Much has been learned in the last decade regarding the initial steps of crystal deposition and ultimate stone formation. There appear to be 3 basic pathways for crystal formation in the upper urinary tract. The first and most common pathway is the overgrowth of calcium oxalate on suburothelial deposits of hydroxyapatite, so-called Randall plaque.1 This pathway is germane to the idiopathic calcium oxalate stone former, by far the largest category of stone formers. Randall plaque forms in the basement membranes of the thin limbs of the loop of Henle as fine particles that produce no visible tissue reaction or cell injury. These particles are laminated microspherials of alternating apatite crystals and organic matrix that coalesce in the interstitium to form a syncythium of crystal islands in an organic sea. This migrates to the suburothelial space, where it appears during surgery as a white, irregularly shaped plaque. Randall plaque occupies 5% to 8% of the total papillary surface area in idiopathic calcium oxalate stone formers and on this minor proportion of surface more than 75% of stones are attached, meaning that overgrowth on plaque is of preeminent importance for stone formation.2