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Atezolizumab

Immune check point inhibitors (ICPIs)

MECHANISM OF ACTION

Tumor cells evade immunosurveillance by activating immune checkpoint pathways that suppress antitumor immune responses; ICPis release the brakes on the immune system, promoting antitumor immune responses by interrupting co-inhibitory signaling pathways and promoting immune-mediated elimination of tumor cells.

MECHANISM OF KIDNEY INJURY

AIN (Acute interstitial nephritis), ATN (Acute tubular necrosis), Water/electrolyte disturbances, Glomerular injury, Tubular injury, Podocyte Injury, Chronic interstitial Nephritis

CLINICAL KIDNEY SYNDROME

AKI, Proteinuria/Albuminuria, Nephrotic syndrome, Rhabdomyolysis

CARDIOVASCULAR ADVERSE EFFECTS

Myocarditis

LYTE ABNORMALITIES

Metabolic acidosis (HAGMA, NAGMA), Hypoalbuminemia, Nephrotic range protenuria, Hyponatremia, Hypokalemia, Hypophosphatemia

RISK FACTORS

PPI use, combination therapy, lower baseline eGFR, history of extrarenal irAEs

MITIGATION STRATEGIES

Early steroid use, stopping PPIs

SUGGESTIONS 

Hold offending drug and rechallenge after AKI/proteinuria resolves, Discontinue offending drug, Treat with steroids taper

NOTES/COMMENTS

None

PHARMACOKINETICS

Molecular Weight

145 kDa

Volume of Distribution

6.9 L

Plasma Protein Binding

Metabolism

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

Bioavailability

---

Half-life elimination

27 days

Time to peak

---

Excretion

No formal studies

Dialyzable?

No

REF:

Gupta JITC 2021, Seethapathy CJASN 2020, Cortazar JASN 2020

PATHOLOGY SLIDES:

ENTRY UPDATES:

Shruti Gupta

United States

Sep 25, 2022

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