One such nidus, first described more than sixty years ago by Alexander Randall, was proposed to be the originating lesion for the formation of calcium oxalate stones (Randall 1936; Randall 1937; Randall 1940). In microscopic studies of renal papilla obtained at necropsy, he demonstrated the presence of 2-3mm lesions in 19.6% of patients that were composed of calcium phosphate and devoid of evidence of inflammation. Adherent to this, in 65 of 1,514 pairs of kidneys, he identified nascent stones composed of calcium oxalate and calcium phosphate. When these stones reached sufficient size, he hypothesized that they would break free, taking with them the underlying plaque. In subsequent work, 256 voided or removed calculi were examined and 106 gave visible evidence of mural attachment (Randall 1940). Later microradiographic studies would confirm the presence of plaque in a papillary location that could be co-localized with stone (Carr 1954). Unfortunately, all earlier studies of stone pathogenesis have suffered from lack of definition of clear clinical stone-forming phenotypes.