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PubMed1999

Nucleation of calcium oxalate crystals by albumin: involvement in the prevention of stone formation.

BACKGROUND: Urine is supersaturated in calcium oxalate, which means that it will contain calcium oxalate crystals that form spontaneously. Their size must be controlled to prevent retention in ducts and the eventual development of a lithiasis. This is achieved, in part, by specific inhibitors of crystal growth. We investigated whether promoters of crystal nucleation could also participate in that control, because for the same amount of salt that will precipitate from a supersaturated solution, increasing the number of crystals will decrease their average size and facilitate their elimination. METHODS: Albumin was purified from commercial sources and from the urine of healthy subjects or idiopathic calcium stone formers. Its aggregation properties were characterized by biophysical and biochemical techniques. Albumin was then either attached to several supports or left free in solution and incubated in a metastable solution of calcium oxalate. Kinetics of calcium oxalate crystallization were determined by turbidimetry. The nature and efficiency of nucleation were measured by examining the type and number of neoformed crystals. RESULTS: Albumin, one of the most abundant proteins in urine, was a powerful nucleator of calcium oxalate crystals in vitro, with the polymers being more active than monomers. In addition, nucleation by albumin apparently led exclusively to the formation of calcium oxalate dihydrate crystals, whereas calcium oxalate monohydrate crystals were formed in the absence of albumin. An analysis of calcium oxalate crystals in urine showed that the dihydrate form was present in healthy subjects and stone formers, whereas the monohydrate, which is thermodynamically more stable and constitutes the core of most calcium oxalate stones, was present in stone formers only. Finally, urinary albumin purified from healthy subjects contained significantly more polymers and was a stronger promoter of calcium oxalate nucleation than albumin from idiopathic calcium stone formers. CONCLUSIONS: Promotion by albumin of calcium oxalate crystallization with specific formation of the dihydrate form might be protective, because with rapid nucleation of small crystals, the saturation levels fall; thus, larger crystal formation and aggregation with subsequent stone formation may be prevented. We believe that albumin may be an important factor of urine stability.

Adult↗
PubMed2000

Oxalate-induced ceramide accumulation in Madin-Darby canine kidney and LLC-PK1 cells.

BACKGROUND: Oxalate exposure produces oxidant stress in renal epithelial cells leading to death of some cells and adaptation of others. The pathways involved in these diverse actions remain unclear, but appear to involve activation of phospholipase A2 (PLA2) and redistribution of membrane phospholipids. The present studies examined the possibility that oxalate actions may also involve increased accumulation of ceramide, a lipid-signaling molecule implicated in a variety of pathways, including those leading to apoptotic cell death. METHODS: Ceramide accumulation was examined in renal epithelial cells from pig kidney (LLC-PK1 cells) and from dog kidney [Madin-Darby canine kidney (MDCK cells)] using the diacylglycerol kinase assay. Sphingomyelin degradation was assessed by monitoring the disappearance of 3H-sphingomyelin from cells that had been prelabeled with [3H]-choline. The effects of oxalate were compared with those of other oxidants (peroxide, xanthine/xanthine oxidase), other organic acids (formate and citrate), and a known activator of sphingomyelinase in these cells [tumor necrosis factor-alpha (TNF-alpha)]. Separate studies determined whether oxalate-induced accumulation of ceramide could be blocked by pretreatment with antioxidants [Mn (III) tetrakis (1-methyl-4-pyridyl) porphyrin (Mn TMPyP, a superoxide dismutase mimetic) or N-acetylcysteine (NAC; an antioxidant)], with an inhibitor of ceramide synthase [fumonisin B1 (FB1)] or with an inhibitor of PLA2 [arachidonyl trifluoromethylketone (AACOCF3)]. RESULTS: Oxalate exposure produced a significant time- and concentration-dependent increase in cellular ceramide. A reciprocal decrease in 3H-sphingomyelin was observed under these conditions. Increases in cellular ceramide levels were also observed after treatment with other oxidants (hydrogen peroxide, and xanthine/xanthine oxidase), activators of sphingomyelinase (TNF-alpha), exogenous sphingomyelinase, or arachidonic acid. Formate produced similar (albeit smaller) effects, and citrate did not. The oxidant-induced increases in ceramide were attenuated by pretreatment with NAC (a glutathione precursor) and MnTMPyP (a superoxide dismutase mimetic), suggesting a role for cellular redox states. The oxalate-induced increase in ceramide was also attenuated by pretreatment with AACOCF3, suggesting a role for PLA2. Pretreatment with FB1 produced a small but statistically insignificant attenuation of the response to oxalate. CONCLUSIONS: Oxalate exposure produces a marked accumulation of ceramide in renal epithelial cells by a process that is redox sensitive and mediated in part by activation of PLA2. Since cellular sphingomyelin decreased as ceramide increased, it seems likely that oxalate actions are mediated, at least in part, by an increase in sphingomyelinase activity, although alterations in ceramide synthase are also possible. Further study is required to define the steps involved in oxalate actions and to determine the extent to which ceramide signaling mediates oxalate actions.

