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PubMed1976

Effect of bile salts and fatty acids on the colonic absorption of oxalate.

These studies were designed to evaluate the effect of bile salts and fatty acids on colonic oxalate absorption. Five millimolar deoxycholate significantly increased oxalate absorption from 34.2 +/- 9.4 nmoles per min per g dry weight to 330.4 +/- 47.3 (P less than 0.001) and changed water absorption to water secretion. Deoxycholate also increased the absorption of urea, decreased the electrical potential difference, and increased colonic clearance of oxalate, observations which are consistent with an increase in colonic mucosal permeability. In contrast, taurocholate did not increase oxalate absorption. Ricinoleic acid also significantly increased the absorption. These results suggest that bile salts and fatty acids increase colonic absorption of oxalate. Oleic acid had similar effects on oxalate absorption but was less effective than ricinoleic acid. Octanoic acid, a medium chain fatty acid, did not alter oxalate absorption of oxalate by a nonspecific alteration of mucosal permeability. These observations may further explain many of the clinical phenomena associated with enteric hyperoxaluria.

Animals↗

PubMedDate not supplied

Oxalate removal by differing dialysis techniques.

Secondary hyperoxalemia is a common feature in patients with chronic renal failure, but oxalate removal is not adequately accomplished by regular dialysis treatment. Oxalate removal in two groups of patients, 11 on continuous ambulatory peritoneal dialysis (CAPD) and 12 on hemodialysis (HD), was investigated. HD patients were studied during a regular bicarbonate dialysis and during hemodiafiltration (HDF) with a high convective component (UF = 66 mL/min) and AN69 filter (Hospal Filtral 12, 1.2 m2, Hospal Industrie, Meyzieu, France). All HD and HDF spent dialysate and all 24 hr CAPD effluents were collected; oxalate concentration was measured by high performance liquid chromatography (HPLC) using an ion exchange column. Both oxalate flux and total extraction were statistically higher during HDF treatments (HDF = 1.87 +/- 0.77 mg/min and 335.9 +/- 131.5 mg/session, respectively; HD = 0.99 +/- 0.74 mg/min, 226 +/- 153 mg/session, respectively; p < 0.02). The positive interaction of convective and diffusive fluxes probably played a major role in oxalate removal during treatment with a high convective component; solute-membrane interactions can occur by using either cellulosic or synthetic fibers. In CAPD patients, oxalate removal (76.42 +/- 50.85 mg/day) was lower than in patients on either HD or HDF, although weekly oxalate extraction was statistically no different between CAPD (535.46 +/- 356 mg/week) and HD (677.72 +/- 460.82 mg/week). It was concluded that HDF is more effective than HD or CAPD in oxalate removal. Long-term studies are needed to demonstrate whether these kinetic findings have clinical relevance.

Adult↗

PubMed2005

[Assessment of oxalate concentration in serum and urine of children with renal stones].

UNLABELLED: Oxalate crystals are the main component of renal stones and oxalate urolithiasis is the most common type both in adults and children. The aim of the work was the assessment of oxalate concentration in plasma and urine of children with renal stones. MATERIAL: The examined group (I) consisted of 29 children (12.0 +/- 3.87 years) with confirmed stones in caliceal-pelvic system. The control group (C) was composed of 30 healthy children. METHODS: The oxalate concentration in plasma and urine was measured using an enzymatic method after 3-4 days of hypooxalate diet. Children with congenital abnormalities of urinary tract were excluded. We found 1-5 stones, 0.35-1.5 in diameter. RESULTS: In I group mean plasma oxalate concentration (4.89 +/- 1.58 micromol/l) was higher than in control group (p<0,05). However urinary oxalate concentration exceeded 95 percentile of those obtained in healthy group only in 16 (55%) children, mainly with II and III degree of urolithiasis. In children with urolithiasis we also found hypercalciuria with normal serum calcium concentration. No correlation between plasma and urinary oxalate concentration was found. CONCLUSIONS: 1. Plasma oxalate concentration in children with renal stones is higher than in healthy children. 2. Hyperoxaluria was found in 16 (55%) children with first attack of nephrolithiasis.

Adolescent↗

PubMed1991

Five treatment procedures evaluated for the elimination of ascorbate interference in the enzymatic determination of urinary oxalate.

