Vitamin B 6 and Oxalic Acid in Clinical Nephrology

Abstract

Vitamin B(6) (VB(6)) is a water-soluble vitamin, which is important for the normal functioning of multiple organ systems. It is metabolized to the active molecule pyridoxal-5-phosphate (PLP). Oxalic acid (OA) is thought to be a uremic toxin that participates in the pathogenesis of the uremic syndrome. The objectives of this study were as follows: (1) to evaluate the plasma and erythrocyte VB(6) (effect of PLP; effect of PLP was in indirect relationship with the concentration of erythrocyte VB(6)), and plasma and urinary OA in marathon runners, in patients with acute intermittent porphyria (AIP) and variegate porphyria, and in patients with stage 1 chronic kidney disease (CKD), chronic glomerulonephritis and nephrotic syndrome (CGNS); (2) to examine the influence of water diuresis in healthy subjects, and the influence of sodium diuresis (high sodium intake) and an intravenous administration of furosemide on the urinary excretion of VB(6) and OA in CKD stage 3-4 patients; and (3) to evaluate the influence of erythropoietin treatment on erythrocyte VB(6) (effect of PLP) in hemodialysis (HD) patients, and the influence of continuous ambulatory peritoneal dialysis (CAPD) therapy on plasma VB(6) and OA and their peritoneal clearance and transfer. This study was conducted at the Nephrological Clinic of L. Pasteur Faculty Hospital and of Medical School of P. J. Safarik University. A combination of 29 marathon runners, 15 patients with CG and NS, 11 patients with AIP, 1 patient with variegate porphyria, 15 healthy subjects, 27 CKD stage 3-4 patients, 30 HD, and 27 CAPD patients were used in the study. After a marathon run, plasma and erythrocyte VB(6) significantly decreased and plasma OA increased. Plasma (15.5 +/- 3.8 nmol/L) and erythrocyte VB(6) (effect of PLP: 42.1% +/- 7.5%) were decreased and plasma OA (9.8 +/- 2.3 micromol/L) was significantly elevated in patients with CGNS and stage 1 CKD. In patients with AIP, deficiency of plasma (24.3 +/- 5.2 nmol/L) and erythrocyte VB(6) (effect of PLP: 46.2% +/- 7.0%) and hyperoxalemia (9.39 +/- 2.5 micromol/L) were present. The urinary excretion of VB(6) and of OA during maximal water diuresis and after intravenous administration of furosemide increased significantly (P < .01), but was not affected by the high intake of NaCl (P > .05). Erythropoietin treatment in HD patients led to the erythrocyte VB(6) deficiency. This finding is an indirect evidence that erythrocyte VB(6) is consumed by the hemoglobin synthesis much more during EPO treatment. In CAPD patients, plasma value of VB(6) (127.3 +/- 66.9 micromol/L) was in the normal range and plasma OA (23.6 +/- 7.4 micromol/L) was significantly elevated. Mean value of peritoneal clearance of VB(6) was 8.8% and of OA was 76.9% of urea clearance. Our study indicates that deficiency of VB(6) led to hyperoxalemia and hyperoxaluria in patients with CKD. Deficiency of VB(6) in CKD stage 4-5 patients potentiates the uremic hyperoxalemia and hyperoxaluria.