Plasma and Hemodynamic Markers During Hepatectomy

Introduction Liver resection is considered the only curative treatment option for mCRC patients without extrahepatic disease and is accepted practice. Despite substantial improvements in surgical techniques, postoperative morbidity and mortality remain an important concern after major resections. Complications of liver resection, although rare, include liver failure and acute kidney injury as indicated by oliguria and increased serum creatinine. The underlying pathophysiological pathways of post-operative renal alteration following liver resection is an increase in portal venous pressure, based on observations in animal models or small cohorts. The corpus of data is derived from patients with liver cirrhosis and subsequent hepatorenal syndrome. These data are limited since cirrhosis cannot distinguish between metabolic changes, portal hypertension and impaired liver function in the elucidation of the pathogenesis of renal alterations. Liver resection is therefore a potent model to evaluate the impact of portal hypertension on the kidney despite stable liver function. The most significant factor determining morbidity and mortality following hepatectomy is the ability of the remnant liver to regenerate. In this context, several growth factors were shown to regulate the highly orchestrated process of liver regeneration (LR). Hypothesis The investigators will therefore test the hypothesis that liver resection leads to a sustained increase of portalvenous pressure with a subsequent episode of oliguric renal impairment, correlating with the quantity of resected liver. Furthermore, the investigators will examine the relationship between postoperative liver regeneration and circulating growth factor levels in patients undergoing hepatectomy. Based on the preclinical data the investigators hypothesize that a circulating growth factor levels will be associated with delayed liver regeneration, an increased incidence of postoperative liver dysfunction and concomitant worse c