We evaluated the efficacies of five treatment procedures for eliminating ascorbate interference in the enzymatic determination of urinary oxalate. Aliquots of urine samples, containing different amounts of added ascorbate and oxalate, were individually subjected to ferric chloride, sodium nitrite, sodium periodate, charcoal, or ascorbate oxidase treatment to eliminate ascorbate interference. Oxalate contents of the urine samples were then determined by a banana oxalate oxidase-horseradish peroxidase-linked assay with 3-methyl-2-benzothiazolinone hydrazone and 3-(dimethylamino)benzoic acid as chromogens. Only those urine samples treated with ascorbate oxidase or charcoal consistently gave recovery of oxalate close to 100%. Treatment with other reagents, though improving the recovery of oxalate, gave inconsistent results. On the basis of these data, we describe procedures for simply and reliably assaying oxalate by using banana oxalate oxidase.

Ascorbic Acid↗

PubMed1990

Measurements of urinary state of saturation with respect to calcium oxalate and brushite (CaHPO4.2H2O) in renal stone formers.

Urinary supersaturation with respect to calcium oxalate and/or brushite (CaHPO4.2H2O) is critical for the formation of calcium stones. The aim of this study is to use concentration product ratio (CPR) as a tool to assess the state of urine saturation with respect to calcium oxalate and brushite. One 24-h urine specimen from each of 16 healthy city dwellers (GI), 18 healthy villagers (GII) and 28 villagers with renal stones (GIII) was collected and analyzed for calcium, sodium, potassium, phosphate, uric acid, citrate and oxalate. The CPRs of calcium and oxalate and of calcium and phosphate before and after equilibration of the urine with the corresponding seeding crystals were also determined. Urinary volume and the excretion rate of calcium, potassium, uric acid, citrate and oxalate of GII and of sodium, phosphate, uric acid and citrate of GIII were significantly less than those of GI. The CPRs for calcium oxalate and brushite were 2.9 +/- 0.3 and 1.7 +/- 0.2 for GI, 2.7 +/- 0.2 and 1.3 +/- 0.1 for GII and 2.5 +/- 0.2 and 1.1 +/- 0.1 for GIII, respectively. The CPR values indicated that urine of all groups was generally supersaturated with respect to calcium oxalate salt (CPRs were above 1) and were not different among the groups. With regard to brushite, urine was also supersaturated but the state of supersaturation was less than that of calcium oxalate. Furthermore, instead of being supersaturated, brushite in many urine specimens of GIII was undersaturated and its mean CPR was even significantly less than that of GI (P less than 0.01).

Adult↗

PubMed1989

Oxalate crystallization in the kidney in the presence of hyperuricemia.

It has been a long time since uric acid was suggested to be a promoting factor in calcium oxalate stones, and a number of in vitro studies have been carried out on the relationship between uric acid or urate and calcium oxalate. Concerning in vivo studies, urate or calcium oxalate stone-forming diets were given alone in most cases, and diets that induce formation of stones with different composition have not been given in combinations. We administered a low-concentration oxalemic diet, and a mixed diet containing oxalic acid and uric acid, and biochemically and histologically studied the effects of oxalate and uric acid on kidney stone formation. In the kidney of the animals given the mixed diet, formation of crystalloids of uric acid or urate was evident when no crystallization was noted in the kidney of those given the low concentration oxalemic diet alone. The morphological differences in the uric acid and urate crystalloids in the kidney and the process leading to crystallization of calcium oxalate were examined under transmission and scanning electron microscopy. Histological examination indicated that these uric acid crystals and urate crystals serve as seeds and induce formation and epitaxial growth of calcium oxalate crystals. Our in vivo study provides additional evidence that uric acid is a promoting factor in calcium oxalate stone formation.

Animals↗

PubMed1989

[The effect of mineral water containing calcium on supersaturation of urine with calcium oxalate].

The influence of mineral waters with different calcium content on the urine composition was investigated. Twelve healthy male test persons were housed for 3 x 24 h (once a week) in a climatic chamber under constant resting conditions. The standardized food intake was distributed equally over 24 h. Six 4-h urine samples were collected and chemically analyzed to study the risk of stone formation. The total amount of mineral water (Staatl. Fachingen or Bad Wildunger Helenenquelle) or of tapwater was administered in three portions (700 ml at 9.00, 350 ml at 13.00, 350 ml at 17.00). After mineral water intake, the calcium concentration in the urine was slightly higher. However, the more highly mineralized water caused a significant increase in the urinary magnesium concentration, which persisted into the night. The citrate concentration was increased as a result of alkalization of the urine. After mineral water intake the oxalate excretion was slightly (but not significantly) higher. However, no increased risk of calcium oxalate stone formation was seen when different supersaturation ratios were used as the basis of calculation. In a second study, further 12 volunteers of both sexes were given an oxalate-rich standard meal and 500 ml of the test waters in addition. The urine oxalate concentration was measured hourly for 6 h after the meal, and the total oxalate excretion was calculated. The renal oxalate excretion after mineral water intake was significantly reduced compared with tapwater controls. This effect may be caused by intestinal binding of oxalate by calcium and indicates a further lowering of the risk of calcium oxalate crystallization.

