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At least 19 recordsLinked to original sources
PubMed1988

The effect of glucose intake on urine saturation with calcium oxalate, calcium phosphate, uric acid and sodium urate.

The effect of simple carbohydrate intake on the state of urine saturation was studied in 44 patients with calcium kidney stones and in 28 healthy subjects. Renal excretion of calcium, magnesium and oxalate significantly increased and pH of urine decreased after an intake of 100 g glucose in stone formers and healthy subjects. In the basic conditions (before glucose administration) urine was supersaturated with calcium oxalate in stone formers (median 0.55) and healthy subjects (0.24; p less than 0.05). Carbohydrate intake caused a significant increase of the degree of urine saturation with calcium oxalate and uric acid. The degree of urine saturation with brushite and sodium urate after glucose administration did not change. These data suggest that excess of simple carbohydrate consumption may increase the degree of urine saturation with some of the compounds important in stone formation.

Calcium Oxalate↗
PubMed2005

Influence of PSSS additive and temperature on morphology and phase structures of calcium oxalate.

Calcium oxalate (CaOx) particles with different morphologies and phase structures were prepared by a facile precipitation reaction of sodium oxalate with calcium chloride in the absence and presence of poly(sodium 4-styrene-sulfonate) (PSSS) at different temperatures. The as-prepared products were characterized with scanning electron microscopy and X-ray diffraction. The influence of experimental conditions including pH, temperature, and concentration of PSSS and CaC2O4 on the morphologies and phase structures of the prepared calcium oxalate particles were investigated. It was found that variations in the concentration of PSSS and CaC2O4, temperature, and pH significantly influenced the crystal structure, morphology, and particle size of the samples. Various crystal morphologies of calcium oxalate, such as plate, leaf-shaped, bipyramid, and cylinder could be fabricated, depending on the experimental conditions. Higher PSSS concentration and reaction temperature favored the formation of metastable calcium oxalate dihydrate (COD) crystals and stable calcium oxalate monohydrate (COM), respectively. Especially, cylinder-shaped CaC2O4 particles were obtained at 80 degrees C in the presence of PSSS for the first time. This research may provide new insight into understanding and potentially regulating the formation of kidney stones and the control of morphology and phase structures of calcium oxalate particles.

Calcium Oxalate↗
PubMed1993

Circadian rhythms of urinary saturation levels of calcium oxalate and calcium phosphate in normal male individuals.

The circadian rhythms of the calcium oxalate, calcium phosphate, and brushite saturation levels as estimated by the AP(CaOx), AP(CaP), and AP(Bru) indices (Tiselius), respectively, were studied in 5 healthy males on three different occasions. These indices were calculated from the data of urinary specimens collected in 2.5-hour fractions except during sleep. The calcium oxalate and brushite saturation levels peaked between 5:30 and 8:00 am, and these were significantly higher than in the other periods. The calcium phosphate saturation level had two peaks that occurred between 8:00 and 10:30 am and between 1:00 and 6:00 pm. The ion-activity products of octacalcium phosphate and hydroxyapatite, calculated from the AP(CaP) index, exhibited a pattern similar to the AP(CaP) values, indicating a high risk of crystallization for both substances at around the same peak periods. In conclusion, early morning was found to be the high risk period for calcium oxalate and brushite crystallization, while two high risk periods for octacalcium phosphate and hydroxyapatite were detected between 8:00 and 10:30 am and between 1:00 and 6:00 pm.

Adult↗
PubMed2005

Effects of luminal oxalate or calcium oxalate on renal tubular cells in culture.

Oxalate or calcium oxalate crystal-induced tissue damage could be conducive to renal stone disease. We studied the response of renal proximal (LLC-PK1 and MDCK-II) and collecting (RCCD1 and MDCK-I) tubule cell lines to oxalate ions as well as to calcium oxalate monohydrate (COM) crystals. Cells grown on tissue culture plastic or permeable growth substrates were exposed to high (1 mM) and extremely high (5 and 10 mM) oxalate concentrations, or to a relatively large quantity of crystals (146 microg), after which cell morphology, prostaglandin E(2) (PGE(2)) secretion, [(3)H]thymidine incorporation, total cell numbers and various forms of cell death were studied. Morphological alterations, increased PGE(2) secretion, elevated levels of DNA synthesis and necrotic cell death were induced by extremely high, but not by high oxalate. Crystals were rapidly internalized by proximal tubular cells, which stimulated PGE(2) secretion and DNA synthesis and the release of crystal-containing necrotic cells from the monolayer. Crystals did not bind to, were not taken up by, and did not cause marked responses in collecting tubule cells. These results show that free oxalate is toxic only at supraphysiological concentrations and that calcium oxalate is toxic only to renal tubular cells that usually do not encounter crystals. Based on these results, it is unlikely that oxalate anions or calcium oxalate crystals are responsible for the tissue damage that may precede renal stone formation.