Animals↗
PubMed2000

Experience with the [13C2]oxalate absorption test.

Hyperoxaluria is the most important risk factor for a formation of calcium oxalate-urinary stones. Usually, the bulk of oxalate will be formed in the human body, but in many patients the oxalate from food plays the decisive role. Conventionally, in urine the endogenous oxalate can not be distinguished from food derived oxalate. We have developed a standardized oxalate-absorption test, applying a physiological dose (50 mg disodium salt of [13C2]oxalic acid) of labelled oxalate. The assay has been published. Now we report on the first extensive applications of this test in 86 volunteers and 135 patients from different groups with calcium oxalate stones or an increased risk of the formation of such stones. In one-third of the patients with calcium oxalate-urinary stones an oxalate hyperabsorption was diagnosed. For these patients, a dietetic stone prophylaxis and/or therapy is indicated.

Absorption↗
PubMed2002

Effect of oxalate on the growth of renal tubular epithelial cells.

PURPOSE: Until recently, oxalate was considered merely as a major component of calcium oxalate stones, forming crystals in the lumen of the renal tubules. However, new evidence suggests that oxalate is not only a major constituent of calcium oxalate stones but also has effect on renal tubular epithelial cells, affecting the pathogenesis of nephrolithiasis. We tried to elucidate the effect of oxalate on the growth of renal tubular epithelial cells of different species and locations and also to interpret the possible role of the oxalate in the pathogenesis of urolithiasis. MATERIALS AND METHODS: Porcine proximal renal tubular epithelial cells (LLC-PK1) and canine distal renal tubular epithelial cells (MDCK) were incubated with different concentrations of oxalate, and the effect of oxalate on the growth of the cells was assessed by methylthiazoletetrazolium assay. RESULTS: Growth of the renal tubular epithelial cells was inhibited with increasing concentrations of oxalate in both proximal and distal lines. CONCLUSION: Oxalate may cause stone formation by affecting the growth of renal tubular epithelial cells as well as by providing a constituent of calcium oxalate stones.

Animals↗
PubMed2005

Oxalate clearance by haemodialysis--a comparison of seven dialysers.

BACKGROUND: In patients with primary hyperoxaluria (PH) and oliguric end-stage renal disease, oxalate removal is largely dependent on the clearance by dialysis. Data on the oxalate clearance of newer dialyser types are scarce or absent. Therefore, we measured oxalate clearances of seven dialysers in a single 52-year-old female patient with PH. Since haemodiafiltration (HDF) has been advocated to increase oxalate clearance, we also assessed the effect of different pre-dilution flows. The goal of the study was to select the dialyser and pre-dilution flow combination with the highest oxalate clearance. METHODS: Oxalate clearances were assessed by simultaneously taking afferent blood and efferent dialysate samples at 30, 60, 120 and 180 min after the start of haemodialysis. Blood flow and dialysate flow were 350 and 500 ml/min, respectively. All dialysers were tested at a pre-dilution flow of 2 l/h. Six dialysers were also tested at either a pre-dilution flow of 4.5 l/h or without HDF, depending on the ultrafiltration coefficient of the dialyser. RESULTS: Oxalate clearances differed markedly between the tested dialysers, ranging from 144+/-10 to 220+/-12 ml/min. The highest oxalate clearances were achieved with HdF100S (219+/-10 ml/min) and Sureflux FB-210U (220+/-12 ml/min) at a pre-dilution flow of 2 l/h. Higher pre-dilution flows (2 l/h vs no HDF or 4.5 vs 2.0 l/h) yielded similar oxalate clearances. CONCLUSION: The highest oxalate clearances were achieved with a high-flux polysulfone and a cellulose triacetate dialyser with a large surface area. Higher pre-dilution flows did not augment oxalate clearance.

