Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OXALATES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources
PubMed1999

Absorption of calcium oxalate does not require dissociation in rats.

Calcium absorption is thought to occur only if calcium is in a soluble or dissociated form, although experimental evidence is lacking. The intestinal absorption of calcium oxalate, a small, neutral and virtually insoluble calcium salt, was elucidated in the whole body of awake rats. Suspensions of 45Ca ascorbate, 14C-oxalic acid and doubly labeled 45Ca-[14C]-oxalate were given by gavage to separate groups of rats. Following dosing, blood samples were drawn for up to 240 min through a previously inserted intravenous catheter. Serum was assayed for radioactive tracers, and data were then plotted as fraction of dose over time. Calcium absorption was 15% [with a loading of 0.3 mmol (15 mg) calcium], oxalic acid absorption was 22% and Ca-oxalate absorption was <2%. Appearance of 45Ca from calcium ascorbate and 14C from oxalic acid differed, whereas 45Ca and 14C from doubly labeled Ca-oxalate had identical serum appearance profiles. Therefore, we conclude that calcium oxalate was absorbed intact. Addition of excess, unlabeled calcium to the doubly-labeled calcium oxalate did not alter the relationship of the serum level of the two tracers, confirming absorption of calcium oxalate as the intact salt. Thus, calcium bound as a small, neutral, calcium salt such as calcium oxalate does not have to be dissociated prior to absorption. Possibly other small compounds would be similarly absorbed. These results alter our current understanding of calcium bioavailability from foods and therapeutic agents.

Absorption↗
PubMed1996

In vitro degradation of oxalic acid by human feces.

BACKGROUND: Oxalic acid-degrading bacteria have been isolated from human faces. Therefore, the possibility exists that oxalic acid in food is degraded in human intestine by such bacteria, and absorption and excretion of oxalic acid is reduced. It may be possible that patients who form idiopathic stones have fewer oxalic acid-degrading bacteria than healthy controls. The purpose of this study is to examine the possibility that oxalic acid in food is degraded in the human intestine. METHODS: Nineteen patients with calcium stones and 13 healthy subjects were included in the study. Samples of feces were diluted with Barber medium containing 1 g/L of oxalic acid dihydrate, and 1%, 0.1% and 0.01% suspensions were prepared. These solutions were incubated under anaerobic conditions at 37 degrees C for seven days. The degradation of oxalic acid was estimated by the decrease of oxalic acid in the medium. RESULTS: The feces of almost all persons with or without calculi degraded oxalic acid to some degree. Incomplete or no oxalic acid degradation was found in 15 of the 19 stone-forming patients and in five of the 13 stone-free controls. CONCLUSION: Large numbers of oxalic acid-degrading bacteria were observed less often in the feces of stone-formers than in the feces of stone-free controls.

Adult↗
PubMed2004

Is calcium oxalate nucleation in postprandial urine of males with idiopathic recurrent calcium urolithiasis related to calcium phosphate nucleation and the intensity of stone formation? Studies allowing insight into a possible role of urinary free citrate and protein.