Adult↗

PubMed1988

Oxalate metabolism in end-stage renal disease: the effect of ascorbic acid and pyridoxine.

Oxalate metabolism was studied in ten patients with end-stage renal disease. No patient with primary hyperoxaluria was included in this study. Five patients were on regular haemodialysis and five patients were on chronic ambulatory peritoneal dialysis (CAPD). Oxalate metabolism was assessed by measurement of plasma oxalate concentration (POx), oxalate metabolic pool size (OxMP), tissue oxalate accumulation rate (TOxA), oxalate production rate (OxPR) and dialysis clearance of oxalate (DCOx). These observations were made on three separate occasions in each of the ten patients: initially when the patients were taking a routine ascorbic acid supplement of 100 mg per day; then after a period of 1 month with no ascorbic acid supplement; and then finally after a further period of 1 month's treatment with pyridoxine 800 mg daily. The values for POx, OxMP and TOxA were significantly increased in all ten patients and in the range observed in some patients with type I primary hyperoxaluria. There was no significant difference between immediate prehaemodialysis POx and the POx in the CAPD patients. The DCOx was very much greater during haemodialysis (mean 85 ml/min) than during CAPD (mean 8 ml/min). The acute fall in POx during haemodialysis was greater than 50% of the immediate pre-haemodialysis concentration. Ascorbic acid in a dose of 100 mg/day had no significant effect on the parameters of oxalate metabolism studied. Pyridoxine in a dose of 800 mg/day produced a significant fall in POx in both haemodialysis and CAPD patients.

Adult↗

PubMed1987

The hyperuricosuric calcium oxalate stone former.

Hyperuricosuric patients may form uric acid kidney stones and mixed stones containing both calcium oxalate and uric acid. Some of these patients form pure calcium oxalate stones. Explanation of this syndrome was based on the plausibility of epitaxial growth of calcium oxalate on uric acid crystals acting as substrates. In spite of convincing crystallographic consideration, laboratory experiments did not demonstrate any growth of calcium oxalate on uric acid seeds. An amino acid evidently adsorbing on uric acid seeds and attracting calcium ions could act as a mediating agent, thus realizing the potential of the epitaxial growth of calcium oxalate on uric acid crystals. Administration of allopurinol to hyperuricosuric calcium oxalate stone formers reduced the level of uric acid, consequently preventing the creation of uric acid crystals in urine. It should have removed the direct cause for the formation of calcium oxalate stones. Though undoubtedly more effective than placebo, the therapy with allopurinol was not unequivocally successful. Combined therapy using allopurinol and other drugs which were proved to be beneficial for idiopathic calcium oxalate stone formers, seems to give improved results. The use of procedures for evaluating the effect of therapy on risk factors has been started to predict success in individual cases.

Calcium Oxalate↗

PubMed1988

[A modification of the estimation of urinary oxalate using a Sigma kit].

The Sigma kit for estimating urinary oxalate is an enzymatic procedure. However, some errors were encountered using the standard assay system of the kit. Firstly, an overestimate of oxalate may arise from the oxidation of ascorbate during the alkaline wash stage of the extraction of oxalate from urine. Secondly, an underestimate of oxalate may occur because of incomplete extraction of oxalate. A modified assay system for measurement of urinary oxalate using the kit is reported. The following points were modified: urine was diluted two-fold with 0.2 M EDTA and and 0.2 M citrate buffer (pH 3.0), oxalate from urine was extracted with 0.06 N sodium hydroxide to prevent the overestimation by the oxidation of ascorbate, and a plate mixer and addition of a small magnet to the vial were used in the steps of both absorption and extraction of oxalate to keep the accuracy of the estimation. The linearity of standard curve, reproducibility and recovery rates of the modified method were studied, and good results were obtained (linearity; r = 0.999, CV of reproducibility; 5.3%, recovery rate; 101% (300 microM) and 103% (600 microM). A good correlation was seen between the modified Sigma method and high performance liquid chromatography (r = 0.991).

Chromatography, High Pressure Liquid↗

PubMed1985

Renal tubular excretory transport of oxalate in the chicken.

