A metabolic relationship between the liver and kidney exists in conbination with the urea cycle. We found different concentrations of serum guandino compounds between patients with acute renal failure and those with acute hepatic failure. We made an experimental model of acute hepatic failure in rats by injecting 1,000 mg/kg of D-galctosamine i. p. and evaluated the metabolic changes in the liver and kidney by measuring guandino compound levels using high performance liquid chromatography. We concluded that when the urea cycle was disturbed, the metabolism in the kidney was activated, and the synthesis of GAA (guandino acetic acid) was accelerated for the purpose of excreting ammonium. Also, we thought it possible to evaluate the metabolic compensative ability of the kidney by determining (serum Arginine)/(serum GAA). In the liver and kidney of rats, we found high levels of GBA (guanidino butyric acid), the metabolic pathway of which is unknown. With the progress of liver damage, the release of GBA into the serum was observed.