In idiopathic recurrent urolithiasis (IRCU) calcium oxalate and calcium phosphate are components of stones. It is not sufficiently known whether in urine the nucleation (liquid-solid transition) of each salt requires a different environment, if so which environment, and whether there is an impact on stone formation. Nucleation was induced by in vitro addition of oxalate or calcium to post-test meal load whole urine of male stone patients (n=48), showing normal daily and baseline fasting oxaluria. The maximally tolerated (until visible precipitates occur) concentration of oxalate (T-Ox) or calcium (T-Ca) was determined; additionally evaluated were other variables in urine, including total, complexed and free citrate (F-Cit), protein (albumin, non-albumin protein) and the clinical intensity (synonymous metabolic activity; MA) of IRCU. In the first of three trials the accumulation of substances in stone-forming urine was verified (trial-V); in the second (clinical trial 1) two strata of T-Ox (Low, High) were compared; in the third (clinical trial 2) IRCU patients (n=27) and a control group (n=13) were included to clarify whether in stone-forming urine the first crystal formed was calcium oxalate or calcium phosphate, and to identify the state of F-Cit. T-Ox was studied at the original pH (average < 6.0), T-Ca at prefixed pH 6.0; the precipitates were subjected to electron microscopy and element analysis. Trial-V: Among the urinary substances accumulating at the indicated pHs were calcium, oxalate and phosphate, and the crystal-urine ratios were compatible with the nucleation of calcium oxalate, calcium-poor and calcium-rich calcium phosphate; citrate, protein and potassium also accumulated. Clinical trial 1: the two strata exhibited an inverse change of T-Ox and T-Ca, the ratio T-Ox/T-Ca and MA. The initial (before induction of Ox or Ca excess) supersaturation of calcium oxalate and brushite were unchanged, with the difference of proteinuria being borderline. Several correlations were significant (p < or = 0.05): urine pH with citrate and volume, protein with volume and MA, T-Ox with T-Ca and MA. Clinical trial 2: in patients with reduced urine volume and moderate urine calcium excess, the first precipitate appeared to be calcium oxalate, followed by amorphous calcium phosphate. Conversely, when the calcium excess was extreme, calcium-rich hydroxyapatite developed, followed by calcium oxalate; F-Cit, not total and complexed citrate, was decreased in IRCU vs. male controls; F-Cit rose pH-dependently, and the ratio F-Cit at original pH vs. F-Cit at pH 6.0 correlated inversely with the nucleation index T-Ox/T-Ca; MA correlated inversely with the ratio F-Cit at pH 6.0, respectively, original pH, but directly with the urinary albumin/non-albumin protein ratio. In summary 1) to study calcium oxalate and calcium phosphate nucleation in whole urine of IRCU patients is feasible; 2) at this crystallization stage the two substances, dominant in calcium stones, appear intimately linked, 3) in stone-forming urine, calcium phosphate may be ubiquitously present, likely as particles < 0.22 microm; 4) together with co-precipitation of calcium oxalate and calcium phosphate, low F-Cit and alteration of proteinuria may act in concert and accelerate stones.

Adult↗
PubMed2000

[Calcium decreases urinary oxalate].

The effects of calcium supplementation on urinary oxalate excretion was tested in 9 normal subjects, 4 males and 5 females between 23 and 49 years of age. In a crossover study 800 mg calcium was orally administered as active absorbable algal calcium (AAACa) (A) and calcium carbonate (B), and compared with non-calcium containing placebo (C). Calcium, oxalate, osmolality, creatinine and pH were measured in the first three morning urine samples and Ca/osmolality, Ca/osmolality/body weight, Ca/creatinine and oxalate/osmolality were calculated to correct for urine dilution. Ca x oxalate product was also calculated and Ca oxalate crystal in the sediment was microscopically examined and semiquantitatively estimated as -, +, ++, and +++ expressed as 0, 1, 2 and 3 respectively. Urinary Ca excretion was similar in A and B, but significantly larger than C, regardless of the method of correction for dilution. Urinary oxalate excretion tended to be lower in A than in B and C. Urine pH was similar among all three groups. Ca x oxalate product was higher in C than in A and B. AAACa, unlike calcium carbonate, appeared to decrease urinary oxalate excretion and Ca x oxalate product more efficiently than Ca carbonate, suggesting a possibility of inhibiting the formation of Ca x oxalate kidney stones. Formation of calcium oxalate was also tested in vitro by adding oxalate to urine samples and aqueous calcium solution.

Administration, Oral↗
PubMed1990

Renal excretion of oxalate in patients with chronic renal failure or nephrolithiasis.

This study was carried out in order to investigate renal oxalate excretion in a group of normal subjects (n = 40), a group of patients with uremia (n = 52) and a group with nephrolithiasis (n = 34). We found that the mean concentrations of oxalate in the 24-hour urine specimens of both patient groups were below the normal range. Although the renal creatinine clearance (CCR) was significantly decreased in some stone patients (n = 14), decreased renal oxalate clearance was noted only in those patients with severe renal failure. Thus, plasma oxalate was found to be elevated only in patients with chronic renal failure (mean +/- SD, 49.7 +/- 12.4 mumol/l), while the normal value was 17.0 +/- 6.7 mumol/l. The mean tubular excretion fraction of oxalate was also found to increase markedly in uremia with a mean of 26.3 +/- 17.3% (in normal subjects, 11.7 +/- 7.5%), but their mean daily urinary excretion of oxalate decreased to 63.2 mumol/day (mean value of 232.6 mumol/day in normal subjects). A positive correlation was observed between oxalate and creatinine, and between oxalate and calcium excretion, which was not found in normal subjects or patients with kidney stones. In nephrolithiasic patients, the daily excretion of oxalate, calcium and phosphate had no discernible increment and the mean excretory ratio of oxalate, calcium or phosphate to creatinine was all within normal limits. But when the CCR of stone patients was below 80 ml/min, their daily excretion of oxalate and calcium decreased significantly (p less than 0.01) and the excretory ratio of phosphate to creatinine markedly increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Pharmacokinetic study on oxalate in rats].

