Renal lithiasis is a multifactorial disease. An important number of etiologic factors can be adequately modified trough diet, since it must be considered that the urine composition is directly related to diet. In fact, the change of inappropriate habitual diet patterns should be the main measure to prevent kidney stones. In this paper, the relation between different dietary factors (liquid intake, pH, calcium, phosphate, oxalate, citrate, phytate, urate and vitamins) and each type of renal stone (calcium oxalate monohydrate papillary, calcium oxalate monohydrate unattached, calcium oxalate dihydrate, calcium oxalate dihydrate/hydroxyapatite, hydroxyapatite, struvite infectious, brushite, uric acid, calcium oxalate/uric acid and cystine) is discussed.
The phytate urinary levels in a group of active calcium oxalate stone formers were studied and compared with those found in healthy people. Urinary phytate was significantly lower for stone formers. If deficit of the capacity to inhibit crystallization of calcium salts is considered an important factor related to calcium stone formation, the excretion of low phytate amounts could be an important risk factor in the development of this type of renal calculi. The influence of dietary phytate on urinary excretion was also studied. Clearly maintenance of a phytate-free diet significantly decreased the urinary excretion of phytate (about 50% after 36 h). This demonstrated the importance of dietary phytate in maintaining adequate urinary levels to permit effective crystallization inhibition of calcium salts and consequently preventing renal stone development.
1 October 2001 in The Journal of Nutritional Biochemistry
Phytate (inositol hexaphosphate; InsP6) was determined in rat tissues fed on diets with different phytate contents, using a GC–mass detection methodology that permitted the evaluation of the total amount of this substance present in such tissues. The highest InsP6concentrations were found in brain (5·89×10-2 (SE 5·7×10-3) MG/G DM), WHEREAS THE CONCENTRATIONS DETECTED IN KIDNEYS, LIVER AND BONE WERE SIMILAR TO EACH OTHER (1·96×10-3 (se 0·20×10-3), 3·11×10-3 (se 0·24×10-3), 1·77×10-3 (se 0·17×10-3) mg/g DM respectively) and 10-fold less than those detected in brain. When rats were fed on a purified diet in which InsP6was undetectable, the InsP6levels of the organs mentioned earlier decreased dramatically (9·0×10-4, 3·8×10-5, 1·4×10-5 mg/g DM in brain, kidneys and liver respectively) and in some cases became undetectable (bone). The addition of InsP6to this purified diet led to the increase of InsP6levels in these tissues. This clearly demonstrated that the majority of the InsP6found in organs and tissues has a dietary origin and is not a consequence of endogenous synthesis. Consequently, considering that InsP6could be involved in some important biological roles, the value of any diet on supplying this substance is noteworthy.