Vitamin B6 status in uremia.

We have studied vitamin B6 status in 26 uremic patients, 18 on maintenance hemodialysis and 8 nonhemodialyzed. The vitamin B6 status was estimated by an assay of erythrocyte aspartate aminotransferase and coenzyme stimulation. Hemodialyzed uremic patients were found to have vitamin B6 deficiency. Patients were treated with 150 mg pyridoxine hydrochloride daily for 4 weeks. Erythrocyte aspartate aminotransferase increased significantly in both groups of uremic patients, the increase being greater in hemodialyzed patients. In vitro pyridoxal phosphate stimulation produces an erythrocyte aspartate aminotransferase activity greater than that obtained before pyridoxine hydrochloride administration. After cessation of pyridoxine hydrochloride treatment, erythrocyte aspartate aminotransferase decreases in hemodialyzed patients, while it remains elevated in nonhemodialyzed patients. The data obtained appear to indicate that vitamin B6 administration to patients with chronic renal insufficiency must be appraised not only for correcting the deficit but also for increasing the intracellular pyridoxal phosphate concentration, which could modify the possible functional impairment at the level of apoenzymes that use pyridoxal phosphate.