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Spontaneous bacterial peritonitis (SBP) may precipitate deterioration of circulatory function with severe hepatic insufficiency, hepatic encephalopathy, and type-1 hepatorenal syndrome (HRS) and has 30% hospital mortality despite infection resolution.1 Predictors of this acute-on-chronic liver failure include ascitic fluid concentrations of granulocytes and cytokines and renal and hepatic insufficiency at diagnosis.1–3 Endotoxemia and the inflammatory response precipitate renal failure (RF) by accentuating splanchnic vasodilatation and impairing cardiac function.3–5 Compensatory activation of the renin-angiotensin and sympathetic nervous systems further decrease renal perfusion. Volume expansion with albumin (1.5 g/kg day one, 1 g/kg day three) significantly reduces the incidence of HRS and hospital mortality.2
In the sole reported trial, only patients with serum bilirubin (bili) >68.4 μmol/l, blood urea nitrogen (BUN) >30 mg/dl or serum creatinine (Cr) >88.4 μmol/l appeared …
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