The pharmacokinetics of oxalate were studied in normal and nephrectomized rats, using radioisotope-labelled oxalate to resolve the mechanism of calcium oxalate stone formation. Plasma disappearance of 14C-oxalate was analyzed with a 2-compartment open model, and each compartment volume, the first-order rate constant for elimination, and the first-order rate constant for transfer between the central compartment and peripheral compartment were obtained. These values were compared with those for inulin. In normal rats, the total distribution volume was 57% of body weight for oxalate and 34% for inulin. The elimination rate constant from the central compartment for oxalate was lower than that for inulin, but oxalate had a much larger central compartment volume than inulin. Thus, the total clearance of oxalate was greater than that of inulin. In nephrectomized rats, total clearance of oxalate decreased to 1/6 of that in normal rats, while total clearance of inulin decreased to 1/27 of that in normal rats. These results suggest that oxalate is more diffusible than inulin, and that oxalate is excreted mainly from the kidney.

Animals↗
PubMed1992

Oxalate transport in cultured porcine renal epithelial cells.

Oxalate-containing kidney stones are the most common type (75%) of renal stones. In order to control oxalate excretion in the urine, a basic understanding of the cellular transport of oxalate is imperative. We have utilized the technique of continuous cell culture to establish and characterize a model system to study renal epithelial cell (LLCPK1) oxalate transport. Our data demonstrate that oxalate uptake in these cells is dependent on time, concentration and energy. The Km for oxalate uptake was 200 microM. Oxalate uptake was decreased at lower temperatures and elevated in an acidic extracellular environment. Both anion exchange inhibitors DIDS and SITS inhibited oxalate uptake. Sulfate, chloride, and bicarbonate decreased oxalate uptake, as did the diuretics bumetanide and furosemide. There was no evidence for the co-transport of oxalate with sodium. Our data show that monolayers of cultured kidney epithelial cells are a valuable model system for study of the basic cellular mechanisms of oxalate transport.

Animals↗
PubMed1977

Intestinal oxalate absorption. I. Absorption in vitro.

Enteric hyperoxaluria and oxalate urolithiasis in patients with ileal resection seem to be caused by intestinal hyperabsorption of oxalate. The mechanism responsible for hyperabsorption of oxalate is not known. Intestinal transport of oxalic acid was therefore examined by an in vitro technique in rat intestine. Oxalic acid was absorbed by a mechanism of simple passive diffusion. The rate of absorption decreased from the colon to the duodenum (colon greater than ileum greater than jejunum greater than duodenum). Bile acids enhanced oxalic acid absorption in the large and small intestine and increased extracellular space; calcium, however, markedly decreased mucosal-serosal transport of oxalic acid. Cholestyramine known to reduce oxalate excretion in hyperuxaluria associated with ileal resection did not directly affect absorption of oxalic acid, but decreased the enhanced absorption of oxalic acid induced by bile acids. The results suggest that the beneficial therapeutic effect of cholestyramine in hyperuxaluria is rather mediated by its bile acid binding activity than by direct binding of oxalic acid.

Animals↗
PubMed2002

Calcium oxalate stone disease: role of lipid peroxidation and antioxidants.

