Abstract
BACKGROUND: Calcium phosphate (CaP) renal stones appear to be increasing in prevalence, and are caused by high urine CaP supersaturation, which arises from genetic hypercalciuria and high urine pH. Renal damage from stones or procedures, or treatments for stone could raise urine pH; alternatively pH may be intrinsically high in some people who are thereby predisposed to CaP stones. METHODS: To distinguish these alternatives we sequenced changes in urine pH and stone CaP content asking which occurs first in patients whose stones showed progressive increase in CaP over time. From 4767 patients we found 62 in whom we could document transformation from calcium oxalate (CaOx) to CaP stones, and 134 CaOx controls who did not transform. Laboratory and clinical finding were contrasted between these groups. RESULTS: Even when patients were forming relatively pure CaOx stones, those destined to increase stone CaP had higher urine pH than controls who never did so. Their higher pH was present before and during treatments to prevent new stone formation. Shock wave lithotripsy was strongly associated with increasing stone CaP but urine pH bore no relationship to number of procedures. CONCLUSION: We conclude that high pH may not be acquired as a result of stones or their treatments but may precede transformation from CaOx to CaP stones and arise from diet or possibly heredity.