The formation of stone minerals

Abstract

It is now generally accepted that normal urine may be supersaturated with respect to calcium oxalate hydrates (1) and a number of calcium phosphate phases such as octacalcium phosphate (Ca₈H₂(PO₄)₆ 5H₂O, OCP) (2), hydroxyapatite (Ca₅(PO₄)₃ OH, HAP) (2) and sometimes dicalcium phosphate dihydrate (CaHPO₄.2H₂O, DCPD) (3). The degree of supersaturation is usually higher in patients with urinary stones (1–3) mainly because they tend to have higher urinary calcium (3). Although the significance of such differences has been questioned, a recent analysis has indicated that they can be amplified by including magnesium analytical data in the assessment (4). Calcium oxalate, a major component of renal stones may consist of the mono- (COM), di-(COD), or tri-(COT) hydrate and the normal urine may be supersaturated with respect to any or all of these phases. Thus the less stable COD and COT may act as precursors to the formation of COM, precipitating and dissolving transiently. There is general agreement that urine contains inhibitors of calcium oxalate crystallization ranging from a number of low molecular weight components such as magnesium, citrate, and pyrophosphate, to the higher molecular weight polypeptides and glycosaminoglycans (5–8). Several investigators have used synthetic urines or mixtures of low molecular weight inhibiting species in an attempt to model more accurately the in-vivo mineralization processes (9). Under physiological conditions, the low molecular weight ions appear to account for only 5–10% of the observed inhibition.