STONE PREVENTION - WHY SO LITTLE PROGRESS

Despite intensive research the knowledge of stone pathogenesis, which is the basis of every rational stone metaphylaxis, has remained rather scanty. Epidemiology shows that stone formation in most patients is o nly a sporadic event, probably resulting from a coincidence of differe nt factors. The hypercalciuria, hypocitraturia, hyperuricosuria and hy peroxaluria frequently found in calcium stone formers can be influence d therapeutically and, in affluent societies, seem to be the result of protein over-consumption. These four factors favour crystallization p rocesses in urine. However, urine is normally protected from nucleatio n, growth and aggregation of calcium minerals by crystallization inhib itors. In urine, crystallization of calcium oxalate can only be induce d by an extreme supersaturation, a deficient inhibitor activity and pr omoters of crystallization. To form a stone, crystals have to be retai ned in the urinary collecting system. Two mechanisms of retention are discussed: large crystal aggregates trapped in collecting ducts of ren al papillae, or a pre-existing calcification of the papilla (mainly ca lcium phosphate) that may be responsible for growth of an initially fi xed particle to a concretion large enough to become symptomatic. An ex cessive oxalate intake combined with a low calcium consumption can pro duce marked hyperoxaluria. In the animal model, hyperoxaluria induces not only calcium oxalate crystallization but also papillary damage and incrustrations. Hypercalciuria at a low pH favours the aggregation of calcium oxalate, and at a high pH the crystallization of calcium phos phate, a promoter of heterogeneous nucleation of calcium oxalate. All these factors and further complex phenomena mentioned in this paper ha ve to be taken in account to perform rational stone metaphylaxis.