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Bevacizumab

VEGF receptor monoclonal antibody

MECHANISM OF ACTION

recombinant, humanized monoclonal antibody that inhibits VEGF preventing microvascular growth.

MECHANISM OF KIDNEY INJURY

TMA (thrombotic microangiopathy) (systemic/kidney limited), Glomerular injury, cryoglobulinemic MPGN, collapsing FSGS

CLINICAL KIDNEY SYNDROME

AKI, Pseudo AKI (false elevation in Cr), Proteinuria/Albuminuria, Nephrotic syndrome, Hypertension, rash, impaired wound healing

CARDIOVASCULAR ADVERSE EFFECTS

HTN worsending, edema , VTE/arterial thrombus , Left ventricular dysfunction, syncope, myocardial rupture, arterial aneurysm, and coronary artery dissection

LYTE ABNORMALITIES

Hypoalbuminemia

RISK FACTORS

MITIGATION STRATEGIES

Hold for proteinuria >2g/day and permanent discontinuation if nephrotic range. Although significance of proteinuria still somewhat unclear.

SUGGESTIONS 

Hold offending drug and re-challenge after AKI/proteinuria resolves, Discontinue offending drug, Check UA with urine culture, Check urine analysis for crystals, WBC, RBC, etc, Check urine protein creatinine ratio, Check TMA work up (send haptoglobin, peripheral smear, LDH)

NOTES/COMMENTS

eGFR < 60 ml/min; no dose adjustment

PHARMACOKINETICS

Molecular Weight

149 kDa

Volume of Distribution

2.7-3.2L

Plasma Protein Binding

Metabolism

No formal studies; but likely catabolism to small peptides and amino acids via protein degradation

Bioavailability

---

Half-life elimination

20 days (range, 11 to 50 days)

Time to peak

---

Excretion

No formal studies

Dialyzable?

No. Use with caution in ESRD patients

REF:

PATHOLOGY SLIDES:

ENTRY UPDATES:

Raad Chowdhury

United States

Sep 25, 2022

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