Urinary stones form as a consequence of urinary supersaturation. Supersaturation occurs as a result of elevated concentrations of urinary solutes. Dietary, metabolic, endocrine, hereditary, and infectious processes alter urinary solute concentrations. Struvite (MgNH4PO. 6H2O) and carbonate-apatite [Ca10(PO4)6CO3] stones form in urine that becomes supersaturated as a by-product of the hydrolysis of urea by the bacterial enzyme urease. Urease-induced stones manifest primarily as branched renal calculi and as bladder calculi. Conventional therapy has usually consisted of surgical removal of the stone combined with a short course of antimicrobial therapy. Such treatment is curative in about 50% of cases. Recurrent stone formation and progressive pyelonephritis occur in those who are not cured. Adjunctive medical treatment with acetohydroxamic acid or hydroxyurea lessens the risk of calculogenesis and decreases growth of residual stones in patients who are not cured by conventional therapy. Patients with urea-splitting urinary infection and renal stones have a major life-threatening disease. The morbidity and expense that result from this disease are great. Long-term (perhaps lifetime) chemotherapy with antimicrobial agents and/or urease-inhibiting drugs combined with judicious and expert surgical intervention can be expected to significantly improve the plight of these unfortunate patients.