formation remain a mystery as well. Urinary stone formation is likely a multifactorial process dependent upon environmental and genetic factors. Furthering the complexity of stone formation, several types of calculi exist, each possibly with a disparate process of formation. Certainly, the formation of cystine stones is genetically based and is dependent upon urinary nucleation and supersaturation. A similar process of increasing supersaturation leading to nucleation also likely explains uric acid stone formation. Urinary mineral supersaturation and nucleation do not appear to adequately explain the entire process of calciumbased nephrolithiasis formation, which remains the most common type of urinary calculi and is often represented by idiopathic calcium stone formation [3]. The relationship between these calcium-based calculi, particularly calcium oxalate, and Randall plaques has been well documented.Randall's work decades ago supports alternate theories of calcium stone formation independent of urinary supersaturation. After performing more than a 1,000 cadaveric renal dissections, Randall implicated the renal papilla tip as the initiating site of calcium-based urolithiasis. He observed calcium salt deposits in nearly 20 % of non-selected cadaveric units [4]. The presence of Randall plaques may be associated with urinary stones in some, but this does not necessarily implicate subsequent stone formation in all. Work by others suggests that these calcium salt deposits are present in nearly all calcium oxalate stone formers. Furthermore, calcium oxalate calculi are adherent to Randall plaques in up to 50 % stone formers [5].The calcium deposits identified by Randall, termed plaques, were located within the renal interstitium of papillae. He postulated that the basement membrane of the collecting ducts calcified and, overtime, eroded into the papillary luminal surface [4]. Randall plaques remain implicated with the process of urolithiasis formation, but how this Abstract The relationship between calcium-based calculi and Randall plaques is well documented, but the role these plaques play in the early process of urinary stone formation remains unknown. The vascular hypothesis of Randall plaque formation has been proposed, and recent works support this concept. The renal papilla's vascular environment is subject to relative hypoxia, hyperosmolar surroundings, and turbulent blood flow. These factors together create an environment prone to vascular injury and may potentiate Randall plaque precipitation. Recent data support the similarity between the vascular calcification process itself and urinary stone formation. Furthermore, epidemiological studies have suggested an association between urinary stones, adverse cardiovascular events, and vascular calcification risk factors. The concept that an initial vascular insult precipitates a Randall plaque and subsequent urolithiasis is compelling and represents an area in need of continued research. This may lead to future novel treatment approaches to urolithiasis.
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