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PubMed1984

Change in inhibitory potential in urine of hyperuricosuric calcium oxalate stone formers effected by allopurinol and orthophosphates.

Allopurinol and orthophosphates were used in the treatment of 25 hyperuricosuric calcium oxalate stone formers. Their urines were tested by the Discriminating Index method, which measures the potential of a urine to retard calcium oxalate precipitation in vitro. The tests were performed before any treatment was begun and about 10 days after the commencement of drug intake. An insignificant effect by allopurinol and a markedly significant effect of orthophosphates on Discriminating Index were found. In a few of the patients, allopurinol seemed to cause a decrease in the urine's potential to retard calcium oxalate precipitation. Therefore the effect of allopurinol in 11 hyperuricosuric patients with no history of calcium oxalate stone formation was tested. In 5 of the 11 patients, the urine's potential to retard calcium oxalate precipitation decreased to levels similar to those of calcium oxalate stone formers. The results of this study suggest that hyperuricosuric calcium oxalate stone formers suffer from the same yet-undefined etiology of stone formation as other calcium oxalate stone formers. The results also question the role of uric acid in calcium oxalate stone formation and the efficacy of allopurinol in preventing this disease. It is suggested that allopurinol may even be related to stone formation in some patients.

Allopurinol↗
PubMed1999

Fungal production of citric and oxalic acid: importance in metal speciation, physiology and biogeochemical processes.

The production of organic acids by fungi has profound implications for metal speciation, physiology and biogeochemical cycles. Biosynthesis of oxalic acid from glucose occurs by hydrolysis of oxaloacetate to oxalate and acetate catalysed by cytosolic oxaloacetase, whereas on citric acid, oxalate production occurs by means of glyoxylate oxidation. Citric acid is an intermediate in the tricarboxylic acid cycle, with metals greatly influencing biosynthesis: growth limiting concentrations of Mn, Fe and Zn are important for high yields. The metal-complexing properties of these organic acids assist both essential metal and anionic (e.g. phosphate) nutrition of fungi, other microbes and plants, and determine metal speciation and mobility in the environment, including transfer between terrestrial and aquatic habitats, biocorrosion and weathering. Metal solubilization processes are also of potential for metal recovery and reclamation from contaminated solid wastes, soils and low-grade ores. Such 'heterotrophic leaching' can occur by several mechanisms but organic acids occupy a central position in the overall process, supplying both protons and a metal-complexing organic acid anion. Most simple metal oxalates [except those of alkali metals, Fe(III) and Al] are sparingly soluble and precipitate as crystalline or amorphous solids. Calcium oxalate is the most important manifestation of this in the environment and, in a variety of crystalline structures, is ubiquitously associated with free-living, plant symbiotic and pathogenic fungi. The main forms are the monohydrate (whewellite) and the dihydrate (weddelite) and their formation is of significance in biomineralization, since they affect nutritional heterogeneity in soil, especially Ca, P, K and Al cycling. The formation of insoluble toxic metal oxalates, e.g. of Cu, may confer tolerance and ensure survival in contaminated environments. In semi-arid environments, calcium oxalate formation is important in the formation and alteration of terrestrial subsurface limestones. Oxalate also plays an important role in lignocellulose degradation and plant pathogenesis, affecting activities of key enzymes and metal oxido-reduction reactions, therefore underpinning one of the most fundamental roles of fungi in carbon cycling in the natural environment. This review discusses the physiology and chemistry of citric and oxalic acid production in fungi, the intimate association of these acids and processes with metal speciation, physiology and mobility, and their importance and involvement in key fungal-mediated processes, including lignocellulose degradation, plant pathogenesis and metal biogeochemistry.

Biodegradation, Environmental↗
PubMed2002

Effect of dissolved cobalt(II) on the ozonation of oxalic acid.

