2011 society of thoracic surgeons
主講人 : R2 顏介立

Introduction
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Acute kidney injury (AKI) occurs in 40% patients after cardiac surgery, 1% requires dialysis
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- Poor outcome and high cost in AKI patient
AKI: consequence of interplay of different pathophysiologic mechanism
Several biomarkers for acute kidney injury
Protective therapy for AKI

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Incidence of post-op AKI:
1%-30% of patient after cardiac surgery
Incidence of hemodialysis:
1%-6% of patient
Different type of cardiac operation:
@ CABG: lowest incidence 2%-5%
@ valvular disease or combied disease: 30%
Different AKI definition
=>new classification critieria

@ Post-op AKI: progressive course with different phase
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Vasomotor change : alteration in vaso-reactivity and renal perfusion
Prerenal azotemia, ATP depletion, oxidative injury
=> bone marrow/ endothelium: proinflammatory state
Inflammatory cells adhere peritubular capillaries=> proximal tubule
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Proliferation of tubule cells=> function reconstitution
 post-operative AKI is acute tubular necrosis

Pathogenesis
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AKI is the consequence of different mechanisms inerplay
Major cause:
1. CPB (cardiopulmonary bypass)
2. patient-related factor( risk factor)

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Pathogenesis
Cardiopulmonary bypass (CPB)
Kidney blood circulation ischemia-reperfusion injury, low cardiac ouput hemodilution, loss of pulsatile flow
Hypothermia
CPB induced systemic inflammation
CPB related emoblization

Risk Factor
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many factor associated with AKI pre-op renal function : baseline creatinine 2-4 =>10-20% hemodialysis baseline creatinine > 4 =>30% hemodialysis pre-op anemia
DM
Intravenous contrast and ACEi
Identified risk factor associated with AKI is important

Biomarkers for AKI
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Problem of conventional renal biomarker
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1. become abnormal too late (urea, creatinine)
2. lack specificity (urine ouput)
New biomarker of AKI ex. cystatin C, NGAL(neutrophil gelatinase associated lipocalin), IL-6, IL-18, KIM-1( kidney injury molecule-1)
, LFABP, NAG…….

Biomarkers for AKI
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Neutrophil gelatinase-associated lipocalin(NGAL)
@Measure tubular stress, increase after tubular injury
@precedes creatinine more than 24hrs!!
Liver type FABP
@ cell uptake fatty acid and promote metabolism
@ increase within 4hr after surgery, accuracy of 81% of AKI development
- KIM-1( kidney injury molecular-1)
@ predict AKI immediately after surgery=>than NGAL
@ more specific to ischemic injury than NGAL

Strategies to prevent AKI
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Difficulty of AKI prevention: complex AKI pathophysiology
Intravenous contrast
vasoconstriction-mediated medullary ischemia and direct cytotoxicity on glomerular cells
delay cardiac surgery beyond 24hrs of exposure to contrast

Strategies to prevent AKI
2. Drugs increasing blood flow a. dopamine: no protective effect and even exacerbate renal tubular injury b. Fenoldopam: increase renal blood flow in dose-dependent manner

Strategies to prevent AKI c. Atrial and brain natriuretic peptide increase GFR and inhibit sodium reabsorption
=> decrease renal dysfunction d. Agent attenuating systemic inflammaatory
-Statins attenuate inflammation and oxidative stress
- Nacetylcysteine, dexamethasone,…..
etc. (anti-inflammation agent)

Strategies to prevent AKI

Strategies to prevent AKI e. CPB use
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The most relevant pathophysiologic mechanism nonpulsatile flow
@ pulsatile perfusion =>improved renal protection
Presta and colleagues research (2009)
Poor oxygen availability to renal medulla when
CPB
@ Hct<26% , oxygen delivery less than
272ml/kg/min
(Ranucci and collegue, 2005)
@pump flow > 3.0L /min/m2
(von Heymann, 2006)

Strategies to prevent AKI
e. CPB use off-pump coronary bypass graft technique
@ controversial renal effect

Cost and Outcomes
post-op AKI has shown to be related to poor prognosis
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Relationship between In-hospital mortality and post-op GFR
(Thakear and colleagues, 2005)
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Less than 30% decline GFR
 Mortality 0.4%
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More than 30% decline
 Mortality 5.9%
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Hemodialysis
=> Mortality 54%

Cost and Outcomes
- AKI contributes to long- term mortality
@10years survival rate with RIFLE criteria
(Hobson and colleague 2009)
Risk: 51% Injury: 42% failure: 26%

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Cost and Outcomes
Duration of AKI with long-term survival
@long term mortality is proportional to AKI duration
@importance of continuous monitoring of renal function

Cost and Outcomes
post-op AKI mortality
Plausible mechanism :
. Fluid overloading, dialysis catheter insertion , impaired host immunity and infection
@ post-op infection:
(Thaker and colleague 2003)
1.6% without AKI, 23.7% with AKI, 58.5 % with hemodialysis

Cost and Outcomes
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Hospital cost and length of stay increase as AKI severity worsen
@ post- op AKI: higher intensive care unit cost(1.7-fold) pharmacy cost(2.3-fold) laboratory cost (1.6-fold)

Conclusion
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Acute kidney injury after cardiac surgery
increase mortality and morbidity. Longer hospitalization and increase cost
-consequence of interplay of different mechanism
- patients who are at high risk
- novel renal biomarker
- protective strategies

Thank you for your attention !!