Membrane injury facilitated the fixation of calcium oxalate crystals and subsequent growth into kidney stones. Oxalate-induced membrane injury was mediated by lipid peroxidation reaction through the generation of oxygen free radicals. In urolithic rat kidney or oxalate exposed cultured cells, both superoxide anion and hydroxyl radicals were generated in excess, causing cellular injury. In hyperoxaluric rat kidney, both superoxide and H2O2-generating enzymes such as glycolic acid oxidase (GAO) and xanthine oxidase (XO) were increased, and hydroxyl radical and transition metal ions, iron, and copper were accumulated. The lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), hydroperoxides, and diene conjugates were excessively released in tissues of urolithic rats and in plasma of rats as well as stone patients. The accumulation of these products was concomitant with the decrease in the antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6 phosphate dehydrogenase (G6PD) as well as radical scavengers, vitamin E, ascorbic acid, reduced glutathione (GSH), and protein thiol. All the above parameters were decreased in urolithic condition, irrespective of the agents used for the induction of urolithiasis. Oxalate binding activity and calcium oxalate crystal deposition were markedly pronounced, along with decreased adenosine triphosphatase (ATPase) activity. Lipid peroxidation positively correlated with cellular oxalate, oxalate binding, gamma-glutamyl carboxylase, and calcium level and negatively correlated with GSH, vitamin E. ascorbic acid, and total protein thiol. Antioxidant therapy to urolithic rats with vitamin E, glutathione monoester, methionine, lipoic acid, or fish oil normalised the cellular antioxidant system, enzymes and scavengers, and interrupted membrane lipid and protein peroxidation reaction, ATPase inactivation, and its associated calcium accumulation. Antioxidant therapy prevented calcium oxalate precipitation in the rat kidney and reduced oxalate excretion in stone patients. Similarly, calcium oxalate crystal deposition in vitro to urothelium was prevented by free radical scavengers such as phytic acid and mannitol by protecting the membrane from free radical-mediated damage. All these observations were suggestive of the active involvement of free radical-mediated lipid peroxidation-induced membrane damage in the pathogenesis of calcium oxalate crystal deposition and retention.

Animals↗
PubMed2006

Calcium oxalate saturation in dialysis patients with and without primary hyperoxaluria.

Calcium oxalate supersaturation of the blood is associated with deposition of crystals in various tissues. We measured the serum levels of oxalate, citrate, calcium, and magnesium to estimate their saturation in 112 hemodialysis patients without primary hyperoxaluria and two boys with primary hyperoxaluria. Serum levels of oxalate and citrate were determined by high-performance capillary electrophoresis, while calcium and magnesium were measured by ICP spectroscopy. The serum levels of oxalate, citrate, calcium, and magnesium were 44.9+/-16.5, 138.1+/-54.9 micromol/l, 2.30+/-0.28, and 1.07+/-0.18 mmol/l, respectively, while the levels in patients with primary hyperoxaluria were 83.9+/-34.3, 197.9+/-63.5 micromol/l, 2.53+/-0.15, and 1.14+/-0.34 mmol/l, respectively. Serum calcium oxalate saturation (SS), as calculated by the Equil program, was significantly correlated with the serum oxalate level. Most patients showed metastable supersaturation (1<SS<8.9), which was associated with a serum oxalate level of more than 30 micromol/l. Serum saturation exceeded the formation product (SS=8.9) in some specimens from patients with type 1 primary hyperoxaluria. The serum calcium oxalate saturation [SS(CaOx)] showed a significant positive correlation with the levels of oxalate [Ox], calcium [Ca], and citrate [Cit]: [SS(CaOx)]=-0.3562+34.634[Ox]+0.394[Ca]-0.483[Mg]+0.101[Cit], (all mmol/l, r=0.9848, P<0.01). This formula is useful for estimating the saturation. In conclusion, the serum oxalate level is a good indicator of calcium oxalate saturation and should be monitored accurately while keeping it lower in dialysis patients.

Aged↗
PubMed2005

Oxalate toxicity in renal cells.