Equipment Design↗
PubMed2004

Oxalate production by Sclerotinia sclerotiorum deregulates guard cells during infection.

Oxalic acid is a virulence factor of several phytopathogenic fungi, including Sclerotinia sclerotiorum (Lib.) de Bary, but the detailed mechanisms by which oxalic acid affects host cells and tissues are not understood. We tested the hypothesis that oxalate induces foliar wilting during fungal infection by manipulating guard cells. Unlike uninfected leaves, stomatal pores of Vicia faba leaves infected with S. sclerotiorum are open at night. This cellular response appears to be dependent on oxalic acid because stomatal pores are partially closed when leaves are infected with an oxalate-deficient mutant of S. sclerotiorum. In contrast to oxalate-deficient S. sclerotiorum, wild-type fungus causes an increase in stomatal conductance and transpiration as well as a decrease in plant biomass. Green fluorescent protein-tagged S. sclerotiorum emerges through open stomata from the uninfected abaxial leaf surface for secondary colonization. Exogenous application of oxalic acid to the detached abaxial epidermis of V. faba leaves induces stomatal opening. Guard cells treated with oxalic acid accumulate potassium and break down starch, both of which are known to contribute to stomatal opening. Oxalate interferes with abscisic acid (ABA)-induced stomatal closure. The Arabidopsis (Arabidopsis thaliana) L. Heynh. mutants abi1, abi3, abi4, and aba2 are more susceptible to oxalate-deficient S. sclerotiorum than wild-type plants, suggesting that Sclerotinia resistance is dependent on ABA. We conclude that oxalate acts via (1) accumulation of osmotically active molecules to induce stomatal opening and (2) inhibition of ABA-induced stomatal closure.

Abscisic Acid↗
PubMed1989

Risk factors for urinary calcium oxalate crystals as revealed by their specific enzymatic assay.

Calcium oxalate crystal concentrations were assayed by a new highly specific enzymatic method in 1200 urine samples from normal subjects and stone formers. Examination of the crystals was also carried out by light microscopy and urines were analysed for oxalate, calcium, magnesium, citrate, urate, pH and osmolality. A striking positive correlation was established between urinary oxalate concentration and calcium oxalate crystal concentration as well as incidence of calcium oxalate crystals and aggregates seen by microscopy. A less striking relationship, also supported by light microscopy, was found between calcium oxalate crystal concentration and urinary calcium concentration. A small rise in calcium oxalate crystalluria was seen with increasing osmolality, but no relationship found between concentration or urinary urate, citrate or magnesium and that of calcium oxalate crystals. Higher levels of calcium oxalate crystal concentration appeared in alkaline urines in association with calcium phosphates. The dominance of urinary oxalate as a risk factor for calcium oxalate crystalluria is confirmed.

Calcium↗
PubMed2004

Mitochondrial dysfunction is a primary event in renal cell oxalate toxicity.

