severe hypersensitivity reactions characterized by dyspnea and hypotension requiring treatment, angioedema, and generalized urticaria have occurred in 2 to 4% of patients receiving paclitaxel in clinical trials. Fatal reactions have occurred in patients despite premedication. All patients should be pretreated with corticosteroids, diphenhydramine, and H 2 antagonists (see DOSAGE AND ADMINISTRATION ). Patients who experience severe hypersensitivity reactions to paclitaxel injection should not be rechallenged with the drug. Paclitaxel injection therapy should not be given to patients with solid tumors who have baseline neutrophil counts of less than 1500 cells/mm 3 and should not be given to patients with AIDS-related Kaposi’s sarcoma if the baseline neutrophil count is less than 1000 cells/mm 3 . In order to monitor the occurrence of bone marrow suppression, primarily neutropenia, which may be severe and result in infection, it is recommended that frequent peripheral blood cell counts be performed on all patients receiving paclitaxel injection.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 98,464 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

Glomerular Injury / Proteinuriacorroborated · ROR 5.4 — on the terms that name the lesion (ROR 2.45)
Hemorrhagic Cystitiscorroborated · ROR 1.54 — on the terms that name the lesion (ROR 4.42)
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 6.0295% CI 5.47–6.63· 426 reports

Glomerular Injury / Proteinuria

ROR 5.4095% CI 5.01–5.81· 718 reports

Electrolyte Disturbance

ROR 3.0195% CI 2.90–3.13· 2,632 reports

SIADH / Hyponatremia

ROR 2.9795% CI 2.79–3.15· 1,103 reports

Acute Interstitial Nephritis

ROR 2.4395% CI 2.12–2.78· 212 reports

Acute Tubular Necrosis

ROR 1.5995% CI 1.26–2.00· 73 reports

Hemorrhagic Cystitis

ROR 1.5495% CI 1.41–1.69· 500 reports

Hypertension

ROR 1.4595% CI 1.40–1.51· 2,602 reports

FAERS outcomes & reporting trend· 16.6% of reports w/ death · 41% w/ hospitalization

16.6%

Reported with a death outcome

16,309 of 98,464 reports

41%

Reported with hospitalization

40,358 of 98,464 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 98,464 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 1.9495% CI 1.84–2.05· 1,372 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

Neutropenia5,423Anaemia4,794Febrile Neutropenia3,718Myelosuppression3,570Thrombocytopenia3,060

Gastrointestinal

Nausea5,499Diarrhoea5,152Vomiting3,818Abdominal Pain2,017

General / constitutional

Fatigue4,222Pyrexia3,902Asthenia2,946

Skin

Rash2,459Erythema2,150Alopecia1,867

Respiratory

Dyspnoea5,114

Nervous system

Neuropathy Peripheral3,933

Metabolic & electrolyte

Decreased Appetite2,347

Immune / infection

Pneumonia2,225

Vascular

Hypertension1,954

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 Paclitaxel 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

Cabazitaxel

Jevtana · Taxane

Profile

Rare AKI; mostly GI-mediated.

PRECYST

Mild#1 · 84% phenotype match

Docetaxel

Taxotere · Taxane

Profile

Fluid retention; low direct renal toxicity.

PRECYSTTMA

Mild#2 · 76% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#3 · 68% phenotype match

Asparaginase

Elspar · Enzyme

Profile

Rare AKI; pancreatitis-mediated.

PRE

Mild#4 · 57% phenotype match

Belzutifan

Welireg · HIF-2α inhibitor

Profile

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

PRE

Mild#5 · 57% phenotype match

Dacarbazine

DTIC · Alkylator

Profile

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

PRE

Mild#6 · 57% phenotype match

Compare Paclitaxel 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
4CabazitaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
5VincristineSIADH — SIADH / HyponatremiaFAERS AKIMild
6VinorelbineSIADH — SIADH / HyponatremiaFAERS AKIMild
7DocetaxelPRE — Prerenal / Hemodynamic AKIFAERS AKIMild
8Paclitaxel· this agentPRE — 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.

Who studies this

The leading contributors to Paclitaxel’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 Paclitaxel; 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 194 clinical records among the 300 most-relevant of 425 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.