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PubMed1979

Histologic study of the early events in oxalate induced intranephronic calculosis.

The early phases of calcium oxalate crystal formation in rat kidneys after intraperitoneal challenge with sodium oxalate were examined. From the results we conclude that the crystals are formed intraluminally in the proximal tubules of the renal cortex. The size, number, and distribution of calcium oxalate particles depend on the amount of sodium oxalate injected and the time interval after its injection. Tubular necrosis and dilation were evident after administration of higher doses of sodium oxalate. The papillary tip and corticomedullary junction were the preferential sites for crystal localization after longer periods of injections of higher doses of sodium oxalate.

Animals↗
PubMed1984

Intestinal oxalate uptake in castrated male and female rats: evidence for altered brush border membrane composition.

The intestinal uptake rate of oxalate (mumoles/h/g tissue wt.) in castrated male (CM) rats, CM rats administered estradiol, and female (F) rats was 1.8, 1.4 and 1.3 times higher than that of male rats, whereas castrated female (CF) rats and CF rats administered testosterone absorbed oxalate at a rate similar to F rats, thereby, suggesting that gonadectomy affected intestinal uptake of oxalate only in male rats The intestinal oxalate uptake rate in all the groups increased linearly with increasing oxalate concentration (0.1- 6.0 mM). Chemical composition of brush border membrane showed significant changes in the sialic acid, phospholipid and cholesterol content following castration, which may lead to ultrastructural changes in the membrane thereby, increasing the absorption of oxalate.

Animals↗
PubMed1996

Oxalate toxicity in LLC-PK1 cells, a line of renal epithelial cells.

PURPOSE: The present studies assessed the possibility that high concentrations of oxalate may be toxic to renal epithelial cells. MATERIALS AND METHODS: Subconfluent cultures of LLC-PK1 cells were exposed to oxalate, and the effects on cell morphology, membrane permeability to vital dyes, DNA integrity and cell density were assessed. RESULTS: Oxalate exposure produced time- and concentration-dependent changes in the light microscopic appearance of LLC-PK1 cells with higher concentrations ( > 140 microM.) inducing marked cytosolic vacuolization and nuclear pyknosis. Exposure to oxalate also increased membrane permeability to vital dyes, promoted DNA fragmentation and, at high concentrations (350 microM. free oxalate), induced a net loss of LLC-PK1 cells. CONCLUSIONS: Since high concentrations of oxalate can be toxic to renal epithelial cells, hyperoxaluria may contribute to several forms of renal disease including both calcium stone disease and end-stage renal disease.

Animals↗
PubMed1987

Inhibition by citrate of spontaneous precipitation of calcium oxalate in vitro.

Effect of citrate on the spontaneous precipitation of calcium oxalate was examined in synthetic media. Citrate significantly increased the formation product of calcium oxalate. This "direct" measure of inhibitor activity, representing activity product at the point of nucleation, rose by 76% by the addition of citrate sufficient to provide trivalent citrate concentration of 1.49 mM. Moreover, citrate inhibited calcium oxalate crystallization by complexing calcium and lowering calcium oxalate saturation. This "indirect" measure of inhibitor activity was assessed from the concentration product of calcium oxalate at the point of nucleation, since this measure should provide a reflection of both ion pair formation and direct inhibitor activity of citrate. The concentration product exceeded the formation product at all ionic (trivalent) citrate concentrations, particularly at high ionic citrate levels. At the ionic citrate concentration of 1.49 mM, the rise in the concentration product was 373%, which was nearly fivefold that observed for the formation product. The presence of ferric or aluminum cations at a physiologic concentration of 2 mg/l did not modify the increase in formation product produced by citrate. Thus, citrate inhibits calcium oxalate crystallization, largely by complexing citrate, but also by directly affecting nucleation. Presence of ferric or aluminum cations at a physiological concentration does not modify the inhibitor action of citrate.

Calcium Oxalate↗
PubMed1987

The effect of serum on the crystallization of calcium oxalate in whole human urine: inhibition disguised as apparent promotion.

The effect of serum on calcium oxalate crystallization was studied in whole human urine. At concentrations between 0.005% to 0.10% (v/v), serum had no effect on the metastable limit of urine as detected by the Coulter Counter. However, serum caused a marked increase in the number and volume of calcium oxalate crystals deposited in response to an oxalate load. That this increase in volume reflected true deposition of calcium oxalate was confirmed by determining calcium concentration and by including control urines containing added serum but no exogenous oxalate. Analysis of particle size distributions showed that the crystals deposited in the presence of serum were smaller than those occurring in the control. Since serum did not affect the limit of metastability, the enhancement of crystal volume is unlikely to be a result of heterogeneous nucleation. We hypothesize that the apparent promotion effect of serum is due to its inhibition of crystal aggregation which increases the crystal surface area available for calcium oxalate deposition.