Cobalt(II) was examined as an ozonation catalyst. Laboratory-scale batch ozonation experiments were run at near-neutral pH and 24 degrees C. A hydroxyl radical probe compound, p-chlorobenzoic acid (pCBA), was also included in the solution matrix. Batch experiments showed that trace amounts of cobalt(II) accelerated the ozonation of oxalate. The rate of oxalate removal increased with decreasing pH from pH 6.7 to pH 5.3. The presence of cobalt(II) also increased the removal rate of pCBA indicating that the generation of hydroxyl radicals are byproducts of cobalt(II)-catalyzed ozonation of oxalate. It is proposed that the first step in the catalytic ozonation reaction pathway is the formation of a cobalt(II)--oxalate complex. Cobalt(II) oxalate is then oxidized by ozone to form cobalt(III) oxalate. The catalytic cycle is completed with decomposition of the cobalt(III) complex to form cobalt(II) and an oxalate radical. Assuming that cobalt, oxalate, and water were in equilibrium, the second-order reaction rate constants at pH 6 for ozonation of the cobalt(II) monooxalate and dioxalate species were 30 +/- 9 and 4000 +/- 500 M-1 s-1, respectively. These are both much greater than the reaction rate constant for the ozonation of free oxalate (kO3 < or = 0.04 M-1 s-1).

Catalysis↗
PubMed2005

Variation in ascorbic acid and oxalate levels in the fruit of Actinidia chinensis tissues and genotypes.

Ascorbic acid and total oxalate were measured in fruit from six genotypes of Actinidia chinensis. Ascorbic acid was separated from oxalate in fruit extracts by HPLC and quantified from absorbance at 245 nm, whereas oxalate was measured enzymatically in the HPLC eluate. Levels of whole fruit mean ascorbic acid in the different genotypes ranged from 98 to 163 mg/100 g of fresh weight (FW), whereas mean oxalate varied between 18 and 45 mg/100 g of FW. Ascorbic acid was highest in the inner and outer pericarp, whereas oxalate was concentrated in the skin, inner pericarp, and seed. Essentially no ascorbic acid was found in the seed. Each tissue clustered separately when the tissue ascorbic acid and oxalate data were normalized to the whole fruit level of ascorbic acid and oxalate in that genotype and plotted against each other, suggesting that oxalate is not a sink for excess ascorbic acid but that oxalate formation is regulated.

Actinidia↗
PubMed2005

Biodegradation of oxalic acid from spinach using cereal radicles.

A high level of oxalate intake constitutes a health risk for infants and metabolically disposed adults. Spinach, acclaimed for its many health benefits, is among the vegetables richest in oxalate. Blanching reduces oxalate unsatisfactorily and unspecifically. An alternative, biological method is proposed on the basis of rye seedlings or radicles (also barley and wheat) containing an oxalate-specific oxalate oxidase by nature. Dissolved oxalate (0.25 mM) was rapidly degraded in the presence of radicles (e.g., 70% within 100 min). With commercial deep-frozen spinach, near-complete degradation of soluble oxalate was achieved at pH 3.5. The total level of oxalate was reduced by half. Similarly high rates occurred from 18 to 35 degrees C. Even at 55 degrees C appreciable rates were observed. The seedling as a whole is effective, too, and enrichment with cereal-specific healthy components would occur. Removal of oxalate from other vegetables, juices, cycled process waters, or feeds is conceivable with fresh or heat-dried cereal seedlings or radicles.

Biodegradation, Environmental↗
PubMed1999

Oxalates in oca (New Zealand yam) (Oxalis tuberosa Mol.).

Oca (Oxalis tuberosa Mol.) or New Zealand yam, in common with other members of this genus, contains oxalate, an antinutritive factor. Twelve South American and two New Zealand cultivars of oca were analyzed for total and soluble oxalate contents of the tubers. The range of total oxalate levels was 92-221 mg/100 g of fresh weight. Levels of soluble and total oxalate extracted from the tubers were not significantly different, suggesting that no calcium oxalate is formed in the tubers. The oxalate concentrations obtained in this study for oca suggest that previously reported values are too low and that oca is a moderately high oxalate-containing food. This is the first report of a tuber crop containing moderate to high levels of soluble oxalates in the tubers and no insoluble oxalates.

Chromatography, High Pressure Liquid↗
PubMed1993

Relationship of protein intake to urinary oxalate and glycolate excretion.