By use of the Sperber in vivo chicken preparation, infusion of radiolabeled oxalic acid ([14C]oxalate) into the renal portal circulation indicated net excretory transfer of unchanged oxalate. At infusion rates of 0.1 to 100 nmol/min, approximately 26% of the oxalate reaching the kidney was excreted directly into the urine. The excretory transport of oxalate was not altered by infusion of probenecid or terephthalic acid, at rates that blocked completely the excretory transport of simultaneously infused p-aminohippuric acid. Because probenecid and terephthalic acid are also known to inhibit uric acid excretory transport in the chicken kidney, these findings suggest that the transport system for oxalate in the chicken kidney is separate from those handling p-aminohippuric acid and uric acid. The excretory transport of oxalate was decreased by the infusion of alpha-ketoglutaric acid, suggesting that oxalate competes at least in part with other endogenous dicarboxylic acids for uptake at the peritubular membrane.

Animals↗

PubMed1982

Stimulation of synovial fibroblasts by calcium oxalate and monosodium urate monohydrate. A mechanism of connective tissue degradation in oxalosis and gout.

The responses of cultured rabbit synovial fibroblasts to amorphous and microcrystalline calcium oxalate were compared with responses to MSUM. Like urate crystals, crystalline calcium oxalate (but not amorphous oxalate) caused marked stimulation of secretion of latent collagenase and PGE2 after 3 days of culture without significant change in cell protein or gross cellular morphology. Collagenase rose from undetectable levels in control cultures to 32.4 +/- 6.0 and 27.4 +/- 7.9 U/mg of cell protein for crystalline calcium oxalate and MSUM, respectively. PGE2 rose from a control level of 0.24 +/- 0.14 to 19.47 +/- 5.15 and 23 +/- 4.84 micrograms/mg of cell protein for crystalline calcium oxalate and sodium urate compared to 1.22 +/- 0.48 microgram for amorphous calcium oxalate. Although the crystalline species studied caused LDH in the media to increase threefold, this was minimal. Cell stimulation by amorphous oxalate and the crystals did not correlate with membranolytic potential as measured with an erythrocyte lysis assay. Stimulation of resident synovial cells by crystalline calcium oxalate and sodium urate may contribute to the chronic inflammation and destruction of joint tissues that occurs in oxalosis and gout.

Animals↗

PubMed1980

Changes in calcium oxalate crystal, morphology as a function of concentration.

Calcium oxalate solutions in a wide range of concentrations were prepared and allowed to precipitate to determine how alterations in the calcium-to-oxalate ratio and the relative calcium oxalate supersaturation affected crystal morphology. The crystals were examined optically and with X-ray diffraction and their morphology was found to be closely related to relative supersaturation. Calcium oxalate monohydrate was the predominant species at all concentrations in which calcium oxalate precipitate was found. Calcium oxalate dihydrate was found only at high concentrations of both calcium and oxalate and underwent transformation to the monohydrate within 24 hr. Calcium oxalate trihydrate was not detected in any sample.

Calcium Oxalate↗

PubMed1995

Crystallization properties in urine from calcium oxalate stone formers.

PURPOSE: We determine whether stone formers and normal subjects can be distinguished in terms of supersaturation with calcium oxalate, and inhibition of calcium oxalate growth and aggregation. MATERIALS AND METHODS: An estimate of the ion activity product of calcium oxalate was obtained from the analysis of calcium, oxalate, citrate and magnesium in 16-hour urine samples obtained between 6 a.m. and 10 p.m. The inhibition of calcium oxalate crystal growth and aggregation was assessed in 8-hour urine specimens obtained between 10 p.m. and 6 a.m. RESULTS: The ion activity product of calcium oxalate was higher and inhibition of crystal aggregation was lower in stone formers than in normal subjects. Inhibition of crystal growth was lower only in male stone formers. Quotient 1 (10(2) x ion activity product of calcium oxalate/inhibition of crystal growth), quotient 2 (10(2) x ion activity product of calcium oxalate/inhibition of crystal aggregation) and quotient 3 (10(4) x ion activity product of calcium oxalate/[inhibition of crystal growth x inhibition of crystal aggregation]) were significantly higher in stone formers. CONCLUSIONS: The biochemical risk situation in calcium oxalate stone formers can be summarized by quotient 2 or 3.

Calcium Oxalate↗

PubMed1996

Oxalate binding to rat kidney mitochondria: induction by oxidized glutathione.

