Effects of vitamin E ingestion on plasma and urinary risk factors for calcium oxalate urolithiasis in two population groups having different stone-risk profiles: evidence of different physiological handling mechanisms

Abstract

It has been demonstrated that vitamin E supplementation reduces calciuria and oxaluria and that it may also prevent oxalate-mediated peroxidative injury, all of which reduce the risk of calcium oxalate urolithiasis. In view of the significant difference in stone occurrence in black (B) and white (W) South Africans, we undertook to investigate the effects of vitamin E supplementation in subjects from these two groups. Five healthy males from each group ingested one capsule (400 IU) of vitamin E daily for 60 days. Blood and 24 h urine samples were collected at baseline and on day 60; 24 h dietary questionnaires were simultaneously completed. Urine composition was determined by routine analyses. Urinary and plasma TBARS were determined using a commercially available assay kit while plasma vitamin E was determined by reverse phase HPLC. Plasma vitamin E increased significantly in W but not in B. Urinary and plasma TBARS did not increase in either group. Urinary citrate increased significantly in both groups but the percentage increase in W (169%) was greater than that in B (82%). No other urinary parameter changed significantly. The increase in plasma vitamin E in W but not in B suggests either that the mechanism by which it is packaged into chylomicrons, which are secreted into the systemic circulation, is suppressed in the latter group or that it is differentially absorbed in the two groups. Similarly, to explain the greater increase in citraturia in W compared to B, we speculate that inhibition of lipogenesis of arachidonic acid by vitamin E, ultimately leading to an increase in citraturia, occurs to a lesser extent in B than in W.

Hyperoxaluria Induces Oxidative DNA Damage and Results in Renal Tubular Epithelial Cell Apoptosis: A Clue to the Pathogenesis of Urolithiasis

“…The use of antioxidants was successful in preventing crystal induced tubular cell injury in some studies [20]. The systemic use of antioxidants in humans, on the other hand, did not have enough satisfying results in preventing the development of renal stone disease [34,35].…”

Protective effects of boron and vitamin E on ethylene glycol-induced renal crystal calcium deposition in rat

“…Flavonoids compounds with lowering urinary citrate and increasing oxalate contribute to the prevention of calcium oxalate stones formation, and it is partly relevant to anti-infl ammatory and antioxidant eff ects of fl avonoids (Ahmed et al 2013). Daily intake of 400 IU VitE for 60 days increased urinary citrate with increasing plasma levels of alpha-tocopherol, which is a key factor in the prevention of kidney stones (Th eka et al 2012). Interaction between the renal tubular epithelial cells and crystals in the urine (Khan 2011) and renal tubular epithelial integrity by secreting various factors such as Osteopontin (OPN) and citrate play a key role in the formation of kidney stones (De Yoreo et al 2006).…”