The relationship of protein intake to urinary oxalate and glycolate excretion was examined in a large cohort (N = 101) of normal individuals on self-selected diets and in 11 individuals on controlled protein diets. On self-selected diets no correlation was detected between protein intake and urinary oxalate or glycolate excretion. A moderate but significant correlation (r = 0.45; P < 0.001) of oxalate with urea excretion was observed in males but not females, suggesting that there may be a link between urea and oxalate synthesis in males. On controlled protein diets mean oxalate excretion in females on days 7 to 10 of a high protein diet (1.8 g/kg body wt) was 20% higher than on a low protein diet (0.6 g/kg body wt; P = 0.02), but there was no difference in males. Glycolate excretion was significantly higher (P < 0.001) on the high protein diet than on the low protein diet in both sexes. Only a weak precursor-product relationship was observed between glycolate and oxalate. A gender effect was apparent on both self-selected and control diets with females excreting more oxalate and glycolate relative to creatinine than males. A pronounced inter- and intra-individual variability in the excretion of oxalate was observed, even on controlled diets. This suggests that genetic factors and physiological changes such as hormonal fluctuations may contribute more to the variability in oxalate excretion than the dietary intake of protein.

Adult↗
PubMed2006

Hydroxyproline ingestion and urinary oxalate and glycolate excretion.

Endogenous synthesis of oxalate is an important contributor to calcium oxalate stone formation and renal impairment associated with primary hyperoxaluria. Although the principal precursor of oxalate is believed to be glyoxylate, pathways in humans resulting in glyoxylate synthesis are not well defined. Hydroxyproline, a component amino acid of collagen, is a potential glyoxylate precursor. We have investigated the contribution of dietary hydroxyproline derived from gelatin to urinary oxalate and glycolate excretion. Responses to the ingestion of 30 g of gelatin or whey protein were compared on controlled oxalate diets. The time course of metabolism of a 10 g gelatin load was determined as well as the response to varying gelatin loads. Urinary glycolate excretion was 5.3-fold higher on the gelatin diet compared to the whey diet and urinary oxalate excretion was 43% higher. Significant changes in plasma hydroxyproline and urinary oxalate and glycolate were observed with 5 and 10 g gelatin loads, but not 1 and 2 g loads. Extrapolation of these results to daily anticipated collagen turnover and hydroxyproline intake suggests that hydroxyproline metabolism contributes 20-50% of glycolate excreted in urine and 5-20% of urinary oxalate derived from endogenous synthesis. Our results also revealed that the kidney absorbs significant quantities of hydroxyproline and glycolate, and their metabolism to oxalate in this tissue warrants further consideration.

Adult↗
PubMed1979

Plasma level and renal clearance of oxalate in normal subjects and in patients with primary hyperoxaluria or chronic renal failure or both.

1. Plasma oxalate has been measured by a radioisotopic method applicable to all concentrations of plasma oxalate and renal function, and also by an enzymatic method which was only applicable to raised concentrations of plasma oxalate. 2. Where the two methods could be applied simultaneously, the agreement between them was good. 3. Plasma oxalate was 86% ultrafiltrable at concentrations of up to 44 micromol/l. 4. Oxalate clearance and the exchangeable oxalate pool were also measured. The ratio of oxalate clearance to creatinine clearance was greater than unity in most normal subjects and patients. 5. These methods were used in normal subjects and in patients with primary hyperoxaluria and/or chronic renal failure. A raised plasma oxalate concentration was found in both conditions. Chronic renal failure is probably the most common cause of a raised plasma oxalate.

Adult↗
PubMed1995

The urinary F1 activation peptide of human prothrombin is a potent inhibitor of calcium oxalate crystallization in undiluted human urine in vitro.

1. The urinary F1 activation peptide of prothrombin is the predominant protein incorporated into calcium oxalate crystals precipitated from human urine. The aim of this study was to examine the effect of pure urinary prothrombin F1 on calcium oxalate crystallization in human urine. 2. Urinary prothrombin F1 was purified from demineralized calcium oxalate crystals precipitated from human urine, and its effects on calcium oxalate crystallization induced by addition of an oxalate load were tested in undiluted, ultrafiltered urine from healthy men, at final concentrations of 0 to 10 mg/l. 3. Urinary prothrombin F1 did not affect the amount of oxalate required to induce crystallization, but the volume of material deposited increased in proportion to increasing concentrations of urinary prothrombin F1. However, the mean particle size decreased in reverse order: this was confirmed by scanning electron microscopy, which showed it to be the result of a reduction in crystal aggregation rather than in the size of individual crystals. Analysis of 14C-oxalate data revealed a dose-dependent decrease in calcium oxalate deposition with an increase in urinary prothrombin F1 concentration, indicating that the increase in particle volume recorded by the Coulter Counter resulted from inclusion of urinary prothrombin F1 into the crystalline architecture, rather than increased deposition of calcium oxalate. 4. It was concluded that urinary prothrombin F1 may be an important macromolecular determinant of stone formation.

