How should kidney function be monitored during Docetaxel therapy?

Weight and clinical edema/effusions each cycle; LFTs/bilirubin before dosing (drives dose adjustment); CBC for neutropenia; creatinine if volume status changes.

How can kidney injury from Docetaxel be prevented?

Corticosteroid premedication (e.g. dexamethasone starting the day before) to limit fluid retention and hypersensitivity

Who is at higher risk of kidney injury from Docetaxel?

Omission or inadequate corticosteroid premedication (worsens fluid retention); Cardiac or volume-overload comorbidity; Higher cumulative docetaxel dose; Concurrent nephrotoxins and volume depletion.

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Printable monograph

Taxane

Docetaxel

Taxotere · DTX

Taxane · approved 1996 · 10 citations · FAERS AKI reporting ROR 1.34 (95% CI 1.24–1.45, 650 AKI reports)

Up to date· through 2025

Deeply sourced7/9 · 6 signals

Met: 10 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 15y)
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 taxane whose hallmark fluid retention rarely translates into true kidney injury.

MildTaxane

Breast cancerProstate cancerNon-small-cell lung cancerGastric cancer

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Docetaxel has low direct renal toxicity. Its characteristic fluid-retention syndrome (peripheral edema, effusions, weight gain) reflects increased capillary permeability rather than tubular injury; AKI directly attributable to docetaxel is uncommon and not well quantified, and the drug has been used successfully even in kidney-transplant recipients.Source: García-Carro et al., Nephron 2022

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Fluid retention builds up cumulatively after several cycles/cumulative dose, while hypersensitivity reactions happen during infusion.

Distilled from: “Fluid retention develops cumulatively (often after several cycles / cumulative dose); hypersensitivity reactions occur during infusion.”

§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, including monotherapy and oxazaphosphorine-free regimens; mechanism unknown.
Thrombotic MicroangiopathyRarequalitative — no citable incidence
Case-level TTP/HUS-type TMA, including monotherapy.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence10 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

Docetaxel — Hepatically cleared; kidney function largely irrelevant to dosing. Fluid retention; monitor hepatic function.

The spared

Mechanism of kidney injury

No characteristic direct nephrotoxin effect. Cumulative capillary-permeability changes cause fluid retention and third-spacing, and, less often, hypersensitivity-related hemodynamic instability can produce prerenal physiology; the kidney parenchyma is generally spared.

Clinical presentation

Progressive peripheral edema, pleural/pericardial effusions, and weight gain accruing over cycles; renal function usually preserved, with any creatinine rise typically prerenal and reversible. Hypersensitivity reactions occur during infusion.

Management

Manage fluid retention with continued corticosteroid prophylaxis and diuretics as needed; treat prerenal AKI with volume optimization. No drug-specific renal therapy is required.Lesion-level management framework

Risk factors

Omission or inadequate corticosteroid premedication (worsens fluid retention)
Cardiac or volume-overload comorbidity
Higher cumulative docetaxel dose
Concurrent nephrotoxins and volume depletion

Prevention

Corticosteroid premedication (e.g. dexamethasone starting the day before) to limit fluid retention and hypersensitivity

Anticancer mechanism· how it treats cancer

Microtubule-stabilizing taxane that binds beta-tubulin, prevents microtubule depolymerization, arrests mitosis, and promotes apoptosis. Used in breast, prostate, lung, gastric, and head-and-neck cancers.

Note · Fluid retention is the signature toxicity; direct renal toxicity is low and the agent is non-renally cleared.

§04

Clinical depth

Renal dose adjustment

Hepatically (CYP3A4) metabolized and biliary excreted - no renal dose adjustment; reduce dose (or avoid) with significant hepatic dysfunction/elevated bilirubin and transaminases, which raise toxicity risk.

Dialyzability & ESKD dosing

Highly protein-bound, large volume of distribution, non-renally cleared; not dialyzable. Tolerated in dialysis and transplant patients with standard dosing and supportive care.

Differential diagnosis

Docetaxel fluid-retention syndrome with prerenal physiology vs cardiac/renal volume overload vs nephrotic-range proteinuria (which docetaxel does not cause). Bland urine with low albumin from third-spacing, not heavy proteinuria, points to the taxane.

Monitoring

Weight and clinical edema/effusions each cycle
LFTs/bilirubin before dosing (drives dose adjustment)
CBC for neutropenia; creatinine if volume status changes

Key trials & series

Nagahisa Transplant Proc 2024 case of safe docetaxel use after kidney transplantation

Clinical pearls

Steroid premedication is what keeps docetaxel fluid retention in check - skipping it worsens edema.
Fluid retention reflects capillary permeability, not kidney injury; creatinine usually stays normal.
Docetaxel can be given in transplant/dialysis patients because it is non-renally cleared.
Hemorrhagic cystitis is reported at case level with docetaxel, including monotherapy and oxazaphosphorine-free TCHP where it resolved after a swap to paclitaxel; mechanism unknown.
TTP/HUS-type thrombotic microangiopathy is reported at case level with docetaxel, including monotherapy with onset days after the first cycle.

