Investigation of GAGS on 24-hour and 2-hour urines from calcium oxalate stone formers and healthy subjects

Gianotti, Magdalena; Genestar, C.; Palou, Andreu; Pons, Antoni; Conte, Antonio Hernandez; Gráses, F.

doi:10.1007/bf02559738

Cited by 11 publications

(3 citation statements)

References 17 publications

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“…1) show that 24-hour urinray GAG excretion and concentration were lower for calcium oxalate stone formers, men and women, than for healthy people. Although these findings are similar to those de scribed in a previous paper [16] employing the method of Blumenkrantz and Asboe-Hansen 117] to determine GAG levels, the urinary mean values were clearly lower using the DMB technique. These differences could be attributed to two facts: (1) The GAG precipitation procedure proposed by Blumenkrantz and Asboe-Hansen [17] could carry pro ducts containing uronic acid, generating positive errors when reacting with o-hydroxydiphenyl.…”

Section: Discussionsupporting

confidence: 72%

Glycosaminoglycans and Oxalocalcic Urolithiasis

Grases

Llompart²,

Conte³

et al. 1994

Nephron

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A very simple analytical procedure with dimethylmethylene blue as photometric reagent was applied for the evaluation of glycosaminoglycan (GAG) urinary excretions and concentrations in both sexes, calcium oxalate stone formers, and a control group. The GAG concentrations varied significantly in stone formers (males and females) and in the control group; moreover, in some individual cases, a deficit of urinary GAGs was clearly detected. Apart from important inhibitory effects of GAGs on heterogenous calcium oxalate nucleation, the low urinary GAG content could be the cause of a pathological epithelium, favoring stone formation. The dimethylmethylene blue method is recommended as a quick screening procedure to determine a GAG deficit.

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Section: Discussionsupporting

confidence: 72%

Glycosaminoglycans and Oxalocalcic Urolithiasis

Grases

Llompart²,

Conte³

et al. 1994

Nephron

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“…Such studies show that in non-stone formers total GAGs excretion varies between 0 and 50 µmoles glucuronic acid/ 24hr. Some studies show a decreased excretion of GAGs in stone formers (95)(96)(97)(98)(99)(100)(101)(102)(103)(104)(105), however; at least an equal number of studies find comparable GAGs excretion by stone formers and non-stone formers (79, 106-115). The differences in results may relate to differences in employed techniques, patient selection, epithelial damage or the contribution of bladder excretions to the total GAG pool (93).…”

Section: High Mw Compounds 521 Glycosaminoglycans (Gags)mentioning

confidence: 99%

Modulators of urinary stone formation

2004

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Urine contains compounds that modulate the nucleation, growth and aggregation of crystals as well as their attachment to renal epithelial cells. These compounds may function to protect the kidneys against: 1, the possibility of crystallization in tubular fluid and urine, which are generally metastable with respect to calcium salts, 2, crystal retention within the kidneys thereby preventing stone formation and 3, possibly against plaque formation at the nephron basement membrane. Since oxalate is the most common stone type, the effect of various modulators on calcium oxalate (CaOx) crystallization has been examined in greater details. Most of the inhibitory activity resides in macromolecules such as glycoproteins and glycosaminoglycans while nucleation promotion activity is most likely sustained by membrane lipids. Nephrocalcin, Tamm-Horsfall protein, osteopontin, urinary prothrombin fragment 1, and bikunin are the most studied inhibitory proteins while chondroitin sulfate (CS), heparan sulfate (HS) and hyaluronic acid (HA) are the best studied glycosaminoglycans. Crystallization modulating macromolecules discussed here are also prominent in cell injury, inflammation and recovery. Renal epithelial cells on exposure to oxalate and CaOx crystals produce some of the inflammatory molecules such as monocyte chemoattractant protein-1 (MCP-1) with no apparent role in crystal formation. In addition, macrophages surround the CaOx crystals present in the renal interstitium. These observations indicate a close relationship between inflammation and nephrolithiasis.

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“…Only is heparin does not appear in human urine. Many investigators [5,14,17,25,33,61,64,65] have studied urinary GAGs, but it remains unclear whether there are qualitative and/or quantitative differences in urinary GAGs between urolithiasis patients and normal individuals. Moreover, we lack detailed knowledge about the role of GAGs in cell membrane function and its influence on cell surface properties.…”

mentioning

confidence: 99%

Glycosaminoglycans and other sulphated polysaccharides in calculogenesis of urinary stones

et al. 1994

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Summary. Naturally occurring glycosaminoglycans (GAGs) and other, semisynthetic, sulphated polysaccharides are thought to play an important role in urolithiasis. Processes involved in urinary stone formation are crystallization and crystal retention. Oxalate transport and renal tubular cell injury are determining factors in these processes. In this article experimental results concerning the possible mechanisms of action of GAGs and other sulphated polysaccharides are reviewed. GAGs are inhibitors of crystal growth and agglomeration and possibly also of nucleation. They can prevent crystal adherence, correct an abnormal oxalate flux and prevent renal tubular cell damage.Sulphated polysaccharides can be divided in two subgroups, namely, glycosaminoglycans (GAGs) and other semi-synthetic sulphated polysaccharides. GAGs are polyanionic polysaccharide chains composed of repeating disaccharides of identical composition and variable lengths. Their molecular weight varies between 2 × 103 and 3 x 106 Da. All have a similar structure with one of the five principal polymers hyaluronate, chondroitin, keratan, dermatan or heparan. All except hyaluronic acid may be covalently attached to protein as proteoglycans [35].GAGs are widely distributed in the body. Many physiological functions are attributed to these substances, but little is known in detail about their synthesis, distribution and metabolism. In adults, approximately 250 mg GAG is produced each day, only 10% of which is excreted in the urine. Urinary GAGs are enzymatic degradation products of proteoglycans that are excreted by glomerular filtration [50]. Renal tubular secretion or reabsorption has not been demonstrated [37]. Their excretion shows a circadian rhythm. Men excrete significantly more GAGs per 24 h than women, the levels varying between 10 and 30 gmol/ day as based upon measurements of the glucuronic acid moiety. Normal urine contains about 2% GAGs. Of the Correspondence to: E. R. Boev6GAG fraction, about 60% is chondroitin sulphate, 18% is keratan sulphate, 15% is heparan sulphate, 4% hyaluronic acid and 2% is dermatan sulphate [29]. Only is heparin does not appear in human urine. Many investigators [5,14,17,25,33,61,64,65] have studied urinary GAGs, but it remains unclear whether there are qualitative and/or quantitative differences in urinary GAGs between urolithiasis patients and normal individuals. Moreover, we lack detailed knowledge about the role of GAGs in cell membrane function and its influence on cell surface properties.

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Investigation of GAGS on 24-hour and 2-hour urines from calcium oxalate stone formers and healthy subjects

Cited by 11 publications

References 17 publications

Glycosaminoglycans and Oxalocalcic Urolithiasis

Glycosaminoglycans and Oxalocalcic Urolithiasis

Modulators of urinary stone formation

Glycosaminoglycans and other sulphated polysaccharides in calculogenesis of urinary stones

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