Calcium Oxalate↗
PubMed1998

Inhibition of growth and aggregation of calcium oxalate crystals in vitro--a comparison of four human proteins.

The aim of this study was to compare directly, in the absence of interfering contaminants, the inhibitory effects of Tamm-Horsfall glycoprotein (THG), human serum albumin (HSA), alpha1-microglobulin and prothrombin fragment 1 (PTF1) on calcium oxalate crystallization. These proteins have been detected in urinary calculi, and with the exception of THG in calcium oxalate crystals generated from undiluted human urine. THG was isolated from the urine of healthy men, while PTF1 was purified from Prothrombinex-HT, a human blood concentrate; HSA and alpha1-microglobulin were obtained from commercial sources. The effects of these proteins were determined, separately, at the same final concentration (32 nM) on calcium oxalate crystallization in a seeded, inorganic reaction system, using Coulter Counter and [14C]oxalate analysis. Analysis of [14C]oxalate data showed that THG, HSA and alpha1-microglobulin had no measurable effect on deposition of calcium oxalate. However, PTF1 significantly inhibited mineral deposition by 19.6%. The average size of the particles precipitated was reduced from the control value of 8.6 microm to 7.3, 5.9, 5.6 and 4.0 microm in the presence of alpha1-microglobulin, HSA, THG and PTF1 respectively. These findings were confirmed by scanning electron microscopy, which also revealed that the smaller particles deposited in the presence of the proteins resulted from reduced crystal aggregation rather than a decrease in the size of the individual crystals. It was concluded that, on a molar basis, PTF1 is a more potent inhibitor of calcium oxalate crystal aggregation than THG, HSA and alpha1-microglobulin. Moreover, unlike those proteins it significantly inhibits the deposition of calcium oxalate. These findings have implications for the putative role of urinary proteins in the formation of calcium oxalate stones.

Alpha-Globulins↗
PubMed2003

Effect of vitamin C supplements on urinary oxalate and pH in calcium stone-forming patients.

BACKGROUND: The contribution of ascorbate to urinary oxalate is controversial. The present study aimed to determine whether urinary oxalate and pH may be affected by vitamin C supplementation in calcium stone-forming patients. METHODS: Forty-seven adult calcium stone-forming patients received either 1 g (N=23) or 2 g (N=24) of vitamin C supplement for 3 days and 20 healthy subjects received 1 g. A 24-hour urine sample was obtained both before and after vitamin C for calcium, oxalate, magnesium, citrate, sodium, potassium, and creatinine determination. The Tiselius index was used as a calcium oxalate crystallization index. A spot fasting morning urine sample was also obtained to determine the urinary pH before and after vitamin C. RESULTS: Fasting urinary pH did not change after 1 g (5.8 +/- 0.6 vs. 5.8 +/- 0.7) or 2 g vitamin C (5.8 +/- 0.8 vs. 5.8 +/- 0.7). A significant increase in mean urinary oxalate was observed in calcium stone-forming patients receiving either 1 g (50 +/- 16 vs. 31 +/- 12 mg/24 hours) or 2 g (48 +/- 21 vs. 34 +/- 12 mg/24 hours) of vitamin C and in healthy subjects (25 +/- 12 vs. 39 +/- 13 mg/24 hours). A significant increase in mean Tiselius index was observed in calcium stone-forming patients after 1 g (1.43 +/- 0.70 vs. 0.92 +/- 0.65) or 2 g vitamin C (1.61 +/- 1.05 vs. 0.99 +/- 0.55) and in healthy subjects (1.50 +/- 0.69 vs. 0.91 +/- 0.46). Ancillary analyses of spot urine obtained after vitamin C were performed in 15 control subjects in vessels with or without ethylenediaminetetraacetic acid (EDTA) with no difference in urinary oxalate between them (28 +/- 23 vs. 26 +/- 21 mg/L), suggesting that the in vitro conversion of ascorbate to oxalate did not occur. CONCLUSION: These data suggest that vitamin C supplementation may increase urinary oxalate excretion and the risk of calcium oxalate crystallization in calcium stone-forming patients.

