Vitamin B6 (VB6) 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

Objective: Vitamin B6 (VB6) 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 VB6 (effect of PLP; effect of PLP was in indirect relationship with the concentration of erythrocyte VB6), 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 VB6 and OA in CKD stage 3-4 patients; and (3) to evaluate the influence of
erythropoietin treatment on erythrocyte VB6 (effect of PLP) in hemodialysis (HD) patients, and the influence of continuous ambulatory peritoneal dialysis (CAPD) therapy on plasma VB6 and OA and their peritoneal clearance and transfer.

Design and Setting: This study was conducted at the Nephrological Clinic of L. Pasteur Faculty Hospital and of Medical School of P. J. Sˇ afarik 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.

Results: After a marathon run, plasma and erythrocyte VB6 significantly decreased and plasma OA increased.
Plasma (15.5 6 3.8 nmol/L) and erythrocyte VB6 (effect of PLP: 42.1% 6 7.5%) were decreased and plasma OA (9.8 6 2.3 mmol/L) was significantly elevated in patients with CGNS and stage 1 CKD. In patients with AIP, deficiency of plasma (24.3 6 5.2 nmol/L) and erythrocyte VB6 (effect of PLP: 46.2% 6 7.0%) and hyperoxalemia (9.39 6 2.5 mmol/L) were present. The urinary excretion of VB6 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 VB6 deficiency.

This finding is an indirect evidence that erythrocyte VB6 is consumed by the hemoglobin synthesis much more during EPO treatment. In CAPD patients, plasma value of VB6 (127.3 6 66.9 mmol/L) was in the normal range and plasma OA (23.6 6 7.4 mmol/L) was significantly elevated. Mean value of peritoneal clearance of VB6 was 8.8% and of OA was 76.9% of urea clearance.

Conclusion: Our study indicates that deficiency of VB6 led to hyperoxalemia and hyperoxaluria in patients with CKD. Deficiency of VB6 in CKD stage 4-5 patients potentiates the uremic hyperoxalemia and hyperoxaluria.

Source - 2010 by the National Kidney Foundation, Inc. All rights reserved.

VITAMIN B6 (VB6) 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),
which serves as a coenzyme for more than 100 enzymes. PLP influences protein and lipid metabolism, metabolism of several amino acids, and formation of antibodies.1–3 Moreover, VB6 catalyzes
transformation of glyoxalate to glycine, which is the salvage metabolic way to prevent oxalate
formation. 4 Causes of VB6 deficiency in chronic kidney disease (CKD) are depicted in Table 1.
5 Clinical symptoms of VB6 deficiency are not marked in patients with CKD or in hemodialysis
(HD) and continuous ambulatory peritoneal dialysis (CAPD) patients. The symptoms are similar to
those of the uremic syndrome.

*IVth Internal Clinic, Hospital of L. Pasteur, Medical School of P. J. Sˇafarik University, Kosˇice, Slovak Republic.
†Institute of Experimental Medicine, Medical School of P. J.S ˇafarik University, Kosˇice, Slovak Republic.
The authors have no known conflicts of interest.

Address reprint requests to Miroslav Mydlı´k, MD, DSc, IVth
Internal Clinic, Hospital of L. Pasteur, Rastislavova 43, 041 90
Kosˇice, Slovak Republic. E-mail: k.derzsiova@fnlp.sk
2010 by the National Kidney Foundation, Inc.
All rights reserved.
1051-2276/$36.00
doi:10.1053/j.jrn.2010.06.009