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Clin Nephrol. 1995 Jun;43(6):405-8.

The pathogenesis of decreased aspartate aminotransferase and alanine aminotransferase activity in the plasma of hemodialysis patients: the role of vitamin B6 deficiency.

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Ono Clinic, Fukuoka, Japan.


The mechanisms responsible for the low plasma (p) AST and ALT activity in HD patients remain elusive. This prospective study was undertaken to clarify the relationship of AST, ALT and pyridoxal-5'-phosphate (PLP) levels (active form of vitamin B6) in these patients. A group of 52 HD patients were given oral pyridoxine HCl (30 mg daily), for 5 weeks. Prior to supplementation (Day 0), 17 (33%) patients had deficient pPLP levels (Group 1), the remainder (35 patients) had normal pPLP values (Group 2). A positive correlation was noted between pPLP and pAST (r = 0.57, p < 0.01) or pALT (r = 0.68, p < 0.01). The mean pAST (9.2 +/- 0.3 vs 13.4 +/- 0.7 U/l) and pALT (8.6 +/- 0.6 vs 11.4 +/- 0.9 U/l) were markedly lower in Group 1 than those in Group 2, respectively. These low AST and ALT levels increased to those seen in Group 2 where no change from basal values was seen despite vitamin B6 supplementation (Day 35). The administration of vitamin B6 resulted in a significant increase in pPLP in both groups (Day 35) but pPLP dropped to subnormal levels in 5 patients in Group 1 and 7 in Group 2 three months after supplementation was stopped (Day 125). The mean AST and ALT of these 12 pPLP deficient patients became lower than those of the remaining 40 patients with normal pPLP values (p < 0.05). In conclusion, low pAST and pALT levels in HD patients are in part due to a deficiency of pPLP which serves as a coenzyme for these transaminases.

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