Physicochemical aspects of urolithiasis

Finlayson, Birdwell

doi:10.1038/ki.1978.53

Cited by 298 publications

(129 citation statements)

References 31 publications

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“…Damage to the cell membranes of renal tubules is one of the most important factors initiating stone formation. Given the fact that the growth time for a crystal to reach an obstructing diameter of ~200 μm is at least 1.5 h (46), it is highly unlikely that a crystal would attach to a healthy tubule with unobstructed urine fl ow (47,48). A crystal is more likely to attach and obstruct the urine fl ow if the primary injury is located in the anatomically narrow part of the tubule (46,48).…”

Section: Formation Of Oxalate Crystals and Onset Of Ksdmentioning

confidence: 99%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Oxalate urolithiasis (nephrolithiasis) is the most frequent type of kidney stone disease. Epidemiological research has shown that urolithiasis is approximately twice as common in men as in women, but the underlying mechanism of this sex-related prevalence is unclear. Oxalate in the organism partially originate from food (exogenous oxalate) and largely as a metabolic end-product from numerous precursors generated mainly in the liver (endogenous oxalate). Oxalate concentrations in plasma and urine can be modifi ed by various foodstuffs, which can interact in positively or negatively by affecting oxalate absorption, excretion, and/or its metabolic pathways. Oxalate is mostly removed from blood by kidneys and partially via bile and intestinal excretion. In the kidneys, after reaching certain conditions, such as high tubular concentration and damaged integrity of the tubule epithelium, oxalate can precipitate and initiate the formation of stones. Recent studies have indicated the importance of the SoLute Carrier 26 (SLC26) family of membrane transporters for handling oxalate. Two members of this family [Sulfate Anion Transporter 1 (SAT-1; SLC26A1) and Chloride/Formate EXchanger (CFEX; SLC26A6)] may contribute to oxalate transport in the intestine, liver, and kidneys. Malfunction or absence of SAT-1 or CFEX has been associated with hyperoxaluria and urolithiasis. However, numerous questions regarding their roles in oxalate transport in the respective organs and male-prevalent urolithiasis, as well as the role of sex hormones in the expression of these transporters at the level of mRNA and protein, still remain to be answered.

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Section: Formation Of Oxalate Crystals and Onset Of Ksdmentioning

confidence: 99%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…In this scenario, clusters of crystal-salt ions can be generated by a central nucleus of cell debris, for example. Higher CaOx SS, probably around 80 is apparently necessary to create homogeneous nucleation (10). This kind of nucleation is characterized by a decrease in the average crystal size caused by intense precipitation and peptization of crystals.…”

Section: Discussionmentioning

confidence: 99%

Changes in calcium oxalate crystal morphology as a function of supersaturation

Carvalho

Vieira

2004

Int. braz j urol.

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Purpose: To study the changes in calcium oxalate crystal morphology induced by different levels of supersaturation (SS) in human urine.Materials and Methods: Twenty-four hours urine samples from 5 normal men were collected. Each specimen was centrifuged and filtered. About 200 mL of each sample was dialyzed overnight. Aliquots of 2 mL of urine was then added to a 24-wells tissue culture plate and checked for crystal absence. Calcium oxalate crystals were precipitated from each sample by adding sodium oxalate and calcium chloride in sufficient quantities to induce spontaneous crystallization. Finally, each plate hole was examined with an inverted polarized microscope (X500 magnification). Initial SS of each sample relative to calcium oxalate was calculated using an iterative computer program.Results: Crystal formation was connecte to relative calcium oxalate (CaOx) SS. At SS of 10, small crystals of similar shape were formed, mainly CaOx dihydrate morphology. At SS of 30, there was an enormous increase in the number of crystals, that kept the same size. SS greater than 50 produced larger crystals with different shapes and multiple crystalline aggregates. Urine was able to tolerate, i.e., to avoid crystal formation, until SS ratios of approximately 10.Conclusions: Relative CaOx SS and the concentration ratio of calcium to oxalate are important determinanting factors of crystal morphology. Non-dialyzable urinary proteins can act as inhibitors and influence the structure of formed crystals. Additional studies from patients with kidney stones are needed in order to establish whether crystal size and habit distribution are different from crystals in normal urine.

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“…15 The thermodynamic conditions of urine lead to crystal nucleation, growth, aggregation and concretion. Despite these favorable conditions not everybody forms urinary stones.…”

Section: Discussionmentioning

confidence: 99%

Proteoglycan core protein in human urine and its possible role on calcium oxalate urolithiasis

Yoshimura

Miyake²,

Tsujihata³

et al. 1999

Int J of Urology

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Background: There are only a few papers reporting on the role of proteoglycan core protein in calcium oxalate stone formation. The present study was carried out to investigate the role of core protein of proteoglycan in human urine on calcium oxalate (CaOx) crystallization. Methods: Proteoglycans were collected from whole human urine. The covalently bound glycosaminoglycans (GAG) of proteoglycans were then digested by GAG lyase. The inhibitory activity on CaOx crystal growth in vitro was measured before and after enzyme digestion of proteoglycans. Sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of the core protein of proteoglycans and the analysis of amino acid sequence were performed. Results:The core protein showed significant inhibitory activity on CaOx crystal growth, which scarcely changed when compared with that of proteoglycans before enzyme digestion. The SDS-PAGE revealed that the core protein was a single unit with a molecular weight of 26 kDa and amino acid sequencing demonstrated high homology to interalpha-trypsin inhibitor (ITI) light chain (bikunin) with Kunitz inhibitor domain as a core protein. Conclusions:The results suggested that human urine contains proteoglycans and a major part of them is ITI light chain (bikunin). The Kunitz inhibitor domain, a core protein of bikunin, has significant inhibitory activity on CaOx crystallization without GAG bound covalently to the core protein.

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Physicochemical aspects of urolithiasis

Cited by 298 publications

References 31 publications

Oxalate: From the Environment to Kidney Stones

Oxalate: From the Environment to Kidney Stones

Changes in calcium oxalate crystal morphology as a function of supersaturation

Proteoglycan core protein in human urine and its possible role on calcium oxalate urolithiasis

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