Association between serum aspartate transaminase and homocysteine levels in hemodialysis patients.

Background: Hyperhomocysteinemia is a common metabolic abnormality in patients undergoing hemodialysis (HD). An impairment of remethylation of homocysteine (Hcy) is seen in these patients but cannot account completely for hyperhomocysteinemia. Homocysteine is derived from transmethylation of methionine that can be metabolized through transamination pathway alternatively. However, the significance of transamination in the metabolism of Hcy in HD patients is not studied.
Methods: A total of 145 patients undergoing HD for more than 3 months were enrolled in the study. Vitamins B were not prescribed routinely to these patients. Among them, 49 patients had positive test results for hepatitis B surface antigen or antihepatitis C virus antibody. Serum Hcy, folic acid, vitamin B12, pyridoxal 5' -phosphate, methionine, and transaminase were measured, and parameters of dialysis adequacy were calculated. Multiple linear regression model was used to analyze the factors determining Hcy levels.
Results: All patients had higher Hcy levels (40.3 +/- 28.3 micromol/L) than the upper limit of reference range 15 micromole/L. The levels of vitamin B(12) were all higher than 160 pg/mL (118 pmol/L). Only 9 patients had serum folic acid lower than 3 ng/mL (6.8 nmol/L). The predialysis Hcy levels were correlated with age, HD duration, folic acid, vitamin B12, and aspartate transaminase (AST) levels among all patients or the subgroup of hepatitis noncarriers with linear multiple regression analysis. In hepatitis carriers, AST levels were not associated with Hcy. A cutoff value of AST less than 14 U/L predicted a predialysis Hcy level higher than 27 micromol/L in noncarriers, with a sensitivity of 83.9% and a specificity of 50.2%.
Conclusion: In addition to vitamin B12 and folic acid, the serum AST levels correlated inversely with predialytic Hcy levels independently in hepatitis noncarrier HD patients. The results suggest that transamination may play an important role in the development of hyperhomocysteinemia when impaired transmethylation is encountered in uremic patients.
(Copyright 2002 by the National Kidney Foundation, Inc.)