[Is sucrose a risk factor in calculus formation?]. / Le saccharose est-il un facteur de risque de la lithogenèse?

The addition of sucrose to drinking water of rats at the rate of 2.5 or 5 grams per 100 ml, for one month, induced hypercalciuria which appeared to be dependent on the degree of supplementation. In spite of these disorders, calcium deposits were not observed in treated animals. This protection against renal calculi was probably due to high urinary excretions of magnesium, phosphorus, zinc and copper. These lithogenesis inhibitors varied, like oxaluria and calciuria, in parallel with dietary sucrose intake.

[The effect of the administration of a high dose of vitamin D3 on calculus formation in rats]. / Effets de l'administration d'une dose élevée de vitamine D3 sur la lithogénèse chez le rat.

Administration of high doses of vitamin D3 (2,600 IU/100 ml of drinking water) to adult rats, for one month, significantly altered renal function (P less than 0.01) and enhanced renal accumulation of oxalate (71.44 x 18.82 micrograms/g of tissue in treated rats vs 38.87 +/- 11.96 micrograms/g in untreated rats; P less than 0.001), phosphate (1.388 +/- 188 micrograms/g in treated rats vs 870 +/- 171 micrograms/g in untreated rats; P less than 0.01) and calcium (477 +/- 107 micrograms/g in treated rats vs 326 +/- 104 micrograms/g in untreated rats; P less than 0.01). Urinary analyses of principal promotors and inhibitors of lithogenesis revealed high calcium excretion (1,576 +/- 0.419 mg/24 hr in treated rats vs 0.969 +/- 0.214 mg/24 hr in untreated rats; p less than 0.01) and decreased magnesium excretion (0.330 +/- 0.135 mg/24 hr in treated rats vs 0.910 +/- 0.168 mg/24 hr in untreated rats; p less than 0.001). Microscopic calcium deposits were found in the medulla, especially in renal papilla. These results suggested that vitamin D3, when administered at high doses for a long time, may induce nephrocalcinosis and alter renal function.