BACKGROUND: In cultured renal epithelial cells, exposure to oxalate, a constituent of many kidney stones, elicits a cascade of responses that often leads to cell death. Oxalate toxicity is mediated via generation of reactive oxygen species (ROS) in a process that depends at least in part upon lipid signaling molecules that are generated through membrane events that culminate in phospholipase A2 (PLA2) activation. The present studies asked whether mitochondria, a major site of ROS production, were targets of oxalate toxicity, and if so, whether mitochondrial responses to oxalate were mediated by PLA2 activation. METHODS: Effects of oxalate and various lipids on mitochondrial membrane potential (DeltaPsim) were measured in Madin-Darby canine kidney (MDCK) cell monolayers using 5,5',6,6'-tetrachloro 1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide (JC-1), a DeltaPsim-sensitive dye. Other studies assayed caspases, serine proteases activated during apoptosis, in response to oxalate or lipid signaling molecules. Additional studies asked whether oxalate or lipids produced by PLA2 activation promoted ROS formation in isolated renal mitochondria. RESULTS: Oxalate exposure decreased MDCK cell DeltaPsim within 30 minutes, a response attenuated by arachidonyl trifluoromethyl ketone (AACOCF3), an inhibitor of cytosolic PLA2 (cPLA2). Exposure to arachidonic acid or to lysophosphatidylcholine (lyso-PC), lipid products of PLA2 activation, or to ceramide, another lipid signal generated in MDCK cells following oxalate exposure, also depolarized MDCK cell DeltaPsim and increased the number of caspase-positive cells. Isolated renal mitochondria responded to oxalate, arachidonic acid, lyso-PC, and ceramide by increasing their accumulation of ROS, lipid peroxides, and oxidized thiol proteins. CONCLUSION: These studies suggest that lipid signaling molecules released after oxalate-induced PLA2 activation trigger marked, rapid changes in mitochondrial function that may mediate toxicity in renal epithelial cells.

Animals↗
PubMed2005

Oxalate is toxic to renal tubular cells only at supraphysiologic concentrations.

BACKGROUND: Oxalate-induced tissue damage may play an initiating role in the pathophysiology of calcium oxalate nephrolithiasis. The concentration of oxalate is higher in the renal collecting ducts ( approximately 0.1 to 0.5 mmol/L) than in the proximal tubule ( approximately 0.002 to 0.1 mmol/L). In the present investigation, we studied the damaging effect of oxalate to renal proximal and collecting tubule cells in culture. METHODS: Studies were performed with the renal proximal tubular cell lines, LLC-PK1 and Madin Darby canine kidney II (MDCK-II), and the renal collecting duct cell lines, rat renal cortical collecting duct (RCCD1) and MDCK-I. Confluent monolayers cultured on permeable growth substrates in a two-compartment culture system were apically exposed for 24 hours to relatively low (0.2, 0.5, and 1.0 mmol/L) and high (5 and 10 mmol/L) oxalate concentrations, after which several cellular responses were studied, including monolayer morphology (confocal microscopy), transepithelial electrical resistances (TER), prostaglandin E(2) (PGE(2)) secretion, lactate dehydrogenase (LDH) release, DNA synthesis ([(3)H]-thymidine incorporation), total cell numbers, reactive oxygen species (H(2)O(2)) generation, apoptotic (annexin V and DNA fragmentation), and necrotic (propidium iodide influx) cell death. RESULTS: Visible morphologic alterations were observed only at high oxalate concentrations. TER was concentration-dependently decreased by high, but not by low, oxalate. Elevated levels of PGE(2), LDH, and H(2)O(2) were measured in both cell types after exposure to high, but not to low oxalate. Exposure to high oxalate resulted in elevated levels of DNA synthesis with decreasing total cell numbers. High, but not low, oxalate induced necrotic cell death without signs of programmed cell death. CONCLUSION: This study shows that oxalate is toxic to renal tubular cells, but only at supraphysiologic concentrations.

Animals↗
PubMed1980

Characteristics of anaerobic oxalate-degrading enrichment cultures from the rumen.

Enrichment cultures of rumen bacteria degraded oxalate within 3 to 7 days in a medium containing 10% rumen fluid and an initial level of 45 mM sodium oxalate. This capability was maintained in serially transferred cultures. One mole of methane was produced per 3.8 mol of oxalate degraded. Molecular hydrogen and formate inhibited oxalate degradation but not methanogenesis; benzyl viologen and chloroform inhibited both oxalate degradation and methanogenesis. Attempts to isolate oxalate-degrading bacteria from these cultures were not successful. Oxalate degradation was uncoupled from methane production when enrichments were grown in continuous culture at dilution rates greater than or equal to 0.078 h-1. Growth of the uncoupled population (lacking methanogens) in batch culture was accompanied by degradation of 45 mM oxalate within 24 h and production of 0.93 mol of formate per mol of oxalate degraded. Oxalate degradation by the uncoupled population was not inhibited by molecular hydrogen or formate. Cell yields (grams [dry weight]) per mole of oxalate degraded by the primary enrichment and the uncoupled populations were 1.7 and 1.0, respectively.