Exposure to oxalate, a constituent of the most common form of kidney stones, generates toxic responses in renal epithelial cells, including altered membrane surface properties and cellular lipids, changes in gene expression, disruption of mitochondrial function, formation of reactive oxygen species and decreased cell viability. Oxalate exposure activates phospholipase A2 (PLA2), which increases two lipid signaling molecules, arachidonic acid and lysophosphatidylcholine (Lyso-PC). PLA2 inhibition blocks, whereas exogenous Lyso-PC or arachidonic acid reproduce many of the effects of oxalate on mitochondrial function, gene expression and cell viability, suggesting that PLA2 activation plays a role in mediating oxalate toxicity. Oxalate exposure also elicits potentially adaptive or protective changes that increase expression of proteins that may prevent crystal formation or attachment. Additional adaptive responses may facilitate removal and replacement of dead or damaged cells. The presence of different inflammatory cells and molecules in the kidneys of rats with hyperoxaluria and in stone patients suggests that inflammatory responses play roles in stone disease. Renal epithelial cells can synthesize a variety of cytokines, chemoattractants and other molecules with the potential to interface with inflammatory cells; moreover, oxalate exposure increases the synthesis of these molecules. The present studies demonstrate that oxalate exposure upregulates cyclooxygenase-2, which catalyzes the rate-limiting step in the synthesis of prostanoids, compounds derived from arachidonic acid that can modify crystal binding and may also influence inflammation. In addition, renal cell oxalate exposure promotes rapid degradation of IkappaBalpha, an endogenous inhibitor of the NF-kappaB transcription factor. A similar response is observed following renal cell exposure to lipopolysaccharide (LPS), a bacterial cell wall component that activates toll-like receptor 4 (TLR4). While TLRs are primarily associated with immune cells, they are also found on many other cell types, including renal epithelial cells, suggesting that TLR signaling could directly impact renal function. Prior exposure of renal epithelial cells to oxalate in vitro produces endotoxin tolerance, i.e. a loss of responsiveness to LPS and conversely, prior exposure to LPS elicits a similar heterologous desensitization to oxalate. Renal cell desensitization to oxalate stimulation may have profound effects on the outcome of renal stone disease by impairing protective responses.

Animals↗
PubMed2006

Oxalate modulates thiobarbituric acid reactive species (TBARS) production in supernatants of homogenates from rat brain, liver and kidney: effect of diphenyl diselenide and diphenyl ditelluride.

The aim of this paper was to investigate the mechanism(s) involved in the sodium oxalate pro-oxidative activity in vitro and the potential protection by diphenyl diselenide ((PhSe)(2)) and diphenyl ditelluride ((PhTe)(2)) using supernatants of homogenates from brain, liver and kidney. Oxalate causes a significant increase in the TBARS (thiobarbituric acid reactive species) production up to 4mmol/l and it had antioxidant activity from 8 to 16mmol/l in the brain and liver. Oxalate had no effect in kidney homogenates. The difference among tissues may be related to the formation of insoluble crystal of oxalate in kidney, but not in liver and brain homogenates. (PhSe)(2) and (PhTe)(2) reduced both basal and oxalate-induced TBARS in rat brain homogenates, whereas in liver homogenates they were antioxidant only on oxalate-induced TBARS production. (PhSe)(2) showed a modest effect on renal TBARS production, whereas (PhTe)(2) did not modulate TBARS in kidney preparations. Oxalate at 2mmol/l did not change deoxyribose degradation induced by Fe(2+) plus H(2)O(2), whereas at 20mmol/l it significantly prevents its degradation. Oxalate (up to 4mmol/l) did not alter iron (10micromol/l)-induced TBARS production in the brain preparations, whereas at 8mmol/l onwards it prevents iron effect. In liver preparations, oxalate amplifies iron pro-oxidant activity up to 4mmol/l, preventing iron-induced TBARS production at 16mmol/l onwards. These results support the antioxidant effect of organochalcogens against oxalate-induced TBARS production. In addition, our results suggest that oxalate pro- and antioxidant activity in vitro could be related to its interactions with iron ions.

Animals↗
PubMed2005

Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy: potentially serious and unappreciated complications of Roux-en-Y gastric bypass.

BACKGROUND: Neither the presence nor prevalence of enteric hyperoxaluria has been recognized after Roux-en-Y gastric bypass (RYGBP). We have noted a high rate of oxalate nephrolithiasis and even 2 patients with oxalate nephropathy in this patient population postoperatively. Our aim was to determine the frequency of the occurrence and effects of enteric hyperoxaluria after RYGBP. METHODS: Retrospective review of all patients at our institution diagnosed with calcium oxalate nephrolithiasis or oxalate nephropathy after standard (n = 14) or distal (n = 9) RYGBP. The mean postoperative follow-up was 55 months. RESULTS: A total of 23 patients (14 men and 9 women; mean age 45 years; mean preoperative body mass index 55 kg/m(2)) developed enteric hyperoxaluria after RYGBP, defined by the presence of oxalate nephropathy (n = 2) or calcium oxalate nephrolithiasis (n = 21) and increased 24-hour excretion of urinary oxalate and/or calcium oxalate supersaturation. Enteric hyperoxaluria was recognized after a mean weight loss of 46 kg at 29 months (range 2-85) after RYGBP. Two patients developed renal failure and required chronic hemodialysis. Of the 21 patients with nephrolithiasis, 14 had no history of nephrolithiasis preoperatively, and 19 of 21 required lithotripsy or other intervention. Of the 23 patients, 20 tested had increased oxalate excretion, and 14 of 15 tested had high urine calcium oxalate supersaturation. CONCLUSION: Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy must be considered with the other risks of RYGBP. Efforts should be made to identify factors that predispose patients to developing hyperoxaluria.