Adult↗
PubMed2002

Oxalate selectively activates p38 mitogen-activated protein kinase and c-Jun N-terminal kinase signal transduction pathways in renal epithelial cells.

Oxalate, a metabolic end product, is an important factor in the pathogenesis of renal stone disease. Oxalate exposure to renal epithelial cells results in re-initiation of the DNA synthesis, altered gene expression, and apoptosis, but the signaling pathways involved in these diverse effects have not been evaluated. The effects of oxalate on mitogen- and stress-activated protein kinase signaling pathways were studied in LLC-PK1 cells. Exposure to oxalate (1 mM) rapidly stimulated robust phosphorylation and activation of p38 MAPK. Oxalate exposure also induced modest activation of JNK, as monitored by phosphorylation of c-Jun. In contrast, oxalate exposure had no effect on phosphorylation and enzyme activity of p42/44 MAPK. We also show that specific inhibition of p38 MAPK by 4(4-(fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridyl)imidazole (SB203580) or by overexpression of a kinase-dead dominant negative mutant of p38 MAPK abolishes oxalate induced re-initiation of DNA synthesis in LLC-PK1 cells. The inhibition is dose-dependent and correlates with in situ activity of native p38 MAP kinase, determined as MAPK-activated protein kinase-2 activity in cell extracts. Thus, this study not only provides the first demonstration of selective activation of p38 MAPK and JNK signaling pathways by oxalate but also suggests that p38 MAPK activity is essential for the effects of oxalate on re-initiation of DNA synthesis.

Animals↗
PubMedDate not supplied

The effect of soaking and cooking on the oxalate content of taro leaves.

Pacific Island people commonly eat taro (Colocasia esculenta var. Schott) as a staple food in their home islands and also like to consume this familiar food when living in New Zealand. Some of these foods are imported from the islands and some attempts are, currently, being made to grow these crops in New Zealand. The taro leaves in this experiment were grown in a greenhouse in the North Island of New Zealand. The soluble oxalate content of the raw leaves was 236.10 mg oxalate/100 g wet matter (WM). Soaking the raw leaves in water for 30 min marginally reduces the soluble oxalate content by leaching into the tap water. Soaking for 18 h results in a 26% reduction in the soluble oxalate content of the raw leaves. During the soaking treatments the insoluble oxalate (calcium oxalate) content of the leaves remained constant (mean 171.64 mg oxalate/100 g WM). Boiling the taro leaves resulted in a 36% loss of soluble oxalates, while the soluble oxalate content of baked tissue was very similar to the raw tissue. The mean insoluble oxalate content of the raw, boiled and baked tissue was 226.28 mg oxalate/100 g WM. Overall, boiling the taro leaves was an effective way of reducing the soluble oxalate content of the cooked tissue.

Colocasia↗
PubMed1981

Urinary oxalate excretion after large intakes of ascorbic acid in man.

The influence of high dose intake of ascorbic acid on the urinary excretion of oxalate was investigated in five healthy male volunteers. Oxalate was measured by a newly developed specific method using isotachophoresis. With intakes of 10 g ascorbic acid (5 X 2 g daily for 5 days; four subjects) mean urinary oxalate excretion was enhanced from about 50 mg to 87 mg (range 60 to 126 mg) per day. At least 25% of the ascorbic acid was absorbed and excreted with the urine. On discontinuing ascorbic acid administration, oxalate excretion returned to baseline values within 24 h. The time-course of oxalate excretion revealed that following the 3rd dose of 2 g ascorbic acid a plateau in urinary oxalate excretion was reached (0.6 microgram ml-1 min-1) which was not exceeded despite additional 2-g doses of ascorbic acid. On termination of ascorbic acid administration the oxalate excretion rate remained at this level for a further 6 h and then decreased to prestudy rates. No effect of high-dose ascorbic acid ingestion was found on the daily urinary excretion of creatinine, uric acid, and inorganic phosphate. Calcium excretion was slightly reduced. In comparison to the large amounts of ascorbic acid ingested, the increase in urinary oxalate excretion as measured by isotachophoresis in these healthy male volunteers was very low, and is thus similar to the change in urinary content of oxalate which results from consuming normal diets.

Ascorbic Acid↗
PubMed1977

Xylitol infusion and oxalate formation in rabbits.

