Critical care conference Acute Kidney Injury: A Relevant Complication After Cardiac Surgery 2011 society of thoracic surgeons 主講人 : R2 顏介立

Introduction - Acute kidney injury (AKI) occurs in 40% patients after cardiac surgery, 1% requires dialysis - 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

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

Classification of AKI criteria

Post-op AKI: progressive course with different phase - 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 - Proliferation of tubule cells=> function reconstitution  post-operative AKI is acute tubular necrosis

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

Pathogenesis - Cardiopulmonary bypass (CPB) - Kidney blood circulation 1. ischemia-reperfusion injury, low cardiac ouput hemodilution, loss of pulsatile flow 2. Hypothermia 3. CPB induced systemic inflammation 4. CPB related emoblization

Risk Factor - 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

Pathogenesis

Biomarkers for AKI - Problem of conventional renal biomarker 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), L-FABP, NAG…….

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

Strategies to prevent AKI - Difficulty of AKI prevention: complex AKI pathophysiology 1. 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 - N-acetylcysteine, dexamethasone,….. etc. (anti-inflammation agent)

Strategies to prevent AKI

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

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

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

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

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

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

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

Conclusion - 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 !! Any question????