PARTNERS WITH
Vandetanib
Tyrosine kinase inhibitors
MECHANISM OF ACTION
Vegf receptor TKI
MECHANISM OF KIDNEY INJURY
unclear cause of AKI.
CLINICAL KIDNEY SYNDROME
AKI, Hypertension (mechanism for HTN; inhibitory effect on the VEGF receptor. Possible impaired angiogenesis ,endothelial dysfunction with associated decrease in nitric oxide production).
CARDIOVASCULAR ADVERSE EFFECTS
LYTE ABNORMALITIES
Hypocalcemia, Hypokalemia, Hypercalcemia, Hyponatremia
RISK FACTORS
Prior CKD, or severe bouts of AKI.
Can worsen cisplatin toxicity when combined.
HTN; type of malignancy (more common in patients with Medullary thyroid cancer and NSCLC)
MITIGATION STRATEGIES
unclear
SUGGESTIONS
Hold offending drug and rechallenge after AKI/proteinuria resolves, Check UA with urine culture, Check Cortisol levels.
HTN > standard antihypertensive medication. if HTN is difficult to control then dose reduction or treatment interruption.
NOTES/COMMENTS
PHARMACOKINETICS
Molecular Weight
Volume of Distribution
Plasma Protein Binding
Metabolism
Bioavailability
Half-life elimination
Time to peak
Excretion
Dialyzable?
Unknown
REF:
10.1200/JCO.2011.36.1709
PMID: 29318210, PMID: 22882307
PATHOLOGY SLIDES:
ENTRY UPDATES:
Raad Chowdhury
MS/USA
Sep 25, 2022