Animals↗
PubMed1998

Conductive pathways for chloride and oxalate in rabbit ileal brush-border membrane vesicles.

To evaluate the possibility that an apical membrane conductive pathway for oxalate is present in the rabbit distal ileum, we studied oxalate ([14C]oxalate) and chloride (36Cl) uptake into brush-border membrane vesicles enriched 15- to 18-fold in sucrase activity. Voltage-sensitive pathways for oxalate and chloride were identified by the stimulation of uptake provided by an inwardly directed potassium diffusion potential in the presence of valinomycin. Additionally, outwardly directed oxalate (or chloride) gradients stimulated [14C]oxalate (or 36Cl) uptake to a greater degree in the absence of valinomycin (when intracellular and extracellular potassium are equal) than in the presence of valinomycin. Voltage-dependent anion uptake was poorly saturable: apparent affinity constants were 141 +/- 17 and 126 +/- 8 mM for chloride and oxalate, respectively. Activation energies for the voltage-dependent uptake processes were low: 4.7 and 6.3 kcal/mol for chloride and oxalate, respectively. Sensitivity profiles of voltage-dependent chloride and oxalate uptake to anion transport inhibitors were similar. We conclude that an anion conductance is present in the apical membranes of ileal enterocytes and that this conductance is a candidate pathway for oxalate efflux from the enterocyte during transepithelial oxalate secretion.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1981

Oxalate secretion in the rat proximal tubule.

Simultaneous capillary and luminal microperfusion studies in the proximal convoluted tubule of the rat were performed to examine the transepithelial secretory flux of [14C]oxalate. Increases in the concentration of oxalate in the capillary solution from 0.096 to 4.3 mM resulted in progressively higher rates of oxalate secretion into the lumen. Further increases in the capillary concentration of oxalate indicated a tendency toward a plateau. The inclusion of para-chloromercuribenzoate, sodium cyanide, indanyloxyacetic acid, furosemide, or para-aminohippurate in the capillary solution significantly lowered the secretory flux of oxalate. the addition of probenecid in a concentration of 10(-4) M inhibited oxalate secretion when the oxalate concentration in the capillary solution ranged between 1.1 and 4.3 mM, but did not affect oxalate secretion at higher capillary concentrations of oxalate. These results indicate that oxalate secretion in the rat proximal tubule is an active carrier-mediated process. When considered in conjunction with prior studies, the present investigations suggest the possibility that more than one oxalate secretory system exists in the rat proximal tubule.

Animals↗
PubMed2004

Molecular mechanism of oxalate-induced free radical production and glutathione redox imbalance in renal epithelial cells: effect of antioxidants.

BACKGROUND: Peroxidation of renal cells is a critical event in the nucleation and formation of calcium oxalate crystals under hyperoxaluric conditions. We previously demonstrated that oxalate-induced peroxidative injury is one of the major mechanisms in promoting crystal attachment to renal epithelial cells. METHODS: In this study we have demonstrated that the mechanism of oxalate-induced peroxidative injury is through the induction of TGF-beta1 and glutathione (GSH) redox imbalance in LLC-PK1 cells. RESULTS: LLC-PK1, renal epithelial cells exposed to oxalate had significantly higher reactive oxygen species (ROS) production; higher TGF-beta1 levels, as measured by ELISA (1.89 +/- 0.035 fold increase) or Western blot (1.65 +/- 0.01 fold increase); increased malondialdehyde formation; increased LDH release, and loss of cell viability. In addition, oxalate exposure significantly decreased GSH content, glutathione reductase, glucose-6-phosphate dehydrogenase activities, and increased oxidized GSH content. Treatment with vitamin E, neutralizing anti-TGF-beta antibody, or diphenylene iodium, an inhibitor of NAD(P)H oxidase, significantly inhibited oxalate-induced ROS production and prevented peroxidative injury and cytolysis. Vitamin E, catalase, or desferoxamine treatment also significantly restored the oxalate-induced cellular GSH redox status toward the control level, and vitamin E treatment significantly attenuated the oxalate-mediated increase in TGF-beta1 protein in cultured LLC-PK1 cells. CONCLUSIONS: This is the first study to demonstrate that the mechanism of oxalate-induced free radical production in renal tubular epithelial cells is through the activation of NAD(P)H oxidase via cytokine TGF-beta1 induction. These results also provide direct evidence that antioxidant therapy might prevent calcium oxalate nucleation and kidney stone formation by preventing oxalate-mediated peroxidative injury and GSH redox imbalance.

