Chemotherapeutic Agents Flashcards
Chemotherapeutic agents that cause AKI:
Cisplatin and carbopplatin- proximal tubular cell necrosis and apoptosis
Ifosfamide- hemorrhagic cystitis and tubular toxicity
Bevacizumab- antiangiogenesis agent
Mitomycin c and gemcitabine- antineoplastic agents
mechanism of AKI in cisplatin and carboplatin:
are accumulated by proximal tubular cells and cause necrosis and apoptosis.
Ifosfomide nephrotoxicity manifests as:
Type II renal tubular acidosis (Fanconi’s Syndrome)
mechanism of AKI in Ifosfamide:
may cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi’s syndrome), polyuria,
hypokalemia, and a modest decline in GFR
mechanism of AKI in Ifosfamide:
may cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi’s syndrome), polyuria,
hypokalemia, and a modest decline in GFR
mechanism of AKI in Ifosfamide:
may cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi’s syndrome), polyuria,
hypokalemia, and a modest decline in GFR
mechanism of AKI in Ifosfamide:
may cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi’s syndrome), polyuria,
hypokalemia, and a modest decline in GFR