Struvite stones

Abstract

The association of putrefying urine and stones has been known since antiquity. The accumulated clinical and experimental evidence points to the bacterial enzyme urease as the primary calculogenic mechanism. The hydrolysis of urea by urease increases urinary ammonia and alkalinity. These substances damage tissue and thereby contribute to bacterial invasion and virulence. Increased levels of urinary pH, ammonia, bicarbonate, and carbonate bring about supersaturation of urine with subsequent crystallization of struvite and carbonate-apatite. It is likely that these crystals are formed by no mechanism other than the hydrolysis of urea. These pathological processes are accompanied by an increased urinary excretion of colloids which may also contribute to calculogenesis. Bacteria that do not make urease do not contribute to the formation of struvite and carbonate-apatite. The role of such bacteria in the pathogenesis of other types of stones is unclear but seems unlikely. Surgical removal of infected renal calculi with or without removal of focal areas of pyelonephritis is practical and successful in most cases. Long-term treatment with antimicrobial agents and/or urease inhibitors can be expected to reduce the incidence of stone recurrence and/or the growth of residual stones. The long-term practicality, safety, and efficacy of these agents, however, has not yet been confirmed. Antimicrobial agents and/or urease inhibitors may contribute to the clinical dissolution of infection stones in selected instances; this concept also awaits further clinical confirmation.