Case study of a patient suffering chronic renal failure complicated with liver cirrhosis causing post-hemodialysis hyperammonemia

The case of a 50-year-old male patient suffering from chronic renal failure complicated with liver cirrhosis is presented. Although deterioration of liver function was slight, the patient repeatedly suffered coma as a result of hyperammonemia caused by portacaval shunt. Hemodialysis was performed to remove sources of hepatic coma and uremic toxins. Hyperammonemia continued, however, and the coma symptoms persisted. Furthermore, the ammonium concentration in arterial blood was found to be significantly increased after hemodialysis. This increase was attributed to increased production of ammonia in the gut during excess protein catabolism in response to hemodialysis and protein meals. By using a slightly acidified dialysate and continuous drip infusion of branche-chain amino acids and glutamate during hemodialysis, and conducting hemodialysis in the afternoon, the post-hemodialysis concentration of ammonia in arterial blood was significantly reduced. At the same time, the pre-hemodialysis level of ammonia approached the normal value and coma symptoms disappeared. The use of a slightly acidified dialysate and continuous drip infusion of branched-chain amino acids and glutamate during hemodialysis appears to suppress amino acid catabolism and reduce production of ammonia in the gut. Moreover, conducting hemodialysis in the afternoon when the ammonium concentration is highest, during digestion of protein in meals, seems to be an effective way of removing ammonia.