It is well established that calcium oxalate stones may be caused by colonic or ileum oxalate (Ox) hyperabsorption (secondary to intestinal dysfunction). Studies have reported that increased intestinal permeability (IP) can cause hyperabsorption of nutrients culminating in passive diffusion of Ox. In South Africa, renal stones occur in the white population (W) but are extremely rare in the black population (B). Previous studies have shown that despite B having a hyperoxalurogenic diet relative to W, urinary Ox in the former is not higher. It has been suggested that different Ox handling mechanisms in the groups are the cause of this disparity. The present study was undertaken to examine whether the IP index, a reliable and accurate measure of intestinal integrity, plays a role in this anomaly. Ten healthy males from each group ingested a dual-sugar isotonic solution containing 5 g lactulose (LA) and 2 g mannitol (MA). IP was assessed by comparing the LA:MA ratio in 5 h urine samples using high performance anion exchange chromatography coupled with pulse amperometric detection to measure the concentration of each sugar. 24 h dietary intake and urine composition were also determined. LA excretion was identical in both groups (0.03 %) while MA excretion was 8.3 % in B and 11.3 % in W. IP index was 0.004 for B and 0.003 for W. It is concluded that IP is not a contributory factor in the apparent different handling of dietary Ox in B and W South Africans. It is speculated that differences in renal transporters may play a role.

Our data imply that the AGT Pro11Leu polymorphism is not directly responsible for the low incidence of stone formation in B. We conclude that other factors must be instrumental in protecting the B population from urolithiasis.

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.

Our results suggest that enzymes which regulate glycolysis may be less active in B than in W, or expression of renal transcellular Glu transporters may be relatively inhibited in B. Effects on phosphatemia are carbohydrate- and race-dependent, thereby prohibiting speculation of a general algorithm linking these variables. Inter-race differences in metabolic handling of carbohydrates might impact on respective nephrolithiasis risk factors in such groups.

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