Adult↗
PubMed1996

Calcium oxalate stone morphology: fine tuning our therapeutic distinctions.

PURPOSE: We determined specific radiographic morphological patterns of crystallographically analyzed pure and mixed calcium oxalate dihydrate and calcium oxalate monohydrate urinary calculi. MATERIALS AND METHODS: A total of 86 greater than 1 cm. calculi crystallographically analyzed as pure calcium oxalate monohydrate, calcium oxalate dihydrate or admixtures of the 2 types was studied to determine whether various forms of calcium oxalate differed in radiographic morphology. RESULTS: Four distinct radiographic patterns could be identified by plain film roentgenography: group 1--14 patients with smooth edged, homogeneously dense calculi, some with dentate shapes (12 had pure calcium oxalate monohydrate stones), group 2--33 with multinodular calculi with irregular edges and variegated areas of more and less radiodensity (32 had greater than 60% calcium oxalate monohydrate), group 3--33 with a uniform, stippled pattern, often with identifiable radial striations, and with a larger amount of calcium oxalate dihydrate than groups 1 or 2, and group 4--6 with poorly radiodense, loosely aggregated crystals with a lacy structure. CONCLUSIONS: At least 4 patterns of calcium oxalate stones are recognizable by plain film roentgenography. Because the fragility of calcium oxalate calculi is determined by the relative calcium oxalate monohydrate and dihydrate content, pretreatment recognition of these radiographic patterns may affect the selection of a therapeutic modality.

Calcium Oxalate↗
PubMed2002

Expression of osteopontin in rat kidneys: induction during ethylene glycol induced calcium oxalate nephrolithiasis.

PURPOSE: Osteopontin is a well-known component of stone matrix and a strong inhibitor of the nucleation, growth and aggregation of calcium oxalate crystals in vitro. To understand its involvement in vivo in calcium oxalate nephrolithiasis we investigated the renal expression and urinary excretion of osteopontin in normal rats, and rats with hyperoxaluria and calcium oxalate crystal deposits in the kidneys. MATERIALS AND METHODS: Calcium oxalate nephrolithiasis was induced by administering ethylene glycol. Immunohistochemistry and in situ hybridization were done to localize osteopontin and osteopontin messenger RNA in the kidneys, while sensitive reverse transcriptase quantitative competitive template polymerase chain reaction was performed to detect and quantify osteopontin messenger RNA expression. Urinary excretion was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis, and then quantified by densitometry of the Western blots. RESULTS: Osteopontin expression in the kidneys was significantly increased after hyperoxaluria and it increased further after the deposition of calcium oxalate crystals in the kidneys. Urinary excretion of osteopontin increased concomitantly. The results reveal differences in renal responses after exposure to oxalate and calcium oxalate crystals. In normal kidneys osteopontin expression was limited to a small number of cells of the thin limbs of the loop of Henle and papillary surface epithelium. During hyperoxaluria osteopontin expression in the kidneys was increased but still mostly limited to cells of the thin limb and papillary surface epithelium. However, after calcium oxalate crystal deposition osteopontin expression was observed throughout the kidneys, including segments of the proximal tubules. CONCLUSIONS: In response to exposure to oxalate and calcium oxalate crystals renal epithelial cells increase the production of osteopontin, which may have a significant role in calcium oxalate nephrolithiasis.

Animals↗
PubMed1997

Clofibrate feeding to Sprague-Dawley rats increases endogenous biosynthesis of oxalate and causes hyperoxaluria.