Increased oxalate binding with negative correlation with reduced glutathione content was observed during lipid peroxidation in rat kidney mitochondria. In presence of oxidized glutathione (GSSG), peroxidized mitochondria lost 48% of protein-SH with concomitant 3-fold increase in oxalate binding activity while control mitochondria lost only 20% protein-SH with only 0.8 fold increase in oxalate binding activity. The GSSG-induced oxalate binding was apparently due to two-fold increased affinity of oxalate to the protein. Reduced glutathione (GSH) inhibited oxalate binding competitively with Ki, 1.4 x 10(-3) M. Urolithic rat kidney mitochondria showed 30-50% increase in oxalate binding activity along with depletion of GSH and protein-SH. These studies suggest that oxalate binding is regulated by thiol status of mitochondria.

Animals↗

PubMed1995

Alterations in intestinal transport of oxalate in disease states.

Normally, absorption of oxalate from dietary sources can occur in all segments of the intestinal tract. However, alterations in both the magnitude and direction of oxalate fluxes across the intestine can occur in disease states. In enteric hyperoxaluria, enhanced absorption of oxalate by the large intestine is caused by increased permeability of a shunt conductance induced by malabsorbed bile salts and fatty acids. In this condition, the contribution of a paracellular passive flux of oxalate moving along its electrochemical gradient will predominate when intraluminal concentrations of free oxalate are high. In contrast, in chronic renal failure, secretion of oxalate can occur across both small and large intestine thereby facilitating extrarenal elimination with subsequent degradation by mucosal substrate-specific microorganisms. Clearly, in recent studies of oxalate transport, the intestine has emerged with an integral role in mass balance of oxalate in health and disease.

Animals↗

PubMed1993

[The effect of different food forms on the urine composition and the risk of calcium oxalate stone formation].

The aim of this 17-day study was to examine the influence of four different diets on urine composition and the risk of calcium oxalate stone formation in 10 healthy male subjects. In the course of phase 0, the subjects were on their individual diet for 2 days. In the following phases I, II, and III the subjects received three different standard diets for a duration of 5 days each. Whereas DIET 1 (normal mixed diet) corresponded to the dietary habits of men aged 19 to 35 years, DIET 2 (balanced mixed diet) and DIET 3 (ovo-lacto-vegetarian diet) were calculated according to the dietary recommendations of the German Society of Nutrition (DGE) for the same age-group. The risk of calcium oxalate stone formation, calculated by the computer program EQUIL of FINLAYSON, was highest on the self-selected diet and on DIET 1, but declined significantly on the intake of DIET 2 by 50% on average compared to DIET 1 and by 61% compared to phase 0. On DIET 3 no further significant decline in the risk of calcium oxalate stone formation was observed. Therefore, it can be concluded that the change of usual dietary habits into a balanced mixed diet significantly reduces the risk of calcium oxalate stone formation. With a vegetarian diet a comparable decline in urine supersaturation of calcium oxalate can be achieved with respect to a mixed diet according to requirements. Since urinary oxalic acid excretion increased significantly, a vegetarian diet is not recommend for calcium oxalate stone patients with absorptive hyperoxaluria.

Adult↗

PubMed1982

Effects of magnesium deficiency on intratubular calcium oxalate formation and crystalluria in hyperoxaluric rats.

Previous studies have shown that magnesium deficiency accelerates renal tubular calcium oxalate monohydrate deposition in rats on chronic hyperoxaluric, lithogenic protocols. The present study was conducted to investigate the effect of magnesium deficiency on intratubular calcium oxalate formation in rats from the 1st day of administration of a hyperoxaluric agent. The objectives were to delineate early ultrastructural features of the formation, mechanisms of retention, and development of renal tubular crystal deposits and to characterize the crystalluria in rats on the hyperoxaluric/hypomagnesuric protocol. Intratubular calcium oxalate monohydrate deposits were found in magnesium deficient rats after only 24 hours of ad libitum administration of 1 per cent ethylene glycol drinking water. Animals on regular food diet did not display renal tubular deposition after 11 days of ethylene glycol administration. Strand- and sheet-like organic material emanating from the luminal wall of the tubules was adherent to the crystals, thereby serving to immobilize them within the tubule. Calcium oxalate monohydrate crystals predominated in the urines of hyperoxaluric/hypomagnesuric animals with intratubular deposits while dihydrate crystals were the primary constituent of urines from rats administered ethylene glycol alone (no intratubular deposition). The results support the supposition that under certain conditions magnesium deficiency is a significant risk factor for intrarenal calcium oxalate deposition and stone formation. Furthermore the identification of calcium oxalate monohydrate crystalluria may be an important indicator of the propensity toward intranephronic calcium oxalate formation and urolithiasis.

Animals↗