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

8 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

8 references · 2010–2025 · 2 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 · LimitedNew-onset systemic sclerosis and scleroderma renal crisis under docetaxel.Debien V et al. · J Scleroderma Relat Disord 2021 · PMID 35387214Docetaxel-triggered new-onset systemic sclerosis with a severe kidney flare featuring scleroderma renal crisis and renal thrombotic microangiopathy.CaseC · LimitedTumor lysis syndrome associated with docetaxel and carboplatin in a case with recurrent endometrial cancer.Ito T et al. · Gynecol Oncol Rep 2018 · PMID 29845102Docetaxel/carboplatin chemotherapy precipitated tumor lysis syndrome with acute renal failure (hyperuricemia/hyperphosphatemia/hyperkalemia) in a solid tumor, fatal outcome.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING: TOXIC DEATHS, HEPATOTOXICITY, NEUTROPENIA, HYPERSENSITIVITY REACTIONS, and FLUID RETENTION Treatment-related mortality associated with docetaxel is increased in patients with abnormal liver function, in patients receiving higher doses, and in patients with non-small cell lung carcinoma and a history of prior treatment with platinum-based chemotherapy who receive docetaxel as a single agent at a dose of 100 mg/m 2 [see Warnings and Precautions (5.1) ]. Avoid the use of docetaxel injection in patients with bilirubin > upper limit of normal (ULN), or to patients with AST and/or ALT > 1.5 x ULN concomitant with alkaline phosphatase > 2.5 x ULN. Patients with elevations of bilirubin or abnormalities of transaminase concurrent with alkaline phosphatase are at increased risk for the development of severe neutropenia, febrile neutropenia, infections, severe thrombocytopenia, severe stomatitis, severe skin toxicity, and toxic death. Patients with isolated elevations of transaminase > 1.5 x ULN also had a higher rate of febrile neutropenia. Measure bilirubin, AST or ALT, and alkaline phosphatase prior to each cycle of docetaxel injection [see Warnings and Precautions (5.2) ] . Do not administer docetaxel injection to patients with neutrophil counts of < 1500 cells/mm 3 . Monitor blood counts frequently as neutropenia may be severe and result in infection [see Warnings and…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 67,030 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· 5 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 3.04
Hemorrhagic Cystitiscorroborated · ROR 2.29 — on the terms that name the lesion (ROR 5.85)
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 3.0495% CI 2.58–3.57· 149 reports

Electrolyte Disturbance

ROR 2.7095% CI 2.57–2.84· 1,615 reports

Hemorrhagic Cystitis

ROR 2.2995% CI 2.10–2.50· 503 reports

SIADH / Hyponatremia

ROR 2.1995% CI 2.01–2.38· 558 reports

Glomerular Injury / Proteinuria

ROR 1.6195% CI 1.37–1.89· 149 reports

FAERS outcomes & reporting trend· 13.2% of reports w/ death · 30.5% w/ hospitalization

13.2%

Reported with a death outcome

8,847 of 67,030 reports

30.5%

Reported with hospitalization

20,424 of 67,030 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 67,030 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 1.3495% CI 1.24–1.45· 650 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Skin

Alopecia16,970

Gastrointestinal

Diarrhoea5,243Nausea3,814Vomiting2,777

Blood & lymphatic

Neutropenia3,371Febrile Neutropenia3,074Myelosuppression2,270Anaemia2,235

General / constitutional

Fatigue3,240Pyrexia2,481Pain2,329Asthenia2,017

Psychiatric

Anxiety3,456

Respiratory

Dyspnoea2,377

Metabolic & electrolyte

Decreased Appetite1,776

Nervous system

Neuropathy Peripheral1,681

Immune / infection

Pneumonia1,389

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 Docetaxel 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

Paclitaxel

Taxol · Taxane

Profile

Low direct nephrotoxicity; vehicle reactions.

PRECYSTGLOM

Mild#2 · 76% phenotype match

Capecitabine

Xeloda · Pyrimidine analog (oral 5-FU)

Profile

Diarrhea-driven prerenal AKI; dose-adjust for CrCl.

PRETMA

Mild#3 · 73% phenotype match

5-Fluorouracil

Adrucil · Pyrimidine analog

Profile

Rare TMA, esp. with mitomycin; mostly renally safe.

TMAPRE

Mild#4 · 73% phenotype match

Eribulin

Halaven · Microtubule inhibitor

Profile

Reduced clearance in renal impairment.

PRE

Mild#5 · 68% phenotype match

Ruxolitinib

Jakafi · JAK1/2 inhibitor

Profile

Tumor lysis in myelofibrosis; renally adjusted.

PRELYTETMA

Mild#6 · 63% phenotype match

Compare Docetaxel 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
7Docetaxel· this agentPRE — 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.

Who studies this

The leading contributors to Docetaxel’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 Docetaxel; 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 116 clinical records among all 171 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.