AKI Patho Fall 2012 Updated version

Ace inhibitors arbs block compensatory

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ACE-inhibitors & ARBs block compensatory vasoconstriction by blocking production and action of angiotensin II Can cause functional AKI Fig 49-3
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ACE-Inhibitor/ARB Renoprotective Effects Slow the progression of chronic kidney disease Reduce proteinuria May be antifibrotic Effects are independent of antihypertensive activity
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NSAID-Induced AKI NSAIDs inhibit COX-mediated prostaglandin production Decreased PGs decreased afferent arteriolar vasodilation Some patients depend on prostaglandins for maintenance of renal perfusion and GFR CKD Volume depletion Decreased CO
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Case LR comes to the hospital for planned surgery On admission, labs are: BP 140/90; BUN 15; SCr 0.6; GFR 33.7 ml/min LR has major blood loss during surgery After surgery, labs are: BP 100/58; BUN 46; SCr = 1.1; GFR 22.4 ml/min
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Does LR have AKI? 1. No, her SCr is normal (0.5-1.3 mg/dl) 2. Yes, her SCr increased by > 1.5-fold 3. Yes, her GFR decreased by >25% 4. Both 2 and 3
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If LR has been diagnosed with prerenal AKI, does she have kidney damage? 1. Yes 2. No
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Intrinsic AKI Damage to kidneys due to ischemia, toxins or other insults Can be a continuation of prerenal failure Can occur in vasculature, glomeruli, tubules or interstitium Tubular damage accounts for 85% of intrinsic renal failure Is the most common cause of AKI in hospitalized patients
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Intrinsic AKI Acute tubular necrosis (ATN) Accounts for 85% of intrinsic renal failure cases Tubules are particularly susceptible to ischemic injury 2 types Ischemic (50%) Nephrotoxic (35%) Is often reversible Except when severe or prolonged ischemia/injury causes renal cortex necrosis
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Intrinsic AKI Ischemic ATN Is a progression of prerenal failure Develops after hours to days of prerenal ischemia Causes Same as prerenal failure
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Intrinsic AKI Nephrotoxic ATN Renal injury caused by direct tubular damage Aminoglycoside antibiotics Amphotericin B Radiocontrast agents Heavy metals (lead, mercury) Endogenous toxins (hemoglobin, myoglobin)
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Phases of ATN Initiation Phase Ischemic injury or toxin exposure Cell death Dysregulation of fluid and electrolyte balance Decreased urine output, decreased GFR Inflammation Continued ischemia or toxin exposure can Delay recovery Extend the injury Kill tubular epithelial cells
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ATN Mechanism Maintenance phase Begins once toxin or ischemia is removed Weeks to months Recovery phase New cells regenerated Diuresis occurs If injury was severe or prolonged, cell regeneration may not occur
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Postrenal AKI No renal damage Obstruction of: Tubules Bladder Bilateral ureters Upstream pressure leads to decreased GFR Pathophysiology: Concepts of Altered Health States. 7 th Ed.
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Clinical Presentation Many patients are asymptomatic Depends on type of AKI Decreased urine output is common Quantification of urination Normal urine output (1200 ml/day) Nonoliguria (>500 ml urine/day) Oliguria (< 500 ml urine/day) Anuria (< 50 ml urine/day)
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AKI or ATN Signs/symptoms of volume depletion Orthostatic hypotension
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ACE inhibitors ARBs block compensatory vasoconstriction by...

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