PARTNERS WITH
Ponatinib
Tyrosine kinase inhibitors
MECHANISM OF ACTION
Cellular TKI inhibiting BCR-ABL and VEFGR
MECHANISM OF KIDNEY INJURY
TMA (thrombotic microangiopathy) (systemic/kidney limited), Glomerular injury possibly via VWF-mediated platelet adhesion and a secondary microvascular angiopathy
CLINICAL KIDNEY SYNDROME
AKI, Proteinuria/Albuminuria, and hypertension which is possibly related to ponatinib kinase activity against vascular endothelial growth factor receptor-2
CARDIOVASCULAR ADVERSE EFFECTS
LYTE ABNORMALITIES
n/a
RISK FACTORS
n/a
MITIGATION STRATEGIES
n/a
SUGGESTIONS
Hold offending drug and rechallenge after AKI/proteinuria resolves, Discontinue offending drug
NOTES/COMMENTS
PHARMACOKINETICS
Molecular Weight
Volume of Distribution
Plasma Protein Binding
Metabolism
Bioavailability
Half-life elimination
Time to peak
Excretion
Dialyzable?
Unknown
REF:
https://www.lumc.nl/sub/4010/att/1683422/1896506
https://pubmed.ncbi.nlm.nih.gov/29318210/
https://pubmed.ncbi.nlm.nih.gov/30692122/
PATHOLOGY SLIDES:
ENTRY UPDATES:
Raad Chowdhury
MN/USA
Sep 25, 2022