Antioxidants↗
PubMed1992

Plasma profiles and dialysis kinetics of oxalate in patients receiving hemodialysis.

Regular dialysis treatment (RDT) does not obviate hyperoxalemia of chronic renal failure (CRF). However, there is emerging evidence suggesting that current dialysis prescription is not always associated to progressive oxalate accumulation. In view of the controversy still concerning this issue, we have investigated on plasma profiles and dialysis kinetics of oxalate in patients on RDT. Oxalate was determined by ion chromatography on serum ultrafiltrates and on the whole dialyzate in 23 stable patients on RDT for end-stage renal failure unrelated to primary hyperoxaluria. Nine patients were on traditional hemodialysis (HD) and 14 on soft hemodiafiltration (HDF). Dialysis prescription was set so as to obtain similar KT/V of urea. Mean dialyzer clearance of oxalate (KdOx) was calculated by standard procedures and was compared to urea (KdUrea) and creatinine (KdCr) clearances. Oxalate removal was measured on the whole spent dialyzate. Distribution volume of oxalate (VOx) was estimated by assuming a single-pool model and was used to estimate the oxalate appearance rate (OxAR). Plasma profiles showed that dialysis patients were virtually always hyperoxalemic. However, the threshold of supersaturation for calcium oxalate was exceeded in only 13 of 138 (9.4%) assayed ultrafiltrates, 13% on HD and 7.1% on HDF. Dialysis reduced plasma oxalate by more than 60%. There was a postdialysis oxalate rebound averaging 9.6% at 30 min from the end of dialysis. Plasma oxalate predialysis was independent of sex, age and time on dialysis. KdOx was mildly higher on HDF than on HD, and was lower than both KdUrea and KdCr, irrespective of the dialysis technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

[Autoradiographic studies of oxalate distribution in rat kidney].

BACKGROUND: We performed macro and micro-autoradiographic studies using 14C-oxalate in normal and hyperoxaluric rats in order to elucidate intrarenal distribution of oxalate and to determine where calcium oxalate crystal can be adhere in the kidney. METHODS: Macro and micro-autoradiographic studies of the kidney in normal rats were carried out at intervals of 15, 30 and 90 min after intravenous administration of 14C-oxalate (37 MBq/kg BW). Hyperoxaluria was induced by vitamin B6 deficient diet. The procedure of macro and micro autoradiography is the same as that in normal rat. RESULTS: In normal rats, macroautoradiogram showed that the radioactivity of 14C-oxalate exists in the whole kidney, and microautoradiogram identified this radioactivity mainly in the extraluminal space of renal tubules at 15 min. Macro and micro-autoradiograms taken 90 min after the injection showed practically no radioactivity of 14C-oxalate in the cortex or the medulla, but it was located in the extraluminal space of the papilla. In hyperoxaluric rats, macroautoradiogram showed some spotty accumulations of 14C-oxalate in the inner medulla and papilla. Microautoradiogram revealed that these accumulations are mainly seen in the extraluminal space. CONCLUSION: These results indicate that in normal rats the injected 14C-oxalate remains in the renal papilla, especially in the extraluminal space, when nearly all oxalate was excreted by urine, and in hyperoxaluric rats 14C-oxalate exists there as calcium oxalate crystal or microlith.

Animals↗
PubMed1999

[Calcium oxalate lithiasis. Relationship between biochemical risk factors and crystalline phase of the stone].