Blood↗
PubMed1992

Investigations on macromolecular precipitation inhibitors of calcium oxalate.

Certain important aspects of the urine oxalate tolerance test (OTT) have been revised. The stirring system has been changed and the test has been adapted to the kinetics of calcium oxalate precipitation. True equilibrium conditions are now ensured during the measurements. Furthermore, the endogenous oxalate concentration is determined and taken into consideration. As a result of these changes, the significance of the test results has greatly improved. The effects of the addition of small amounts of zinc on the precipitation of calcium oxalate have been used in a new variation of the OTT. This new test makes it possible to discriminate much faster and more simply between recurrent stone-formers and other subjects. Tamm-Horsfall protein (THP) has been tested for its effect on the precipitation of calcium oxalate by means of OTT. THP inhibits the precipitation of calcium oxalate, but THP of stone-formers has a diminished inhibitory activity. The inhibitory activity of this protein strongly depends on the method by which it is isolated.

Calcium Oxalate↗
PubMed1993

Oxalate status in stone-formers. Two distinct hyperoxaluric entities.

A retrospective analysis of oxalate status in 115 stone-forming individuals revealed hyperoxaluria in 30%. These individuals could be divided into two distinct groups according to urinary oxalate excretion patterns and plasma oxalate levels. The cause of hyperoxaluria in one group may be explained on the basis of increased absorption of dietary oxalate and decreased renal clearance. Hyperoxaluria in the other group appears to be a consequence solely of enhanced endogenous production of oxalate. These two entities can be distinguished from one another in the context of a routine metabolic evaluation of calcium stone disease when urine and plasma oxalate measurements are included.

Adult↗
PubMed1990

Effects of oral pyridoxine upon plasma and 24-hour urinary oxalate levels in normal subjects and stone formers with idiopathic hypercalciuria.

The effect of pyridoxine hydrochloride, 200 mg/day (0.97 mmol/day) for 3 weeks, upon plasma and urinary oxalate has been determined in ten normal subjects and seven patients with idiopathic hypercalciuria while both groups were on low-oxalate diets. Patients had higher basal urinary oxalate levels than normal subjects. In normal subjects pyridoxine administration decreased plasma oxalate levels and raised urinary oxalate. The patients showed no change in either plasma or urinary oxalate.

Calcium↗
PubMed1985

Developmental morphology of calcium oxalate foreign body stones in rats.

Calcium oxalate bladder stones were induced in male rats by implanting plastic foreign bodies and by adding ethylene glycol to their drinking water. The foreign body surface was first coated with cellular debris and some amorphous material. Encrustation with crystals of calcium oxalate started on the third day of implantation. Within 2 weeks the entire surface of a foreign body was covered with crystals and some noncrystalline material. Calcium oxalate monohydrate crystals consisted of platelike crystallites arranged in hemispherulitic or spherulitic habit. Calcium oxalate dihydrate crystals wee basically dipyramidal, a majority of them showing interpenetrant twinning. The stone grew by confluent crystal growth and crystal aggregation. A transformation of calcium oxalate monohydrate crystals to calcium oxalate dihydrate also occurred. The matrix consisting of cellular debris and urinary macromolecules was universally distributed in the stone including the inside of crystal bodies.

Animals↗
PubMed1988

Kinetic factors influencing the dissolution behavior of calcium oxalate renal stones: a constant composition study.

A constant composition method has been used to examine the dissolution kinetics of calcium oxalate renal stones over a wide range of undersaturation in vitro. Demineralization experiments have been carried out with the concentrations of calcium and oxalate ions and ionic strength (hence the solution undersaturation) held constant by the potentiometrically controlled addition of medium electrolyte solution as diluent, triggered by a calcium ion electrode. Kinetic data for renal stones have been compared with results obtained for synthetic calcium oxalate. In addition, constant composition results have been directly compared with results obtained using conventional dissolution methods for both calculi and synthetic calcium oxalate. Overall, calcium oxalate renal stones exhibited markedly different kinetic dissolution behavior as compared with synthetic controls. The renal stone samples dissolved more slowly at all undersaturations, exhibited increased kinetic orders of reaction, and showed reduced sensitivity to solution hydrodynamics. Stones composed of mixed hydrates of calcium oxalate (mono- and di-) came to dihydrate equilibrium in conventional experiments and underwent net dissolution in solutions supersaturated to monohydrate under constant composition conditions. No conversion of di- to monohydrate was observed under these experimental conditions. These results indicate that stone dissolution is strongly influenced by adsorbed inhibitors, presumably including matrix components, which may complicate efforts to develop systemic and/or irrigation measures effective for in situ solubilization.

Calcium Oxalate↗
PubMed2004

Intestinal transport of an obdurate anion: oxalate.

