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PubMed1991

[Effects of urinary pH and acid-base balance on the formation of calcium oxalate stone].

The effects of urinary pH and acid-base balance on the calcium oxalate stone formation was investigated by two experiments. 24-hr urine samples were collected from 15 recurrent CaOx stone formers, 9 single stone formers and 6 age-matched controls. Inhibitory effect of 1% urine in various pH (4.0-9.0) were calculated by a seed crystal method. In the seed crystal system, there were no significant differences in the inhibitory activity of aggregation (Ia) and in the inhibitory activity of size (Is) for each pH of metastable solution between the stone former group and the control group. However, the value of Ia and Is showed a tendency of rise in proportion to a rise in pH. Rats model for calcium oxalate urolithiasis were fed with three different diets (1% NH4Cl, 5% NaHCO3 and 8% NaHCO3 diet) for three weeks. On the fourth week, 24-hr urine samples were collected. In the animal experiment, calcium oxalate stone formations were predominantly recognized in the kidney of the 1% NH4Cl diet group. The biochemical data showed an increase of urinary calcium and oxalate, and a decrease of urinary citrate. These results suggest that low urinary pH and metabolic acidosis are promoters of the calcium oxalate stone formation.

Acid-Base Equilibrium↗
PubMed1999

Oxalate-induced exposure of phosphatidylserine on the surface of renal epithelial cells in culture.

A molecular mechanism of crystal attachment to renal cells after injury has been proposed in which the exposure of phosphatidylserine (PS) on the cell membrane surface following injury provides attachment sites for calcium-containing crystals. Annexin V was used to determine whether injury to kidney cells by oxalate in culture resulted in PS exposure on the cell surface. When continuous cultures of intermedullary collecting duct cells were exposed to various levels of oxalate, a dose-dependent increase in PS exposure was observed on the cell surfaces. Initially, only scattered cells expressed PS on the surface. However, as the level of oxalate increased, groups of cells began to express PS, suggesting that the injured cells may have an influence on neighboring cells. Exposure of PS on the cell membrane surface correlated with a corresponding increase in calcium oxalate monohydrate crystal attachment to the cells. This indicates that damage to kidney epithelial cells by elevated concentrations of urinary components, in this case oxalate, could result in exposure of PS on cells, which could provide a point of fixation or nucleation for calcium-containing crystals.

Annexin A5↗
PubMed2000

Oxalate-induced changes in renal epithelial cell function: role in stone disease.

Many studies on the etiology of stone disease have focused on the properties of urine that affect crystal nucleation and growth. More recent studies have focused on the properties of the renal epithelium and the role of injury in crystal retention. The latter studies have shown that oxalate exposure per se can damage renal epithelial cells and enhance crystal binding. This overview summarizes findings of specific biochemical and genetic alterations observed in renal epithelial cells after exposure to oxalate. In LLC-PK1 and MDCK cells, oxalate exposure produces marked effects on membranes, causing a redistribution of phosphatidylserine and activation of two lipid signaling cascades, one involving phospholipase A(2) (PLA(2)) and one involving ceramide. Longer exposure to oxalate leads to membrane damage and cell death. Adaptive responses are also observed, including proliferation (for replacement of damaged cells) and induction of various genes (for cellular replacement and repair). Many or all of these responses are blocked by antioxidants, and many can be mimicked by PLA(2) agonists/products. This finding suggests links between oxalate-induced increases in oxidant stress, lipid signaling pathways, and subsequent molecular responses that may eventuate in renal cell damage or death. Whether such changes play a role in stone disease in vivo, and whether strategies to inhibit these changes would be beneficial therapeutically, is unknown.

Animals↗
PubMed1975

Oxalate retinopathy: an experimental model of a flecked retina.

The clinical picture resembling fundus albipunctatus was seen to develop in rabbits following subcutaneous injection with dibutyl oxalate. On histologic examination, the flecks were found to be due to intracellular accumulation of calcium oxalate in the RPE cells. The clinical and histologic features of this animal model closely resemble the recently described entity of oxalate retinopathy in humans which was seen in the presence of high circulating oxalate levels. It is suggested that the presence of metabolic disorders or toxicity which are known to cause oxalate depositions should be sought in patients with fundus albipunctatus.

Animals↗
PubMed2003

[Detection of Oxalobacter formigenes in human feces and study of related genes in a new oxalate-degrading bacterium].