OBJECTIVES: To identify biochemical risk factors specific to each crystalline phase of calcium oxalate (calcium oxalate monohydrate and calcium oxalate dihydrate) in order to allow more specific medical management of calcium oxalate stones and better prevention of recurrences. MATERIAL AND METHODS: The authors compared the urine biochemistry (morning and 24-hour) of 19 patients with stones containing more than 95% of calcium oxalate monohydrate with those of 16 patients with stones containing more than 60% of calcium oxalate dihydrate (calcium phosphate < 12%). RESULTS: Urinary calcium, expressed as excretion rate and as concentration, and the calcium/citrate ratio were significantly higher in the calcium oxalate dihydrate group than in the calcium oxalate monohydrate group: (9.2 +/- 3.8 mmol/24 h versus 4.4 +/- 1.7 mmol/24 h); (4.9 +/- 2.1 mmol/l versus 2.4 +/- 1.1 mmol/l); (3.3 +/- 1.6 versus 1.6 +/- 0.7). The mean pH of the morning urine was lower in the calcium oxalate monohydrate group, just below the cut-off value of 5.5. CONCLUSION: There is a strong correlation between predominantly calcium oxalate dihydrate stones and hypercalciuria or calcium/citrate ratio > 3. The close relationship between urine biochemistry and crystalline phases of calcium oxalate confirms the clinical value of morphoconstitutional analysis of urinary stones. Identification of risk factors, based on stone analysis, allows more specific medical management of the stones and, in the longer term, better prevention of recurrences.

Calcium Oxalate↗
PubMed2000

Ascorbate conversion to oxalate in alkaline milieu and Proteus mirabilis culture.

BACKGROUND AND PURPOSE: Ascorbate breakdown reportedly accounts for 30% to 55% of urinary oxalate excreted. Three potential degradation routes can be postulated: bowel, endogenous, and urinary. Because the pH of normal urine ranges from 4.5 to 8.0, the urinary oxalate concentration in the presence of ascorbate may be influenced by urinary pH and environment, so we studied ascorbate conversion to oxalate in standard buffer solution and in urine. About 10% of infection stones associated with Proteus mirabilis are reportedly composed of calcium oxalate, and their pathogenesis is not well explained. Therefore, we studied whether a pH change induced by P. mirabilis contributes to ascorbate conversion to oxalate in vitro. RESULTS: Oxalate production from ascorbate increased as a function of pH (7.0-10.0) and incubation time (30 minutes-24 hours) in standard and urine specimens. Two-hour exposure to pH 10 in a urinary milieu containing approximately 3 mM ascorbate converted approximately 40% of the ascorbate to oxalate, whereas 24-hour exposure to pH 8 in a urinary milieu that was approximately 3 mM ascorbate converted approximately 20% of the ascorbate to oxalate. The pH in Proteus cultures increased to 9.0 at 24 hours of culture. The ascorbate concentration in the culture medium significantly decreased at 12 hours and 24 hours, and the oxalate concentration increased significantly at 24 hours. CONCLUSION: Urinary ascorbate, if present at a high concentration in association with Proteus mirabilis infection, appears to be locally degraded to oxalate, potentially leading to calcium oxalate deposition on infection stones.

Ascorbic Acid↗
PubMed1985

Calcium oxalate urolithiasis in the rat: is it a model for human stone disease? A review of recent literature.

Calcium oxalate stone disease is the most common human urinary stone disease in the Western Hemisphere. To understand different aspects of the disease, calcium oxalate urolithiasis in the rat is used as a model. Spontaneous calcium oxalate urolithiasis is very rare in rats. Thus the disease is experimentally induced and the rats are generally made hyperoxaluric either by administration of excess oxalate, exposure to the toxin ethylene glycol, or various nutritional manipulations. All the experimental models show renal injury associated with crystal deposition. Calcium oxalate crystals are in most cases intraluminal in renal tubules and often attached to the basal lamina of the denuded epithelium. Rat renal papillary tips and fornices appear to be the preferential sites for the deposition of large calcium oxalate calculi. Where urinary supersaturation of calcium oxalate has been studied the crystal forming rat urines are shown to have higher urinary supersaturation of calcium oxalate than their controls. Oxalate metabolism in the rat is nearly identical to that in humans. Thus, in a number of respects, experimental calcium oxalate urolithiasis in the rat is similar to calcium oxalate stone disease in man.

Animals↗