In this review, we focus on the role of gastrointestinal transport of oxalate primarily from a contemporary physiological standpoint with an emphasis on those aspects that we believe may be most important in efforts to mitigate the untoward effects of oxalate. Included in this review is a general discussion of intestinal solute transport as it relates to oxalate, considering cellular and paracellular avenues, the transport mechanisms, and the molecular identities of oxalate transporters. In addition, we review the role of the intestine in oxalate disease states and various factors affecting oxalate absorption.

Animals↗
PubMed2005

Effects of trace metals on the inhibition of calcium oxalate crystallization.

The aim of this study was to examine the possible effects of some trace metals on the inhibition of calcium oxalate crystallization. A test of urinary lithogenic risk was used to follow the crystallization of calcium oxalate from artificial urine in the presence of several metal ions assayed in their physiological concentrations. Interactions of these metal ions with known inhibitors of such crystallization (phytate, pyrophosphate, citrate and chondroitin sulphate) were also investigated. None of the metals affected the inhibition of calcium oxalate crystallization at concentrations approximating those found in normal urine, with the exception of the Fe3+ ions. Interactions of Fe3+ with some urinary components produced both synergic (phytate and pyrophosphate) and negative (citrate) effects on preventing crystallization. These effects are explained in terms of the affinity of the inhibitors for the calcium oxalate crystal surface and their ability to form stable complexes in urine. Because of the minimal concentrations, we conclude that physiological concentrations of trace elements in urine have no significant influence on calcium oxalate crystallization. In this sense, ferric ions, which exhibit an intrinsic high inhibitory capacity of calcium oxalate crystallization at physiological concentrations, even increased by the concomitant presence of phytate and pyrophosphate, are probably unable to act as powerful inhibitors in the presence of physiological urinary concentrations of citrate, due to the formation of highly stable complexes in solution without inhibitory activity.

Calcium Oxalate↗
PubMed1999

Effect of cola consumption on urinary biochemical and physicochemical risk factors associated with calcium oxalate urolithiasis.

Since stone formers are advised to increase their intake of fluid, the present study was undertaken to determine the effect of cola beverage consumption on calcium oxalate kidney stone risk factors. Fourteen males and 31 females provided 24-h urines before and after an acute load of cola. Relative supersaturations, activity products and empirical risk indices, ratios and quotients were calculated from urinary biochemical data to assess calcium oxalate crystal and stone formation risk. Several risk factors changed unfavourably following consumption of cola. In males, oxalate excretion, the Tiselius risk index and modified activity product increased significantly (P < 0.05). In females, oxalate excretion increased significantly while magnesium excretion and pH decreased significantly (P < 0.05). Scanning electron microscopy showed that urines obtained from both sexes after cola consumption supported calcium oxalate crystallization to a greater extent than the control urines. It is concluded that consumption of cola causes unfavourable changes in the risk factors associated with calcium oxalate stone formation and that therefore patients should possibly avoid this soft drink in their efforts to increase their fluid intake.

Adult↗
PubMed2005

Intestinal oxalate absorption in patients with continent urinary diversion.

The objective of the study is to evaluate the post-operative effect of an orthotopic ileal neobladder or a Mainz pouch I bladder replacement on the extent of intestinal oxalate absorption. Gastrointestinal oxalate absorption was measured in six patients with an orthotopic ileal neobladder and in six patients with a Mainz pouch I bladder replacement. The function test applied was the [13C2]oxalate absorption test. With a range of 5.1-12.4%, the oxalate absorption of these patients was well within the reference range for healthy volunteers. The results from our small study indicate that such continent urinary diversions present no hazard for oxalate hyperabsorption and subsequent calcium oxalate urolithiasis.

Aged↗
PubMed1984

Effect of pyridoxine deficiency on intestinal absorption of calcium and oxalate: chemical composition of brush border membranes in rats.

[U-14C]oxalic acid and 45Ca uptake was measured in control and vitamin B6-deficient rats. Calcium and oxalate uptake rates were significantly increased from the intestine of vitamin B6-deficient rats as compared to pair-fed controls. Oxalate uptake in pair-fed control rats follows a passive diffusion. In pyridoxine-deficient rats, the oxalate uptake increases nonlinearly as the oxalate concentration in the incubation medium increased, indicating a two-component system--a saturable sodium-independent uptake and a linear nonsaturable passive-diffusion component. The brush border membrane composition reveals that membrane sialic acid, cholesterol, and protein contents were markedly reduced. These aberrations in the chemical composition of brush border membrane may be responsible for the enhanced oxalic acid uptake in vitamin B6-deficient rats.

Animals↗
PubMed1990

Does Tamm-Horsfall mucoprotein inhibit or promote calcium oxalate crystallization in human urine?

