Transaminase activities in serum of long-term hemodialysis patients.

Wolf et al. (1) found little or no serum aspartate aminotransferase (EC 2.6.1.1) activity in the sera of 11 of 19 patients undergoing long-term hemodialysis. The authors concluded that low aminotransferase (transaminase) activities seen in these patients may have been due to loss of the enzyme and (or) to pynidoxine depletion during long-term dialysis. We recently examined the sera of 54 long-term hemodialysis (HD) patients for aspartate aminotransferase and alanine aminotransferase (EC 2.6.1.2) activities, and found most of the patients’ activities to be within the normal range of 3 to 15 U. In our study we used both manual colonimetric and manual uv-kinetic methodologies (Sigma)1 and analyzed preand post-dialysis serum samples collected from patients who had been on maintenance dialysis for at least six months. Hemodialysis was regularly performed with parallel-flow Western Gear or Drake-Willock units for an 8-h period three times a week. All patients in our study received 5 mg of pyridoxine per day (“Theragran-M” or its equivalent) as a dietary supplement. Our study group of 54 HD patients demonstrated mean pre-dialysis aspartate and alanine aminotransferase activities of 9 U and 5 U, respectively, with standard deviations of 4 U and 3 U, respectively. These activities were not significantly different from post-dialysis serum aminotransferase activities, suggesting that the dialysis itself had no immediate deleterious effect on either of the two enzymes. We did note, however, that three of our patients had aspartate aminotransferase activities of less than 3 U, while seven patients (including two of the above three) had alanine aminotransferase activities of less than 3 U, indicating long-term dialysis for these patients may have adversely affected enzyme activity or function. The discrepancies in aminotransferase activities reported by Wolf et al. and those found in our study might be explained by differences in methodology (2), by the small sample size selected by Wolf’s group, or by differences in patient pynidoxine status. Depletion of ascorbic acid, pantothenic acid, folic acid, and biotin in plasma of patients undergoing chronic HD has been demonstrated (3,4). For this reason we believe that gradual