The most important phosphates involved in urinary stone disease are carbonate apatite, brushite, and struvite. Overall, phosphate stones account for 12–20% of all stones, with a downward trend for struvite and an increase in carbonate apatite being observed in the last decade. The physicochemical basis for the formation of phosphate calculi is supersaturation. Once the solubility product has been exceeded, a metastable process of supersaturation begins, with slow crystalline growth. If a critical limit of supersaturation is exceeded, large-scale spontaneous precipitation of crystals occurs in a second stage. No urinary tract infection is involved in brushite stone formation. Although infection is not a prerequisite for the formation of carbonate apatite stones, infective conditions favor carbonate apatite formation. Struvite is the characteristic infection calculus, formed as a result of urinary tract infection with urease-producing bacteria. During the first episode of urinary stone disease a definitive diagnosis of the type of stone involved is very difficult without analysis of the latter by infrared spectroscopy or X-ray diffraction. In recurrent disease, appropriate treatment can be initiated on the basis of the previous stone analysis in the majority of cases. The best means of preventing recurrent disease involving any type of phosphate stone is definitive calculus removal by shock-wave lithotripsy, percutaneous stone removal, or open surgery (especially in children). Chemolysis via acidification of the urine with Suby G solution or hemicidrin supported by oral acidification, achieved by the metabolism of L-methionine, and antibiotic therapy (especially for infectious stones) are important adjuvant modalities of therapy. After therapy of phosphate stones, metaphylaxis involving controlled urinary acidification with L-methionine supports the treatment of infection and, at a pH value of less than 6.2 and urine dilution to 2.5 l/24 h, prevents the crystallization of struvite, brushite, and carbonate apatite.