Most cases of nephrolithiasis are associated with the relatively common metabolic abnormality of idiopathic hypercalciuria (1). These patients generally absorb an excess amount of dietary calcium leading to increased urine calcium excretion and supersaturation with respect to calcium oxalate and calcium phosphate; they subsequently form stones. Other patients with nephrolithiasis, who have had an intestinal bypass procedure, absorb oxalate in excess leading to increased urine oxalate excretion and supersaturation with respect to calcium oxalate; they also subsequently form stones. In these and other causes of nephrolithiasis, the site of the initial solid phase has long been the subject of debate. Over 65 years ago, A. Randall demonstrated that interstitial crystals located at, or adjacent to, the papillary tip, Randall’s plaques, were common in stone formers (2). He found that these crystals were composed not of calcium oxalate, the most common solid phase found in patients with nephrolithiasis, but of calcium phosphate (3). He believed that the calcium phosphate crystals formed in the papillary interstitium and then eroded into the urinary space, serving as a heterogeneous nucleation surface for calcium oxalate. B. Finlayson later argued that, due to rapid flow of the renal ultrafiltrate through the tubule, there was insufficient time for formation of a lumenobstructing solid phase (4), which also suggested that an intratubular site of stone formation was unlikely. However, other investigators found that calcium oxalate crystals adhered to cultured tubular cells (5), where they could either be endocytosed or remain on the cell surface, serving as a nidus for growth into larger, clinically significant, calculi.