The first objective of the present study was to examine the presence of Oxalobacter formigenes (an oxalate-degrading bacterium in the human intestine) according to sex in a large number of Japanese. The second objective was to study the presence of three related genes in Bifidobacterium breve, which is considered to be a new oxalate-degrading bacterim. Fecal samples were collected from 55 male and 37 female healthy volunteers. O. formigenes was detected by a polymerase chain reaction (PCR) and a culture-based method. DNA was amplified by the PCR method including the site of important base sequences of each gene in order to detect oxc, frc, and OxlT. O. formigenes was present in 80% of 54 male and 62% of 34 female subjects in the PCR-based assay, while it was present in 62% of 40 male and 50% of 24 female subjects in the culture-based assay. The partial base sequences of the three related genes in B. breve were determined. The RNA polymerase-binding site in promoters and the rho-independent termination sequence were preserved in oxc and frc. In conclusion, the rate of the presence of O. formigenes was the same as in previous reports. Female subjects showed a 15% lower rate than males. B. breve is considered to be an oxalate-degrading bacterium since it was found to have oxalic acid-degrading ability and three genes involved in oxalate degradation.

Adult↗
PubMed1992

Oxalate production from glyoxylate by lactate dehydrogenase in vitro: inhibition by reduced glutathione, cysteine, cysteamine.

Lactate dehydrogenase is known to act as a dismutase converting glyoxylate to oxalate and glycolate. LDH (sources: human erythrocytes, human plasma; rabbit muscle; rat liver) activity was assayed at 340 nm using glyoxylate (5.0 mmol/l) and NADH. The LDH activity (approx. % of control) in all the cases decreased respectively in the presence of 5.0 and 10.0 mmol/l of cysteine (45 and 20), cysteamine (45 and 20), and GSH (55 and 30). This decrease in LDH activity resulted in decreased oxalate production from glyoxylate (0.5 mmol/l). A 50% inhibition in oxalate production was observed in presence of 0.3 mmol/l cysteine, 0.35 mmol/l cysteamine, and 2.0 mmol/l GSH. The results suggest that the net LDH activity towards oxalate production may be regulated by the free SH-groups in the cell. This possibility needs evaluation as a tool to lower endogenous oxalate production and the associated risk of stone formation.

Animals↗
PubMed2005

[Effects of oxalate on acid phosphatase adsorption and its activity on soil colloids and minerals].

By a batch method, this paper studied the effects of different concentration and pH of oxalate, an important root exudate, on the adsorption of acid phosphatase and its activity on < 2 microm colloids of yellow brown soil and latosol, and on minerals goethite and kaolinite. The results showed that the acid phosphatase adsorption by goethite was less affected by the concentration of oxalate; while the adsorbed amount of this enzyme by the other test colloids and kaolinite was sharply decreased with the increasing oxalate concentration (0-5 mmol x L(-1)) first, and then gradually increased to the level equal to or less than the blank, which may be related to the coordination type of oxalate on soil colloids and minerals, and their surface charge change and dissolution. In the systems oxalate existed, the adsorbed amount of acid phosphatase by soil colloids and minerals decreased in order of goethite >> yellow brown soil > kaolinite > latosol. The pH value for the maximum adsorption of acid phosphatase was between the IEP of the enzyme and the PZC of test colloids and minerals. After the enzyme was immobilized on colloids and minerals, the pH of its maximum specific activity had no change, or shifted to a higher value.

Acid Phosphatase↗
PubMed1990

Crystal growth of calcium oxalate monohydrate and calcium carbonate from dilute solutions.

By controlling evaporation, calcium carbonate (calcite) is precipitated together with calcium oxalate monohydrate from equimolar (1 x 10(-5) M) solutions of calcium chloride and sodium oxalate under decreasing (37.5 degrees - 32.7 degrees C) and increasing temperature (22 degrees-42 degrees, 22 degrees-45 degrees, 22 degrees-50 degrees C), and initial pH's of 6.6 and 6, respectively. If, however, the pH of the solutions is, respectively, 8 and 8.5 and the temperature is 32 degrees C, oxalate breaks down to carbonate and calcium precipitates solely as calcite. This process materializes as the pH of both solutions initially adjusts to about 7.5. Both the quality and the size of the crystals of calcite and calcium oxalate monohydrate varied markedly. Euhedral crystals of calcite, measuring in excess of 200 micrometers in cross-section, and grown at 37.5 degrees C were remarkably ordered as shown by the lack of twinning, streaks and/or diffuseness around the diffracta, which is evidenced by single-crystal x-ray diffraction analysis. In contrast, calcium oxalate monohydrate was almost always disordered due to twinning along the (101) plane and never exceeded 100-150 micrometers along a coordinate axis.

Calcium Carbonate↗
PubMed1989

Kochia scoparia oxalate content.