Animals↗
PubMed1994

Clinical and biochemical differences in patients with pure calcium oxalate monohydrate and calcium oxalate dihydrate kidney stones.

To examine the factors and patient characteristics predisposing to formation of calcium oxalate monohydrate or calcium oxalate dihydrate kidney stones, we compared blood and 24-hour urine tests, gender distribution and patient age in 2 groups of patients with pure calcium oxalate monohydrate (422) and calcium oxalate dihydrate (68) stones treated at the lithotripsy unit of the Wellesley Hospital and University of Toronto during 4 years. The calcium oxalate monohydrate group included relatively more women (31% versus 16% in the calcium oxalate dihydrate group, chi-square 7.89, p = 0.005). Patients were older in the calcium oxalate monohydrate group (59 +/- 13 versus 51 +/- 13 years, p = 0.001). The calcium oxalate monohydrate group had lower urinary calcium (4.19 +/- 2.34 versus 7.19 +/- 3.38 mmol. per day, p < 0.0001), calcium oxalate relative saturation rate (6.9 +/- 3.9 versus 8.9 +/- 3.3, p = 0.001), brushite relative saturation rate (0.7 +/- 0.8 versus 1.2 +/- 0.9, p = 0.0001) and urinary pH (5.72 +/- 0.75 versus 5.93 +/- 0.72). When corrected for patient age and gender, the calcium oxalate dihydrate group still had higher urine calcium levels. Higher urine pH in the calcium oxalate dihydrate group was age-related. In summary, we present evidence that calcium oxalate dihydrate stones are relatively more common among younger male patients with higher urine calcium levels and higher urine pH.

Adult↗
PubMed1993

Modification of estimation of the urinary ion-activity products of calcium oxalate and calcium phosphate.

Tiselius proposed simplified estimates of the ion-activity products of calcium oxalate, calcium phosphate, and brushite as the AP(CaOx) index, the AP(CaP) index, and the AP(Bru) index, respectively, which allowed assessment of the urinary saturation levels of these lithogenic substances. A number of urinary variables (calcium, magnesium, oxalate, phosphate, citrate, urine volume, and pH) are necessary to derive these indices. In addition, these three indices have correction factors corresponding to the urinary collection periods, although these periods were originally quite limited. In this study, the factors were shown to vary as a function of time. Therefore, they were incorporated into these indices after proper calculation so as to be usable for any collection period less than 24 hours. This means that the factors will now prove more useful in evaluating the urinary saturation levels after short-term collections.

Calcium Oxalate↗
PubMed2002

Oxalate and calcium oxalate mediated free radical toxicity in renal epithelial cells: effect of antioxidants.

In a previous study we demonstrated that oxalate induced free radical injury can promote calcium oxalate stone formation. In the present study, we tested whether the antioxidants vitamin E, superoxide dismutase (SOD), catalase and desferoxamine (DFO) can provide protection against oxalate toxicity in LLC-PK(1) cells. LLC-PK(1) cells were exposed to oxalate (1.0 mM) or oxalate+calcium oxalate monohydrate crystals (COM, 500 microg) for 3, 6, and 9 h. Cellular injury was assessed by lactate dehydrogenase (LDH) release. Malondialdehyde (MDA) content, catalase and glutathione peroxidase activities were also measured. The effect of vitamin E (200 microM), DFO (1.0 mM), SOD (400 U), and catalase (400 U) on oxalate-exposed cells was tested. LLC-PK(1) cells exposed to oxalate showed a significant increase in LDH release and MDA content, which was further elevated when COM crystals were added. Cellular glutathione peroxidase and catalase activities were decreased on exposure to oxalate. The addition of vitamin E, SOD, catalase and DFO significantly reduced the release of LDH and restored glutathione peroxidase and catalase activities towards the control level. The increased formation of MDA on oxalate or oxalate+COM toxicity was restored towards normalization by antioxidants and antioxidant enzymes. The protection rendered by vitamin E was greater than that of SOD, catalase and DFO. We conclude that oxalate associated free radical injury may promote stone formation by providing cellular debris for crystal nucleation and aggregation and augment crystal attachment to other tubular cells. Antioxidant administration may prevent calcium oxalate nucleation and retention in the renal tubules by preventing oxalate mediated peroxidative injury.

Animals↗
PubMed1985

Estimation by infrared spectrophotometer of the calcium oxalate dihydrate to calcium oxalate monohydrate ratio.

