AKI Patho Fall 2012 Updated version

Diarrhea dehydration drugs heart failure infection

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diarrhea, dehydration Drugs Heart failure Infection Trauma Rhabdomyolysis For all people Age > 65 CKD
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Common Risk Factors Hospital-Acquired AKI Volume depletion Hypotension Low cardiac output Nephrotoxic drugs Radiocontrast Dyes ICU-Acquired AKI Same as hospital-acquired AKI, plus: Sepsis/septic shock Major surgery Multiorgan failure
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Etiology (See Figure 51-1) AKI Prerenal AKI Intrinsic AKI Postrenal AKI -Volume depletion -Decreased effective circulatory blood volume --Bladder outlet obstruction -Ureteral obstruction -Renal pelvis/tubular obstruction -Vascular damage -Glomerular damage -Acute tubular necrosis -Acute interstitial nephritis
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Case: Evaluate the following labs A 58 y/o male (5’10”, 73kg) is admitted to the intensive care unit after an acute MI. PMH: diabetes, hyperlipidemia, CKD On Admission The next day BUN (mg/dl) 16 65 SCr (mg/dl) 1.1 2.2 CrCl (ml/min) 76 38 Urine output 70-80 ml/h 30 ml/h x 4 hours
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Does the patient have AKI? 1. Yes 2. No
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Classify the patient’s AKI by RIFLE category 1. Risk 2. Injury 3. Failure 4. Loss 5. ESKD
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Prerenal Failure Prerenal azotemia Hypoperfusion of renal parenchyma No physiologic kidney damage Reversible if cause is corrected before kidney damage occurs Prolonged prerenal failure can lead to kidney injury and ischemic acute tubular necrosis Is the most common cause of AKI in outpatients
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Prerenal Failure Associated with Systemic Hypotension Decreased intravascular volume GI losses Renal losses Dehydration Hemorrhage Skin losses Third-spacing Decreased effective circulating blood volume Hypotension Septic shock Anaphylactic shock Excessive use of antihypertensives Decreased cardiac output Cardiogenic shock Heart failure
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Prerenal Failure Not Associated With Systemic Hypotension Bilateral renal artery occlusion/stenosis Unilateral renal artery occlusion/stenosis in a single kidney Cholesterol or thrombotic emboli
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Compensation Normal GFR can be maintained in patients with mild prerenal failure via: Stimulation of sympathetic nervous system and renin angiontensin-aldosterone syndrome ADH release Vasoconstriction Thirst stimulation Afferent arteriolar dilation (NO, PGs, kallikrein, kinins) Efferent arteriolar constriction (angiotensin II)
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Functional AKI A type of prerenal failure Occurs due to changes in afferent or efferent arteriolar tone in patients at risk for prerenal AKI Caused by specific drug classes that interfere with compensation mechanisms Results in abrupt GFR decrease ACE inhibitors, angiotensin receptor blockers (ARBs) and non-steroidal antiinflammatory drugs (NSAIDs) are most common offenders
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Normal Glomerular Autoregulation In response to decreased renal blood flow, kidneys maintain GFR & urine output via Net afferent arteriole dilation Prostaglandins Efferent arteriole constriction Angiotensin II Figure 49-2
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ACE-Inhibitor/ARB Associated Functional AKI 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
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