Using two different experimental techniques, Tamm-Horsfall mucoprotein (THM) has been reported both to inhibit and to promote calcium oxalate (CaOx) crystallization in ultrafiltered human urine. In this study, these two techniques were used to compare the effects of THM on CaOx crystallization in the same ultrafiltered urine samples. Urine was collected from 10 healthy men and ultrafiltered (10,000 Da). Each sample was divided and to one half was added sufficient human THM to give a final concentration of 35 mg/L. CaOx crystallization was induced in the samples by addition of an oxalate load and by evaporation. Using the evaporation technique THM significantly increased the deposition of CaOx determined as 14C-oxalate, from 9,772 cpm to 43,652 cpm (P less than 0.01). Using the oxalate load method THM had no effect on the metastable limits of the urine with respect to CaOx, and significantly increased the volume of particulate material deposited from 26,000 to 39,995 microns 3/microliters - an increase of 54%. This increase was reduced to 21% when values were corrected for the volume of THM particles recorded in control samples to which no oxalate load was added. Using 14C-oxalate, it was shown that this increase in volume could not be attributed to an enhanced deposition of crystalline CaOx, but was probably the result of an increased polymerization of THM in the presence of CaOx crystals. Despite this, the average size of the particles precipitated in the presence of THM (6.5 microns) was significantly (P less than 0.01) less than that observed in the absence of THM (12.1 microns). It was concluded that the effect of THM on CaOx crystallization in urine depends upon the methodology used to assess it and that promotion would only be expected in vivo in cases of extreme dehydration. Under usual physiological conditions THM would be expected to inhibit CaOx crystal aggregation and to have little effect, if any, on the amount of crystalline material deposited.

Adult↗
PubMed2005

The association of different urinary proteins with calcium oxalate hydromorphs. Evidence for non-specific interactions.

It has been proposed that various urinary proteins interact specifically with different calcium oxalate hydromorphs and these interactions have important implications regarding the understanding of the onset and progress of kidney stone disease. Calcium oxalate monohydrate and dihydrate crystals were grown and characterised thoroughly to establish sample purity. These crystals were then incubated in artificial urine samples containing isolated urinary macromolecules. Crystal growth was prevented by saturating the incubation mix with calcium oxalate, and this was confirmed through electron microscopy and calcium measurements of the incubation mix. The surface interactions between the different calcium oxalate hydrates and urinary proteins were investigated by the use of Western blots and immunoassays. The same proteins, notably albumin, Tamm-Horsfall protein, osteopontin and prothrombin fragment 1, associated with both hydrates. There was a trend for more protein to associate with calcium oxalate dihydrate, and greater quantities of different proteins associated with both hydrates when Tamm-Horsfall protein was removed from the incubation mix. There is no evidence from this study to indicate that particular proteins interact with specific calcium oxalate hydrates, which in turn suggests that these protein-mineral interactions are likely to be mediated through non-specific charge interactions.

Adult↗
PubMed2005

Counteraction of oxalate induced nitrosative stress by supplementation of l-arginine, a potent antilithic agent.

BACKGROUND: Our understanding of nitrosative stress in the process of urolithiasis is far from complete. Earlier studies carried out in our laboratory demonstrate the presence of nitrated THP in stone formers, l-arginine (l-arg) a precursor of nitric oxide (NO), attenuates the endothelial dysfunction caused by reactive nitrogen species. We investigated the role of l-arg in ethylene glycol (EG)-induced urolithic rat model and observed its antilithic and antioxidative properties. METHODS: Hyperoxaluria was induced using 0.75% EG in drinking water. l-arg [1.25 g/kg body weight] was given orally for a period of 28 days. RESULTS: EG-treated rats showed significant loss in body weight and increase in the activities of oxalate synthesizing enzymes such as glycollic acid oxidase in liver. Lactate dehydrogenase activity in liver and kidney was increased. The activity of the free radical producing enzyme xanthine oxidase, tissue oxalate and calcium levels were significantly increased in EG-treated rats. Depletion in the antioxidant enzymes, membrane bound ATPases and thiol status was observed in these rats. l-arg co-supplementation to EG-treated rats maintained the activities of the oxalate synthesizing enzymes and free radical producing enzymes with in the normal range. Tissue oxalate and calcium levels were also maintained near normal in l-arg treated hyperoxaluric rats. l-arg, by its cytoprotective effect, maintained the thiol status, thereby preserving the activities of the membrane bound ATPases and preventing proteinuria and subsequent weight loss in EG-treated rats. CONCLUSION: l-arg feeding prevents the retention of calcium oxalate crystals in hyperoxaluric rats by way of protecting the renal cells from oxidative injury and also by providing a second line of defense through the normalization of the oxalate metabolism. It reduces the risk of stone formation, by curtailing free radicals and hyperoxaluria as both of them have to work in close association to form stones.

Animals↗