According to the theoretical expression for calibration curve as a function of the optical absorption ratio of two peaks and with the analysis of the infrared spectra of the mixture samples of commercial calcium oxalate monohydrate and synthesized calcium oxalate dihydrate, the following quadratic equation was obtained; Y = 1.79 X2 - 30.90 X + 107.04 in which Y is the percentage of the purity of calcium oxalate dihydrate and X is the ratio of the relative optical absorption at 660 cm.-1 (the wave number at a characteristic absorption peak of calcium oxalate monohydrate) to that at 610 cm.-1 (that of calcium oxalate dihydrate) by regarding the line as a base-line that links the absorption valley at around 700 cm.-1 with that at 550 cm.-1 The linear correlation coefficient of the actual purity to the estimated purity obtained from this formula of calcium oxalate dihydrate is 0.995. When this formula is applied to the results derived from the infrared spectra of the mixture samples of commercial calcium oxalate monohydrate and calcium oxalate dihydrate obtained from urinary stones in duplicate in each percentage, the linear correlation coefficient is 0.991. This estimation method by infrared spectrophotometer of the calcium oxalate dihydrate to calcium oxalate monohydrate ratio gave a very close correlation between actual and estimated purity of calcium oxalate dihydrate and seems useful in the study of calcium oxalate urolithiasis.

Calcium Oxalate↗
PubMed1983

A simple technique for assessing the propensity for crystallization of calcium oxalate and brushite in urine from the increment in oxalate or calcium necessary to elicit precipitation.

In an effort to develop a simple and reliable method with which to assess the propensity for spontaneous nucleation of calcium oxalate and brushite in urine, the permissible increment of oxalate and calcium was calculated. This represented the additional amount of oxalate or calcium that could be added to urine in three hours before spontaneous precipitation of calcium oxalate or brushite was initiated. The permissible increment of oxalate inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of calcium oxalate, which was previously shown to reflect a quantitative measure of the likelihood for spontaneous nucleation. Similarly, the permissible increment of calcium inversely correlated (P less than 0.001) with the formation-product ratio-activity-product ratio discriminant score of brushite. The permissible increments in oxalate and calcium were significantly lower (P less than 0.001) in patients with renal stones than in control subjects. Moreover, treatment with thiazides, allopurinol, sodium cellulose phosphate, orthophosphate, and diphosphonate significantly raised the permissible increment of oxalate in patients with stones. Thus, the permissible increment was reliable in discriminating "stone-forming" from control urine and in assessing response to treatment.

Calcium↗
PubMed1990

Comparison of urinary tract infection in calcium oxalate and calcium phosphate stone formers.

To compare the frequency of urine infection in calcium oxalate and calcium phosphate stone formers, we reviewed charts from patients whose last renal stone submitted for analysis was predominantly composed of calcium phosphate in 118 and of calcium oxalate in 223. Positive cultures were commoner, but not significantly, in the phosphate than the oxalate stone formers, both in men (17 vs. 7.6%) and women (22 vs. 15%). Bacteria frequently producing urease were found in only 4% of the phosphate group. Urine leucocytes were slightly more frequent in the oxalate group for men and significantly so for women. The results do not support the concept that calcium phosphate stones are mainly due to infection with urease-producing or other bacteria.

Calcium Oxalate↗
PubMed2003

Conversion of calcium oxalate to calcium phosphate with recurrent stone episodes.

PURPOSE: We have extended our previous observation that the percent occurrence of calcium oxalate stones decreased while that of calcium phosphate stones increased with each new stone event. MATERIALS AND METHODS: The National VA Crystal Identification Center has analyzed veteran patient urinary tract stones from VA hospitals throughout the United States since 1983. We reviewed the composition of 33,198 stones with emphasis on the changes in composition. More than 11,786 stones came from 5,088 recurrent stone formers. Stones were analyzed using high resolution x-ray powder diffraction and Fourier transform infrared spectroscopic techniques. When the stones were investigated as a function of time, it was determined that there was greater variability when samples were more than 30 days apart. RESULTS: The percent occurrence of whewellite, weddelite, apatite, brushite and uric acid in stones increased between 1.0% and 5.9% since our previous study. The percent occurrence of struvite decreased by 2.6%. The percent of calcium oxalate stones decreased while that of calcium phosphate stones increased with each new event. However, the total percent occurrence of all calcium containing stones did not significantly change with recurrent stone events. CONCLUSIONS: Our study suggests a strong trend for the conversion of stone disease from calcium oxalate to calcium phosphate containing stones, which could influence the progression and severity of disease.

Apatites↗
PubMed1978

[Influence of oxianthraquinones on the crystallization of calcium oxalate and calcium phosphate: dissolution of calciumcontaining urinary calculi (author's transl)].

Ruberythric acid and alizarin glucuronide, the biologic secretion product obtained from the alizarin derivative, stop the crystallization of calcium oxalate and calcium phosphate in the physiologic milieu of the urine. This effect is thought to be due to a soluble alizarin glucuronide: calcium chelate (2:1 mol). From this finding, we deduce that the solubility of calcium oxalate and calcium phosphate in the urine of humans can be increased through the oral administration of oxianthraquinone.

