Axitinib

Tyrosine kinase inhibitors

MECHANISM OF ACTION

Second generation TKI blocking VEGF receptor (VEGF receptor TKI)

MECHANISM OF KIDNEY INJURY

AIN (Acute interstitial nephritis), TMA (thrombotic microangiopathy) (systemic/kidney limited). HTN; vascular endothelial growth factor (VEGF) signaling pathway inhibition . Reduction of vasodilator production such as NO and enhance production of vasoconstriction such as endothelin 1

CLINICAL KIDNEY SYNDROME

AKI, Proteinuria/Albuminuria, Nephrotic syndrome, Hematuria, Hypertension, BLE edema, Anasarca.
HTN; variable; up to 81% of patients with all grade HTN and up to36% of patients experienced severe (grade 3) hypertension

CARDIOVASCULAR ADVERSE EFFECTS

Hypertension, CHF, possible increase in MACE

LYTE ABNORMALITIES

Hypoalbuminemia

RISK FACTORS

MITIGATION STRATEGIES

n/a

SUGGESTIONS

Hold offending drug and rechallenge after AKI/proteinuria resolves, Discontinue offending drug, Add ACEi/ARB, Check GN work up (ANA, ANCA, DsDNA, SPEP with FLC, Hep B sero, Hep C sero, HIV, C3, C4, anti-GBM, cryoglobulins), Check TMA work up (send haptoglobin, peripheral smear, LDH), If nephrotic proteinuria or TMA, discontinue.

NOTES/COMMENTS

PHARMACOKINETICS

Molecular Weight

Volume of Distribution

Plasma Protein Binding

Metabolism

Bioavailability

Half-life elimination

Time to peak

Excretion

Dialyzable?

REF:

https://doi.org/10.1053/j.ajkd.2015.02.340
PMID: 29318210

PATHOLOGY SLIDES:

ENTRY UPDATES:

Raad Chowdhury

MN/USA

Sep 25, 2022

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