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MORNING REPORT
Patrick Sandiford, 2/10/2014
COCAINE
• Cocaine (benzoyl methylecgonine) is available in two forms: cocaine
hydrochloride and alkaloid cocaine (freebase/crack)
• Plasma half life is 45-90 minutes
• Low renal clearance, elimination predominantly controlled by
biotransformation through plasma and liver cholinesterases. These produce
benzoyl and ethyl methylecgonine which are water-soluble metabolites
excreted in urine.
• Common major toxic effects: MI, CVA, mesenteric ischemia, placental
infarcts
RENAL INFARCTION
• Common risk factors for renal infarction include valvular heart disease,
atheroembolic events, hypercoagulopathy, systemic vasculitis, blunt trauma,
collagen vascular disorders, endocarditis.
• Pathophysiology of Renal Infarction:
• Affect on vascular reactivity and renal hemodynamics
• Inability to inhibit update of catecholamines into synapse
• Inhibition of re-uptake of NE in sympathetically innervated tissues and
subsequent release of NE and Epi from adrenal medulla.
• Prothrombotic
• Most cases of renal infarction involve right kidney (longer artery, more prone to
ischemia)
• Although no definitive model yet
RENAL INFARCTION
• Diagnosis of exclusion, many remain idiopathic
• No clear management – vasospasm vs. thrombosis or both
• Most proceed with conservative approach
REFERENCES
• S. BEMANIAN ET. AL, COCAINE-INDUCED RENAL INFARCTION: REPORT OF A
CASE AND REVIEW OF THE LITERATURE. BMC NEPHROLOGY 2005, 6:10, 22
SEPTEMBER 2005
• UPTODATE.COM
REFERENCES
• S. BEMANIAN ET. AL, COCAINE-INDUCED RENAL INFARCTION: REPORT OF A
CASE AND REVIEW OF THE LITERATURE. BMC NEPHROLOGY 2005, 6:10, 22
SEPTEMBER 2005
• UPTODATE.COM

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Renal infarction morning report 2-10-2014

  • 2. COCAINE • Cocaine (benzoyl methylecgonine) is available in two forms: cocaine hydrochloride and alkaloid cocaine (freebase/crack) • Plasma half life is 45-90 minutes • Low renal clearance, elimination predominantly controlled by biotransformation through plasma and liver cholinesterases. These produce benzoyl and ethyl methylecgonine which are water-soluble metabolites excreted in urine. • Common major toxic effects: MI, CVA, mesenteric ischemia, placental infarcts
  • 3. RENAL INFARCTION • Common risk factors for renal infarction include valvular heart disease, atheroembolic events, hypercoagulopathy, systemic vasculitis, blunt trauma, collagen vascular disorders, endocarditis. • Pathophysiology of Renal Infarction: • Affect on vascular reactivity and renal hemodynamics • Inability to inhibit update of catecholamines into synapse • Inhibition of re-uptake of NE in sympathetically innervated tissues and subsequent release of NE and Epi from adrenal medulla. • Prothrombotic • Most cases of renal infarction involve right kidney (longer artery, more prone to ischemia) • Although no definitive model yet
  • 4. RENAL INFARCTION • Diagnosis of exclusion, many remain idiopathic • No clear management – vasospasm vs. thrombosis or both • Most proceed with conservative approach
  • 5. REFERENCES • S. BEMANIAN ET. AL, COCAINE-INDUCED RENAL INFARCTION: REPORT OF A CASE AND REVIEW OF THE LITERATURE. BMC NEPHROLOGY 2005, 6:10, 22 SEPTEMBER 2005 • UPTODATE.COM
  • 6. REFERENCES • S. BEMANIAN ET. AL, COCAINE-INDUCED RENAL INFARCTION: REPORT OF A CASE AND REVIEW OF THE LITERATURE. BMC NEPHROLOGY 2005, 6:10, 22 SEPTEMBER 2005 • UPTODATE.COM