Bendamustine
Treanda · Alkylator
Tumor lysis-mediated AKI is the principal risk; TMA is rare.
PRETMALYTE
ModerateOpen →
Taxane
Paclitaxel
Taxol · PTX
A taxane that mostly spares the kidney, with reactions tied to its vehicle rather than the tubule.
MildTaxane · approved 1992
Breast cancerOvarian cancerNon-small-cell lung cancer
Signature kidney injury
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
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.
Onset
Infusion reactions occur during or shortly after administration (typically first/second exposure); any prerenal AKI follows the hemodynamic instability.
Reversibility
Reversible
Anticancer mechanism
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.
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.
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
Note · Low direct nephrotoxicity; renal events are vehicle/hypersensitivity- and hemodynamics-driven and reversible.
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.
Where it strikes
Nephron segments
Vasculature / Endothelium
Glomerular & peritubular capillaries
Injury signatures
Prerenal / Hemodynamic AKI
Beyond the kidney
Class-level context for the major non-renal toxicities of taxanes.
Neurologic
Neuropathy, encephalopathy, ICANS, PRES
- Peripheral neuropathy (taxanes, vinca)
Hematologic
Cytopenias, thrombosis, TMA
- Myelosuppression
Immune / Infusion
CRS, infusion reactions, irAEs, anaphylaxis
- Hypersensitivity (taxane vehicles)
Evidence
4 peer-reviewed references. Citation metadata via PubMed / NLM.
LandmarkRe-visiting Hypersensitivity Reactions to Taxanes: A Comprehensive Review.Picard M et al. · Clin Rev Allergy Immunol 2015 · PMID 24740483Comprehensive review of taxane hypersensitivity mechanisms (Cremophor/complement and IgE) and desensitization, the basis of the hemodynamic renal risk.PMIDOnconephrology: Update in Anticancer Drug-Related Nephrotoxicity.García-Carro C et al. · Nephron 2022 · PMID 35717937Reviews relative nephrotoxicity of chemotherapy classes, including the low direct renal toxicity of taxanes.PMIDOnconephrology: The intersections between the kidney and cancer.Rosner MH et al. · CA Cancer J Clin 2020 · PMID 32853404Authoritative review contextualizing chemotherapy-associated renal effects.PMIDOnconephrology.Kala J et al. · Crit Care Clin 2021 · PMID 33752861Context for prerenal and hemodynamic AKI mechanisms during chemotherapy.
Related agents
Other agents sharing the same signature kidney injury.