Anthraquinones↗
PubMed1984

[Abnormalities in the erythrocyte membrane transport of oxalate in calcium oxalate lithogenesis].

The high incidence of a family history and the observation of abnormally high intestinal absorption and urinary excretion of oxalate suggest to consider idiopathic calcium oxalate nephrolithiasis as a metabolic disease characterized by a disorder in oxalate transport. To test this hypothesis, the flux of 14C Oxalate through the membrane of red blood cells was investigated in 24 calcium oxalate stone formers; 18 of the 24 "idiopathic" calcium oxalate stone formers showed an increased oxalate self exchange (75%). Our data seem to support the possibility that "idiopathic" calcium oxalate nephrolithiasis may be considered as a metabolic disease marked by a defect in transmembrane transport of oxalate.

Adult↗
PubMed2005

Citrate provides protection against oxalate and calcium oxalate crystal induced oxidative damage to renal epithelium.

PURPOSE: Oxalate and calcium oxalate (CaOx) crystals are injurious to renal epithelial cells. The injury is caused by the production of reactive oxygen species (ROS). Citrate is a well-known inhibitor of CaOx crystallization and as such it is one of the major therapeutic agents prescribed. Since citrate increases cellular reduced nicotinamide adenine dinucleotide phosphate and glutathione (GSH), we hypothesized that exogenously administered citrate should act as an antioxidant and protect cells from oxalate induced injury. MATERIALS AND METHODS: We exposed LLC-PK1 and MDCK cells to 500 microM/ml oxalate or 150 mug/cm calcium oxalate crystals for 30, 60 and 180 minutes with or without 3 mg/ml citrate in the medium. We determined cell viability by lactate dehydrogenase release and trypan blue exclusion, ROS involvement by changes in hydrogen peroxide and GSH, and lipid peroxidation by quantifying 8-isoprostane. RESULTS: The presence of citrate was associated with significant decrease in lactate dehydrogenase release (p <0.001) and staining with trypan blue (p <0.05). In addition, there was a significant increase in GSH (p <0.005) and a decrease in the production of hydrogen peroxide (p <0.05) and 8-isoprostane (p <0.0005) secretion into the culture medium when citrate was present in the medium. CONCLUSIONS: Citrate protects cells from oxalate and CaOx crystal induced injury by preventing lipid peroxidation through a decrease in ROS production. The results provide additional data for the beneficial role of citrate therapy for CaOx nephrolithiasis.

Calcium Oxalate↗
PubMed1995

Alterations in MDCK and LLC-PK1 cells exposed to oxalate and calcium oxalate monohydrate crystals.

Structural analysis of human kidney stones reveals the presence of cellular membranes and other cell fragments. Experimentally, calcium oxalate crystallization is facilitated when an exogenous nephrotoxin is given with ethylene glycol, thus providing cellular degradation products to act as heterogeneous nuclei. In this report, we tested whether oxalate alone could act as a cell toxin capable of producing damaged cells without the presence of an exogenous agent. Cultured LLC-PK1 and MDCK cells, when exposed to 1.0 mmol KOx, a concentration at the limit of metastability for calcium oxalate nucleation, were severely damaged as measured by specific lactate dehydrogenase (LDH) release in the spent media and by trypan blue exclusion. This effect was magnified by the addition of pre-formed calcium oxalate monohydrate crystals; the injury was significantly amplified when compared to exposure to oxalate alone. Scanning electron microscopy studies illustrated attachment of crystals to cells with loss of cell-to-cell and cell-to-substrate contact, as cells were released from the monolayer. In both oxalate and combined crystal-oxalate studies, more cells were released from the monolayer and exhibited considerably more damage when compared to controls. Oxalate, at the limit of metastability for calcium oxalate, is a cell toxin and can produce cellular degradation products. This effect is increased significantly by the addition of calcium oxalate monohydrate crystals.

Animals↗
PubMed1987

Role of magnesium in the growth of calcium oxalate monohydrate and calcium oxalate dihydrate crystals.

Since about 85% of synthesized calcium oxalate dihydrate (COD) crystals proved not to have changed into calcium oxalate monohydrate (COM) crystals at 30 min of incubation time at 37 degrees C when our evaluation method of the COD-to-COM ratio was being used, we made a comparative study of the inhibitory effects of magnesium, one of the well-known inhibitors of calcium oxalate stone formation, on the growth of seeded COM and COD crystals. The results demonstrated that magnesium in identical concentrations might have stronger inhibitory effects on the growth of COM crystals than on that of COD crystals and suggested that these different effects of magnesium on the growth of COM and COD crystals might arise not only from the difference between the specific surface areas of COM and COD crystals, but also from that between the direct inhibitory effects of magnesium on these two types of calcium oxalate crystal growth.

Calcium Oxalate↗