Kochia scoparia was collected periodically during the growing seasons of 1984, 1985 and 1986. The 10, 16 and 16 samples, respectively, from these years were air dried, hammer milled and analyzed at a later date for soluble and total oxalates. An additional 6 samples from New Mexico were analyzed from the 1987 growing season. A maximum of 4.7% soluble oxalates and 11.4% total oxalates were present in 1986 Colorado kochia following heavy rainfall. This concentration of soluble oxalate could cause chronic oxalate poisoning (alkalosis) in cattle.

Oxalates↗
PubMed1989

[The application of peroxyoxalate-chemiluminescence in biochemical analysis: determination of oxalate].

A new sensitive method for the determination of oxalate is presented. By using the chemiluminescence decay of monoperoxyoxalic acid very low concentrations of oxalate can be determined (up to 100 nmol/l). Oxalate determinations in urine require the precipitation of calcium oxalate, in order to avoid oxalate-unspecific side emissions. This could be avoided by combination with a specific enzymatic partial reaction, which would also permit the determination of low concentrations of other organic species (e.g. citrate, pyruvate, malate).

Luminescent Measurements↗
PubMed1988

[An architectural study of mixed uric acid and calcium oxalate stones by polarized light microscopy of thin section].

The architecture of mixed uric acid and calcium oxalate stones was studied by polarized light microscopy. Some uric acid stones contained calcium oxalate stones (whewellite or weddellite) as a nucleus. Other uric acid stones contained calcium oxalate crystals in the nucleus or inner portion. A uric acid stone covered with layers of calcium oxalate was also found. In the mixed stones, nuclei of randomly mixed fine grained whewellite and uric acid were seen and both crystals appeared in alternating sequence in the outer layers. Weddellite crystals dissolved layers of uric acid and invaded into them in the nuclear or peripheral zones. Whewellite may precipitate in the same or a similar condition as uric acid precipitates, whereas weddellite may precipitate in a different condition. We discussed the pathogenesis of mixed uric acid and calcium oxalate stones, heterogeneous nucleation and epitaxial growth based on a morphologic study of the mixed stones.

Calcium Oxalate↗
PubMed1987

Glycoprotein calcium oxalate crystal growth inhibitor in urine.

Urine is normally supersaturated with respect to calcium oxalate. Inhibitors of the growth and aggregation of calcium oxalate crystals are present in urine and probably protect against calcium stone formation. These inhibitors are deficient in stone formers. The major inhibitor of calcium oxalate crystal growth is a non-dialyzable, anionic macromolecule. An acidic glycoprotein has been isolated from urine and human kidney tissue culture medium which inhibits calcium oxalate crystal growth in vitro. This glycoprotein crystallization inhibitor has a molecular weight of 14,000 daltons and contains 2-3 residues of gamma-carboxyglutamic acid. The dissociation constant for the calcium oxalate crystal-inhibitor complex is about 10(-7) M. The glycoprotein isolated from the urine of calcium stone formers has a decreased affinity for crystal surface, and a proportionally weaker inhibitory activity; it also lacks gamma-carboxyglutamic acid.

Calcium Oxalate↗
PubMedDate not supplied

Pathogenesis of acquired renal cysts in hemodialysis patients. The role of oxalate crystal deposition in renal tubules.

Although the mechanism responsible for the genesis of acquired renal cysts in hemodialysis patients has not been clearly defined, obstruction of the nephron by deposition of oxalate crystals may be an important factor. We performed this study to investigate this possibility. In 51 dialysis patients, the number and size of acquired cysts as well as kidney size were examined using sonography. Plasma oxalate levels were measured with capillary gas chromatography. Cysts were found in 6 of 18 (33.3%), 12 of 15 (75%), and 15 of 17 (88.2%) dialysis patients treated for 5, 10, and more than 10 years. The mean kidney size was significantly greater in hemodialysis patients with cysts than in those without cysts. There was a significant correlation between plasma oxalate levels and kidney size, particularly in patients dialyzed for longer periods (r = 0.638, P less than 0.01). Mean plasma oxalate levels of dialysis patients with renal cysts were significantly higher than those of noncystic patients (P less than 0.05). Although further evaluation is necessary to confirm these observations, our results suggest that oxalate crystal deposits in renal tubules secondary to hyperoxalemia in hemodialysis patients are a significant contributing factor to the formation of acquired renal cysts in these patients.

Cysts↗
PubMed1986

Phase transitions of calcium oxalate trihydrate and epitaxy in the weddellite-whewellite system.

