Vitamin B6 deficiency in uremia and its implications for the depression of immune responses

Abstract

By serial determinations of the glutamic oxaloacetic transaminase (GOT) activity of erythrocytes, a marked biochemical vitamin B6 deficiency was found in 48 out of 69 patients with advanced chronic azotemia (serum creatinine > 4 mg/100 ml); 37 on chronic intermittent dialysis and 32 being treated conservatively. As an index for vitamin B6 status, the stimulation effect of pyridoxal 5' phosphate on the erythrocyte EGOT activity (activation coefficient, α(EGOT)) was used, with values ≥ 1.7 indicating a biochemical vitamin B6 deficiency. Increased activation coefficients were restored to normal by the oral administration of 300 mg of vitamin B6 (pyridoxine HCl) daily for 2 wk. From measurements of the GOT activity of nondeficient erythrocytes after incubation with plasma of uremic patients, any inhibitory effect of plasma constituents in uremia on the enzyme activity can be excluded. Hemodialysis improved elevated EGOT ratios significantly. On the basis of these findings it is suggested that inhibition of pyridoxal kinase activity rather than insufficient vitamin B6 supply is the most likely explanation for the depletion of vitamin B6 coenzyme in uremia. Diminution of reactivity in mixed lymphocyte cultures of uremics could be reversed by treating the patients with vitamin B6 orally. It is concluded that suppression of cell mediated immunity in uremia is probably due in part to vitamin B6 depletion.