The Hyperoxaluric Syndromes

Wandzilak, T. R.; Williams, Hibbard E.

doi:10.1016/s0889-8529(18)30297-4

Cited by 17 publications

(13 citation statements)

References 76 publications

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“…Various chronic gastrointestinal disorders can cause fat malabsorption that leads to calcium soap formation, which reduces the intraluminal calcium level and allows free oxalic acid to become available for absorption. Malabsorption of bile and fatty acids also increases the permeability of the colonic mucosa to oxalic acid (shunt conductance) 18,19 . Oxalate‐degrading bacteria exist in the gastrointestinal tract and have been suggested to regulate oxalate homeostasis by preventing its absorption, catabolizing free oxalic acid, and enhancing oxalate secretion from the blood.…”

Section: Discussionsupporting

confidence: 52%

“…Malabsorption of bile and fatty acids also increases the permeability of the colonic mucosa to oxalic acid (shunt conductance). 18,19 Oxalate-degrading bacteria exist in the gastrointestinal tract and have been suggested to regulate oxalate homeostasis by preventing its absorption, catabolizing free oxalic acid, and enhancing oxalate secretion from the blood. Calcium is an essential nutrient for humans, and it is absorbed through both active and passive transport mechanisms.…”

Section: Discussionmentioning

confidence: 99%

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Urinary oxalic acid excretion differs after oral loading of rats with various oxalate salts

et al. 2003

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Background : To compare urinary oxalate excretion after the oral administration of oxalic acid, disodium oxalate, or calcium oxalate in rats. Methods : Male Wistar rats were divided into four groups of six rats each and were intravenously hydrated with normal saline, and then were administered normal saline (control group), 10 mg of oxalic acid, equimolar disodium oxalate, or equimolar calcium oxalate via a gastrostomy. Urine specimens were collected just before administration and at hourly intervals up to 5 h afterwards. The urinary oxalate, calcium, magnesium and phosphorus levels were measured. Results : Urinary oxalate excretion peaked at 1-2 h after administration of oxalic acid or equimolar disodium oxalate, while administration of calcium oxalate only caused a small increase of urinary oxalate excretion. Cumulative urinary oxalate excretion during 5 h was 1.69 ± 0.10 mg (mean ± SD; 17%), 1.43 ± 0.13 mg (13%), and 0.22 ± 0.03 mg (2%) after the administration of oxalic acid, disodium oxalate, and calcium oxalate, respectively. Urinary calcium excretion showed a decrease in the oxalic acid and disodium oxalate groups, while urinary magnesium or phosphorus excretion did not change significantly. Conclusion : The upper gastrointestinal tract seems to be the major site of oxalic acid absorption and only free oxalate is absorbed irrespective of whether it is the sodium salt or not. After binding to calcium in the gut, oxalic acid absorption seems to be inhibited in the presence of calcium and this means that calcium oxalate is poorly absorbed (at least in the upper gastrointestinal tract).

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Urinary oxalic acid excretion differs after oral loading of rats with various oxalate salts

et al. 2003

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“…Oxalate is the most important determinant of the level of urinary supersaturation [36,51,57,58,74,83,84]. Plasma oxalate is filtered freely into Bowman's space and undergoes bidirectional transport across the tubular epithelium [63,68,69,80].…”

Section: Renal Handling Of Oxalatementioning

confidence: 99%

“…Plasma oxalate is filtered freely into Bowman's space and undergoes bidirectional transport across the tubular epithelium [63,68,69,80]. It has been proposed that the secretion of oxalate is possibly enhanced in stone for-mers [3,4,14,15,74,84]. Oxalate secretion requires its crossing of the basolateral plasma membrane facing the interstitial space and blood supply and its subsequent transport through the cell, followed by passage of the apical plasma membrane facing the tubular fluid.…”

Section: Renal Handling Of Oxalatementioning

confidence: 99%

“…The transport of oxalate across membranes is mediated by anion-exchange proteins related to erythrocyte band 3 protein (AE1) [1,8,66]. Although the incidence of a mild form of hyperoxaluria has been reported in stone formers [65,74,83,84], in many clinical studies their 24-h urine oxalate excretion is not significantly higher than that of subjects without stones [28,33]. Although the incidence of a mild form of hyperoxaluria has been reported in stone formers [65,74,83,84], in many clinical studies their 24-h urine oxalate excretion is not significantly higher than that of subjects without stones [28,33].…”

Section: Renal Handling Of Oxalatementioning

confidence: 99%

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Cell cultures and nephrolithiasis

et al. 1997

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While the physical chemistry of stone formation has been intensively studied during the last decade, it has become clear that the pathophysiology of renal stone disease cannot be explained by crystallization processes only. In recent years, evidence has emerged that the cells lining the renal tubules can have an active role in creating the conditions under which stones may develop. Since it is difficult to study these mechanisms in vivo, cultured renal tubular cells have become increasingly popular for the study of physiological and cell biological processes that are possibly linked to stone disease. In this paper, we discuss the possible contribution of cellular processes such as transepithelial oxalate transport and crystal--cell interaction to the formation of renal stones. Experimental studies that have been performed with cultured renal cells to elucidate the mechanisms involved in these processes will be summarized.

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Oxalate transport and calcium oxalate renal stone disease

Verkoelen

Romijn

1996

Urol. Res.

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Hyperoxaluria is considered to play a crucial role in calcium oxalate (CaOx) renal stone disease. The amount of oxalate excreted into the urine depends on intestinal absorption, endogenous production, renal clearance and renal tubular transport. Since a primary disorder has not been found so far in most CaOx stone formers and since oxalate is freely filtered at the glomerulus, most studies are presently focussed on alterations in epithelial oxalate transport pathways. Oxalate can be transported across an epithelium by the paracellular (passive) and transcellular (active) pathway. Oxalate transport across cellular membranes is mediated by anion-exchange transport proteins. A defect in the structure of these transport proteins could explain augmented transcellular oxalate transport. Little is known about the physiological regulation of oxalate transport. In this review cellular transport systems for oxalate will be summarized with special attention for the progress that has been made to study oxalate transport in a model of cultured renal tubule cells. Better understanding of the physiological processes that are involved in oxalate transport could yield information on the basis of which it might be possible to design new approaches for an effective treatment of CaOx stone disease.

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The Hyperoxaluric Syndromes

Cited by 17 publications

References 76 publications

Urinary oxalic acid excretion differs after oral loading of rats with various oxalate salts

Urinary oxalic acid excretion differs after oral loading of rats with various oxalate salts

Cell cultures and nephrolithiasis

Oxalate transport and calcium oxalate renal stone disease

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