Demographics and Characterization of 10,282 Randall Plaque-Related Kidney Stones

Letavernier, Emmanuel; Vandermeersch, Sophie; Traxer, Olivier; Tligui, M.; Baud, Laurent; Ronco, Pierre; Haymann, Jean‐Philippe; Daudon, Michel

doi:10.1097/md.0000000000000566

Cited by 42 publications

(47 citation statements)

References 37 publications

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“…Recent work by Letavernier et al [16] reports data on over 10,000 such stones, each of which showed morphologic signs of having formed on Randall's plaque. Specifically, each stone was identified as showing residue of Randall's plaque, typically as part of a concave region of the stone, suggesting that the stone had formed up against the surface of the papilla.…”

Section: Resultsmentioning

confidence: 99%

What can the microstructure of stones tell us?

2016

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How stones are retained within the kidney while small in size is still not fully understood. In this paper we show two examples of how stones are retained during early growth: One is growth on Randall’s (interstitial) plaque, and the other is growth on mineral that has formed as a luminal plug in a terminal collecting duct. These two mechanisms of stone retention during early growth have distinctive morphologic features that can be seen by methods that show the microscopic structure of the stones. Stones growing on Randall’s plaque display an apatite region that is typically not large in size (less than 0.5 mm across) but which usually shows luminal spaces, which are signs of its origin in the connective tissue of the papilla. Stones growing on ductal plugs also show attachment to a piece of apatite, but the apatite regions are typically larger (often >1 mm long and >0.5 mm wide), and they are solid, without spaces running through them. We propose that knowing the mechanisms of stone retention during early stone formation could allow for better treatment of stone diseases.

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Section: Resultsmentioning

confidence: 99%

What can the microstructure of stones tell us?

2016

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“…In a large series of stones analyzed in a French laboratory using infrared spectroscopy and morphoconstitutional analysis, 34% of 30,149 intact stones collected between 1989 and 2013 that were at least 85% CaOx showed evidence of having formed over Randall’s plaque 11 . Moreover, a marked increase in the frequency of nucleation of stones over plaque occurred between 1990 and 2010 in men and in women, particularly in young adults.…”

Section: Formation Of Idiopathic Calcium Stonesmentioning

confidence: 99%

Idiopathic hypercalciuria and formation of calcium renal stones

2016

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The most common presentation of nephrolithiasis is idiopathic calcium stones in patients without systemic disease. Most stones are primarily composed of calcium oxalate and form on a base of interstitial apatite deposits, known as Randall’s plaque. By contrast some stones are composed largely of calcium phosphate, as either hydroxyapatite or brushite (calcium monohydrogen phosphate), and are usually accompanied by deposits of calcium phosphate in the Bellini ducts. These deposits result in local tissue damage and might serve as a site of mineral overgrowth. Stone formation is driven by supersaturation of urine with calcium oxalate and brushite. The level of supersaturation is related to fluid intake as well as to the levels of urinary citrate and calcium. Risk of stone formation is increased when urine citrate excretion is <400 mg per day, and treatment with potassium citrate has been used to prevent stones. Urine calcium levels >200 mg per day also increase stone risk and often result in negative calcium balance. Reduced renal calcium reabsorption has a role in idiopathic hypercalciuria. Low sodium diets and thiazide-type diuretics lower urine calcium levels and potentially reduce the risk of stone recurrence and bone diseas

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“…The subsequent formation of CaOx crystals may account for kidney stone formation. As proposed previously, hyperoxaluria is considered a major risk factor for urinary stone, and experimental induction of hyperoxaluria can lead to crystalluria and CaOx crystal deposition in the kidney [6,7]. In addition, recurrent idiopathic stone formers always show mild hyperoxaluria; meanwhile, amount and size of CaOx crystals, alongside disease severity, are highly related to urinary excretion of oxalate (Ox) [8].…”

Section: Introductionmentioning

confidence: 96%

“…With respect to sub-urothelial crystals, injury or degradation of urothelium is considered to play an important role as this leads to crystal exposure to the urinary environment favouring further stone formation. Some scholars speculate that urothelial injury could promote crystal retention and the development of a stone nucleus allowing stone formation on the renal papilla [7,12]. Furthermore, renal cell injury can also promote crystal-cell interaction and crystal retention in the tubules.…”

Section: Introductionmentioning

confidence: 97%

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

et al. 2016

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Hyperoxaluria and cell injury are key factors in urolithiasis. Oxalate metabolism may be altered by renal dysfunction and therefore, impact the deposition of calcium oxalate (CaOx) crystals. We investigated the relationship of renal function, oxalate metabolism and CaOx crystal deposition in renal ischemia. One hundred male Sprague-Dawley rats were randomly divided into four groups. Hyperoxaluria model (Group A and B) was established by feeding rats with 0.75 % ethylene glycol (EG). The left renal pedicle was clamped for 30 min to establish renal ischemia Groups (B and C), while Groups A and D underwent sham operation. Then, serum and urine oxalate (Ox), creatinine (Cr) and urea nitrogen (UN) levels were evaluated by liquid chromatography mass spectrometry (LCMS) and ion mass spectrum (IMS) at days 0, 2, 4, 7, and 14. CaOx crystallization was assessed by transmission electron microscope (TEM). A temporal and significant increase of serum Cr and UN levels was observed in Groups B and C compared to values obtained for Groups A and D (P < 0.05). Ox levels in serum and urine were significantly higher in Groups A and B than in the other two groups from day 7 (P < 0.05). In addition, CaOx crystallization was observed in both Groups A and B, but Group B showed earlier and more pronounced crystal deposition in the renal tissue. Our results indicated that renal tubular injury induced by renal ischemia might not affect Ox levels but could promote CaOx crystal retention under hyperoxaluria.

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Demographics and Characterization of 10,282 Randall Plaque-Related Kidney Stones

Abstract: Supplemental Digital Content is available in the text

Cited by 42 publications

References 37 publications

What can the microstructure of stones tell us?

What can the microstructure of stones tell us?

Idiopathic hypercalciuria and formation of calcium renal stones

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

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