The phase changes calcium oxalate trihydrate-weddellite, weddellite-calcium oxalate monohydrate and calcium oxalate trihydrate-whewellite are individually examined at the atomic level from a theoretical point of view; concomitantly the topological requirements necessary for phase stability are clarified for each structure type. In solution a sequential series of phase transitions according to the steps calcium oxalate trihydrate-weddellite-whewellite is not likely to be energetically favoured; direct conversion of calcium oxalate trihydrate to whewellite should be, instead, ordinarily expected. It is formally demonstrated that along two axial directions a set of atoms is in essentially identical positions in both weddellite and whewellite. This notwithstanding, it is concluded that epitactic catalysis cannot and should not be considered a common mechanism for the formation of whewellite from weddellite (and vice versa) or of kidney stones in general.

Calcium Oxalate↗
PubMed1979

[The influence of uric acid on the calcium oxalate stone formation (author's transl)].

Statistic analysis of data from 209 calcium oxalate stone patients and 42 stone-free patients pertinent to the concentration and excretion of uric acid in urine and of uric acid levels in the serum yielded no significant difference between the two groups. Only 17% of the calcium oxalate stone patients suffered from hyperuricuria and hyperuricemia was found only in 15% of these patients. Based on these findings, our in-vitro experiments as to the influence of uric acid on calcium oxalate stone formation yielded the following results: firstly, precipitates in urine form only at uric acid concentrations which in-vivo are rate exceptions humans, and secondly, the precipitates at pH 5.5--6.0 always contain uric acid, and a precipitation of calcium oxalate only is never observed. From the experiments one has to conclude that there exists no "salting-out effect" of uric acid on calcium oxalate in urine but rather that precipitate formation reflects the individual solution- and crystallization characteristics of the precipitating compounds.

Calcium Oxalate↗
PubMed1985

Acute oxalate nephropathy after massive ascorbic acid administration.

A single 45-g dose of intravenous ascorbic acid, a metabolic precursor of oxalate, was administered to a patient as adjuvant therapy for primary amyloidosis and the nephrotic syndrome. Acute oliguric renal failure occurred. Postmortem histopathologic examination of renal tissue revealed extensive intratubular deposition of crystalline material, which was confirmed as calcium oxalate by a microincineration technique. There were no extrarenal deposits of calcium oxalate. Plasma oxalate and ascorbic acid concentrations were increased. We conclude that therapy with high-dose ascorbic acid is a potential cause of oxalate nephropathy.

Acute Kidney Injury↗
PubMed1979

Calcium oxalate dihydrate crystal growth.

Calcium oxalate dihydrate (COD), although thermodynamically unstable with respect to calcium oxalate monohydrate (COM), is more commonly seen in human urine. For the first time, a COD-seeded crystal growth assay has been developed. Seed crystals of COD were precipitated from filtered urine by the addition of ammonium oxalate and were stored dry and added to a supersaturated calcium oxalate solution to initiate an experiment. The growth rate in the COD-seeded system was 22 per cent of that for a COM-seeded system, for equivalent surface areas. Urine samples from normal subjects have similar inhibitory activity in the COD- and COM-seeded systems, as do pyrophosphate and heparin, which are known inhibitors of COM crystal growth. These results indicate that the technically simpler COM-seeded growth assay is suitable for measurement of inhibitors of calcium oxalate growth in urine.

Calcium Oxalate↗
PubMed1979

Attenuation by monosodium urate of the inhibitory effect of glycosaminoglycans on calcium oxalate nucleation.

The interaction between mucopolysaccharide (glycosaminoglycans) and monosodium urate, with respect to their effects on spontaneous precipitation of calcium oxalate, was explored in vitro. Heparin and, to a lesser extent, chondroitin sulfate were found to inhibit calcium oxalate precipitation. The formation product ratio (FPR, limit of metastability or the minimum supersaturation required for spontaneous nucleation) of calcium oxalate was increased 29 per cent by 0.05 mg of heparin per liter, and by 70 per cent with 1 mg of heparin per liter. The increment produced by heparin was much less pronounced when the solution containing the mucopolysaccharide was preincubated with crystalline monosodium urate. Pretreatment of the solution containing heparin (0.05 mg per liter) by monosodium urate (0.5 mg per ml) virtually eliminated the inhibitory action of heparin. Studies with radioactive heparin indicated that monosodium urate binds heparin. In contrast, the inhibitory effect of chondroitin sulfate was unaltered by prior exposure to monosodium urate. The results indicated that monosodium urate may attenuate the inhibitor activity of certain mucopolysaccharides such as heparin and facilitate the calcium oxalate precipitation. The findings provide further support for the important etiologic role of hyperuricosuria in the formation of calcium oxalate stones.

Calcium Oxalate↗