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This thesis examines various groups of athletes to assess whether they are at risk with regard to kidney stone formation. Particle size distribution analysis (Coulter counter), ultra-structural analyses (SEM) and urine analysis were conducted. The background to various factors relating to stone formation is discussed as well as the general theory behind the techniques employed. The methods utilized and data obtained are described. Particle size distribution analysis and scanning electron· micrographs suggest that marathon runners and cyclists may be at risk with respect to stone formation. Dehydration and urinary tract trauma are thought to occur in the former whereas dehydration only is operative in the latter. Results obtained from Na/Ca ratio analyses are found to correspond with the particle size analyses thereby suggesting that this ratio may have potential as a useful index of stone-forming risk. The enormous spread of values amongst each class of athlete shows, however, that physical exertion is not the sole factor affecting the Na/Ca ratio.

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Mice homozygous for the disrupted renal type 11a sodium/phosphate (Na/Pi) cotransporter gene, Npt2, (Npt2 KO) exhibit renal Pi wasting and hypercalciuria, predisposing factors for renal stone formation. We observed that Npt2 KO mice, but not wild-type littermates form renal stones. The renal stones were evident in newborn, weanling and adult mice and composed of calcium (Ca) and Pi. The presence of renal calcification correlated with the absence of Npt2 gene expression and the presence of genes responsible for the synthesis (1alpha-hydroxylase) and catabolism (24-hydroxylase) of 1,25-dihydroxyvitamin D, whose elevated levels contribute to the hypercalciuria and renal calcification in Npt2 KO mice. The renal calcification was associated with increased osteopontin (OPN) mRNA expression and colocalized with OPN, the latter associates with renal stones in vivo and inhibits Ca mineralization in vitro). These data demonstrate that hyperphosphaturia and hypercalciuria, secondary to Npt2 gene disruption, are sufficient for the development of renal calcification.

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