The effects of clofibrate feeding (5 g/kg diet) on oxalate metabolism were investigated in male and female rats. Following clofibrate feeding, 24-hour urinary excretion of oxalate increased until 4 days and then reached a plateau. Whereas the contribution of dietary oxalate (1.4 g/kg diet, as potassium salt) to urinary oxalate was less than 5% in both control and clofibrate-treated male rats, the contribution of dietary glycolate (1.0 g/kg diet, as sodium salt) to urinary oxalate was six times higher in clofibrate-treated male rats compared with controls, indicating that the clofibrate-induced hyperoxaluria is due to increased endogenous biosynthesis of oxalate. This was supported by the increased lactate dehydrogenase (LDH) activity observed in liver supernatants of clofibrate-treated rats compared with controls, and the increased rate of conversion of glycolate and glyoxylate to oxalate by clofibrate-treated male rat liver supernatants. Female rats had lower excretion of urinary oxalate and lower levels of liver glycolic acid oxidase (GAO) as compared with males. Clofibrate-treated female rat liver supernatants had higher LDH levels and produced more oxalate from glyoxylate. Thus, it can be concluded that the increase in LDH activity may be the cause of the increased endogenous biosynthesis of oxalate leading to increased urinary excretion of oxalate in male and female rats treated with clofibrate.

Alcohol Oxidoreductases↗
PubMed1983

Sequential studies of oxalate dynamics in primary hyperoxaluria.

We have measured the total plasma clearance, renal clearance and equilibrium distribution volume of [14C]oxalate, and the urinary oxalate excretion rate and plasma oxalate levels at approximately 6 months intervals for up to 2.5 years in five patients with primary hyperoxaluria. The renal clearance and distribution volumes of [99mTc]DTPA (diethylenetriaminepenta-acetate) were measured simultaneously to provide estimates of glomerular filtration rate (GFR) and extracellular fluid volume (ECF). The same measurements were made on each of five normal volunteers. Clearances and distribution volumes were measured with a modified single injection technique. The oxalate clearance was two to three times the simultaneously measured GFR in the patients and control subjects. The renal clearance of oxalate was less than the total plasma clearance in the patients. The oxalate distribution volume was approximately 1.5 times the ECF in both the patients and controls. Only small changes were observed over a 2.5 years period in these particular patients. The plasma oxalate concentration was derived from the urinary oxalate excretion rate and the plasma [14C]oxalate clearance. It was raised in the patients. The oxalate removal rate was derived from the total plasma clearance and the plasma oxalate concentration.

Adolescent↗
PubMed2000

A novel basic protein from human kidney which inhibits calcium oxalate crystal growth.

OBJECTIVES: To isolate calcium oxalate-binding proteins from human kidney and characterize the functional properties. MATERIALS AND METHODS: Calcium oxalate crystals were prepared and allowed to interact at two different pH values with Triton-extracted human kidney homogenate. The proteins in the homogenate were isolated and fractionated on a cellulose column, and purified by high-performance liquid chromatography. The protein with the greatest oxalate binding activity at pH 4.5 was analysed for its amino-acid composition and characterized by Scatchard plot analysis, crystal growth, nucleation and aggregation studies. RESULTS: Three major protein fractions were eluted when calcium oxalate monohydrate was adsorbed at both pH values (designated as fractions I-III, according to their order of elution). The yield of fraction I and III was increased when adsorbed at an acidic pH. However, only fraction III had maximum oxalate binding activity at pH 4.5. When purified, this protein had maximum oxalate binding activity of approximately 270 pmol/mg protein and a molecular weight of approximately 23 kDa. Amino acid analysis showed that 18% of the total molar proportion was of basic amino acids, e.g. lysine and arginine, while acidic amino acids accounted for only 11%. Both alanine and glycine constituted approximately 41% of the total molar proportion. Modifications to the lysine group abolished oxalate-binding activity of the protein. The protein inhibited crystal growth by 82% at 0.8 micromol/L, while it inhibited the nucleation and aggregation of the crystals by 6% and 28%, respectively, at 49 nmol/L. The inhibition of both nucleation and aggregation was higher at pH 5.7 than at pH 7.4. Significantly, the protein induced the formation of intertwined calcium oxalate dihydrate crystals in a medium known to induce the formation of individual dihydrate crystals. CONCLUSION: The protein described here is the first reported basic inhibitor of calcium oxalate crystal growth with oxalate-binding activity at pH 4.5 that modulates calcium oxalate crystallization. It is suggested that this protein may play a physiologically significant role in inhibiting stone formation in acidic urine.

Calcium Oxalate↗