Sunitinib

Tyrosine kinase inhibitors

MECHANISM OF ACTION

VEGF receptor TKI

MECHANISM OF KIDNEY INJURY

AIN (Acute interstitial nephritis), TMA (thrombotic microangiopathy) (systemic/kidney limited)

CLINICAL KIDNEY SYNDROME

AKI, Proteinuria/Albuminuria, Nephrotic syndrome, Hypertension
extra-renal; rash, impaired wound healing

CARDIOVASCULAR ADVERSE EFFECTS

LYTE ABNORMALITIES

Hypoalbuminemia, Hypophosphatemia, Hypocalcemia

RISK FACTORS

MITIGATION STRATEGIES

n/a

SUGGESTIONS

Hold offending drug and rechallenge after AKI/proteinuria resolves, Discontinue offending drug, Add ACEi/ARB, Check TMA work up (send haptoglobin, peripheral smear, LDH)

NOTES/COMMENTS

Sunitinib: 95%; SU12662: 90%

PHARMACOKINETICS

Molecular Weight

398.474 g/mol

Volume of Distribution

2.2 L

Plasma Protein Binding

95%

Metabolism

Hepatic; primarily metabolized by CYP3A4 to the primary active metabolite, SU12662.

Bioavailability

100%

Half-life elimination

Sunitinib: 40 to 60 hours; SU12662: 80 to 110 hours

Time to peak

6 to 12 hours

Excretion

Feces (~61%); urine (16%)

Dialyzable?

REF:

PMID: 18752081
PMID: 23580811
PMID: 18752081
PMID: 29318210

PATHOLOGY SLIDES:

ENTRY UPDATES:

Raad Chowdhury

MN/United States

Sep 25, 2022

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