It has been suggested that hepatic
urea synthesis, which consumes HCO-3, plays an important role in
acid-base homeostasis. This study measured
urea synthesis rate (Ra
urea) directly to assess its role in determining the
acid-base status in patients with end-stage
cirrhosis and after orthotopic
liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]
urea. Six healthy volunteers served as controls. Ra
urea was 5.05 +/- 0.40 (SE) and 3.11 +/- 0.51 micromol. kg-1. min-1, respectively, in controls and patients with
cirrhosis (P < 0. 05). Arterial base excess was 0.6 +/- 0.3 meq/l in controls and -1.1 +/- 1.3 meq/l in cirrhotic patients (not different). After OLT, Ra
urea was 15.05 +/- 1.73 micromol. kg-1. min-1, which accompanied an arterial base excess of 7.0 +/- 0.3 meq/l (P < 0.001). We conclude that impaired Ra
urea in cirrhotic patients does not produce metabolic
alkalosis. Concurrent postoperative metabolic
alkalosis and increased Ra
urea indicate that the
alkalosis is not caused by impaired Ra
urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic
alkalosis by augmenting Ra
urea, thus increasing HCO-3 consumption and moderating the severity of metabolic
alkalosis produced elsewhere.