Until recently, the sequence of events that leads to the formation of urinary calculi were poorly understood, most fundamentally due to the lack of appropriate in-vivo data. Earlier theories of calculogenesis proposed that stones could result from tubular epithelial injury due to oxalate toxicity, a lack of urinary inhibitors of crystal formation or crystal epitaxy on a pre-existing nidus (Khan, Finlayson et al. 1979). Theoretical work on free and fixed particle growth indicated that a transit time from the collecting duct to the bladder of only 10 minutes provided insufficient time for a crystal to grow to a clinically meaningful size (Jonassen, Cooney et al. 1999). Morphological classification of the directional growth of calculi supported the necessity for a fixed point of origin, in the absence of obstruction (Hinman 1979). These observations suggested that most stones must initiate from a fixed point or nidus in the collecting system or renal papilla.