Oxalate levels in the plasma and urine fractions of fasted normal, oxythiamin treated (20 mg/kg) and 4-deoxypyridoxine treated (300 mg/kg) rabbits were determined following infusion with either xylitol or glucose at a dose of 2 g/kg body weight. Biochemical determinations showed that transient thiamin or pyridoxine deficient states had been induced in the antivitamin treated rabbits. In the first 24 hour following infusion with either carbohydrate, urinary oxalate levels remained within the normal range for all groups. Oxythiamin hastened the appearance of the transient, elevation in plasma oxalate concentrations seen in rabbits after infusion with glucose. After xylitol infusion, the elevation of plasma oxalate was not significnatly above normal. 4-Deoxypyridoxine enhanced peak plasma oxalate levels above those of controls for both sugars. Glucose, at an equivalent dose to xylitol, resulted in higher plasma oxalate levels than xylitol for all groups. Infusions of [U-14C]xylitol and [U-14C]glucose solutions into 4-deoxypyridoxine treated rabbits demonstrated a conversion of the administered radioactive carbon into 14C oxalate of 0.01% with a high dilution of the specific activity. The results suggest that oxalate production from xylitol is negligible; any toxicity related to xylitol administration is not a consequence of oxalate production.

Animals↗
PubMed2006

Oxalate accumulation and regulation is independent of glycolate oxidase in rice leaves.

Cellular oxalate, widely distributed in many plants, is implicated to play important roles in various functions and is also known to affect food qualities adversely in fruits and vegetables. How oxalate is regulated in plants is currently not well understood. Glycolate oxidase (GLO) has long been considered as an important player in oxalate accumulation in plants. To gain further insight into the biochemical and molecular mechanisms, the possible roles of GLO in the process were studied. Drastically different levels of oxalate could be achieved by treating rice with various nitrogen forms (nitrate versus ammonium). While nitrate stimulated oxalate accumulation, ammonium reduced its level. Such treatments resulted in similar pattern changes for some other related organic acids, such as glycolate, oxaloacetate, and malate. By feeding plants with exogenous glycolate it was possible almost completely to restore the ammonium-decreased oxalate level. Under the two treatments few differences were observed for GLO mRNA levels, protein levels, and in vitro activities. Both K(m) for glycolate/glyoxylate and K(i) for oxalate remained almost the same for GLO purified from either nitrate- or ammonium-fed leaves. A further in vivo study, with transgenic plants carrying an estradiol-inducible GLO antisense gene, showed that, while the estradiol-induced antisense expression remarkably reduced both GLO protein levels and activities, oxalate levels were not significantly altered in the estradiol-treated transgenic plants. Taken together, it is suggested that oxalate accumulation and regulation is independent of GLO in rice leaves.

Alcohol Oxidoreductases↗
PubMed2001

Oxalate removal by daily dialysis in a patient with primary hyperoxaluria type 1.

BACKGROUND: Dialysis patients with primary hyperoxaluria are exposed to risks and hazards associated with calcium oxalate salt deposition in body tissues, since regular dialysis treatment does not adequately correct hyperoxalaemia. The purpose of this study was to evaluate oxalate mass removal using various dialysis modes in a patient suffering from primary hyperoxaluria type 1 (PH1). METHODS: Oxalate kinetics during daily haemodialysis was compared with that of standard haemodialysis (STD HD) and haemodiafiltration (HDF) using high flux dialysers (FB 170 H and FB 210 U, Transdial, Paris, France). All dialysis sessions lasted for 4 h. Blood was withdrawn and spent dialysate was collected in plastic bags every hour to evaluate mass removal. Oxalate concentration in plasma and in spent dialysate was determined by an enzymatic method. Oxalate generation, distribution volume and tissue deposition were calculated using single-pool models adapted from previous studies. RESULTS: Although no significant difference was found in mass removal per session between dialysis strategies and dialyser types, weekly mass removal with daily HD was about 2 times greater than with STD HD or HDF. Even when daily HD was performed, the oxalate generation rate-mass removal ratio (G/R ratio) remained at a value of approximately 2. CONCLUSION: Although daily HD sessions led to a substantial increase in weekly oxalate removal, all three types of renal replacement therapy were insufficient to compensate for estimated oxalate generation. To eliminate sufficient amounts of oxalate generated in PH1 patients, at least 8 h of daily dialysis with a high-flux membrane would probably be required. Renal replacement therapy for PH1 patients needs be improved further.

Female↗