The Determination of Oxalate in Urine and Plasma by High Performance Liquid Chromatography

Fry, Ian D R; Starkey, B.J.

doi:10.1177/000456329102800607

Cited by 41 publications

(18 citation statements)

References 24 publications

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“…It has been suggested that a Cl--oxalate exchanger, situated on the luminal membrane, may be involved in a mechanism for transcellular, electroneutral NaCl reabsorption similar to that previously described for formate (Schild et al 1987 France, Holland, McGhie & Wallace, 1988;Petrarulo, Bianco, Marangella, Pellegrino, Linari & Mentasi, 1990;Fry & Starkey, 1991). These data suggest that a mechanism similar to that previously described for formate may be present in the rat proximal tubule; however, the relative contribution of this mechanism to NaCl reabsorption by the proximal tubule as a whole remains to be elucidated.…”

Section: Effect Of Oxalate On Fluid Reabsorptive Ratementioning

confidence: 75%

Effect of formate and oxalate on fluid reabsorption from the proximal convoluted tubule of the anaesthetized rat.

Wareing

Green

1994

The Journal of Physiology

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1. It has recently been suggested that both formate and oxalate may be involved in the reabsorption of chloride from the proximal convoluted tubule (PCT). Reabsorption is achieved via a mechanism coupling Na+-H+ exchange to C--anion exchange thus facilitating net NaCl transport. This possible mechanism was investigated further by observing the effect of luminal addition of formate and oxalate on proximal tubule transport in anaesthetized rats, previously prepared for in vivo microperfusion. 2. Addition of formate (0-25 mmol I1) to the luminal perfusate resulted in a significant stimulation of fluid reabsorptive rate. 3. Oxalate was found to have a concentration-dependent effect on fluid reabsorption.Luminal oxalate concentrations below 0 05 mmol I1 stimulated fluid reabsorption, while an oxalate concentration of 0'5 mmol 11 inhibited fluid reabsorption.4. The presence of formate (0f25 mmol I' ) and oxalate (0O001 mmol I' ) in the same luminal perfusate stimulated fluid reabsorption from the proximal tubule lumen, but the effects of formate and oxalate were not additive. 5. The removal of bicarbonate from the luminal perfusate and its replacement with phosphate had no significant effect on fluid reabsorptive rate. An alteration in perfusate pH was also ineffective. Addition of oxalate at high and low pH failed to stimulate fluid reabsorption compared with pH-matched control perfusions. 6. The experimental data suggest the involvement of both formate and oxalate in the reabsorption of NaCl from the proximal tubule lumen, though their influence may not be exerted through the same mechanisms.

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Section: Effect Of Oxalate On Fluid Reabsorptive Ratementioning

confidence: 75%

Effect of formate and oxalate on fluid reabsorption from the proximal convoluted tubule of the anaesthetized rat.

Wareing

Green

1994

The Journal of Physiology

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“…In addition to glomerular filtration, there is net tubular secretion of oxalate [51, 52, 53], mainly in the proximal tubule, although there is also evidence for oxalate transport in collecting duct and papillary cells [54, 55]. Total daily oxalate excretion by the kidney is estimated at 10–40 mg per 24 h (0.1–0.45 mmol per 24 h) in healthy children and adults, with the average excretion being slightly higher in males than in females [34, 37, 56, 57, 58]. Only a minor part is eliminated through the gastrointestinal tract [6].…”

Section: Hyperoxaluria – Disturbed Oxalate Homeostasismentioning

confidence: 99%

“…Plasma or serum oxalate levels in healthy children and adults are mainly reported to be in the range of 1–3 μmol/L [57, 58, 113, 114, 115, 116]; depending on the method used, however, higher normal limits of up to 11 μmol/L have been reported [117, 118]. As GFR declines, renal oxalate clearance is decreasing, which leads to increased plasma oxalate as depicted in Figure 1C [59, 119, 120, 121, 122, 123, 124, 125].…”

Section: Oxalate and Ckdmentioning

confidence: 99%

Oxalate, inflammasome, and progression of kidney disease

Ermer

Eckardt²,

Aronson³

et al. 2016

Current Opinion in Nephrology and Hypertension

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Purpose of review Oxalate is an end product of metabolism excreted via the kidney. Excess urinary oxalate, whether from primary or enteric hyperoxaluria, can lead to oxalate deposition in the kidney. Oxalate crystals are associated with renal inflammation, fibrosis and progressive renal failure. It has long been known that as glomerular filtration rate (GFR) becomes reduced in chronic kidney disease (CKD), there is striking elevation of plasma oxalate. Taken together, these findings raise the possibility that elevation of plasma oxalate in CKD may promote renal inflammation and more rapid progression of CKD independent of primary etiology. Recent findings The inflammasome has recently been identified to play a critical role in oxalate-induced renal inflammation. Oxalate crystals have been shown to activate the nucleotide-binding domain, leucine-rich repeat inflammasome 3 (also known as NALP3, NLRP3 or cryopyrin), resulting in release of Interleukin-1β and macrophage infiltration. Deletion of inflammasome proteins in mice protects from oxalate-induced renal inflammation and progressive renal failure. Summary The findings reviewed in this article expand our understanding of the relevance of elevated plasma oxalate levels leading to inflammasome activation. We propose that inhibiting oxalate-induced inflammasome activation, or lowering plasma oxalate, may prevent or mitigate progressive renal damage in CKD, and warrants clinical trials.

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“…The determination of plasma oxalate based on different methodological approaches in adult populations also provided similar outcomes [21,27,32,34,36,37,39,41,44,64]. Several methods were used to evaluate normative data on plasma oxalate in pediatric populations; however, numbers of subjects included and age representation were limited or confined to one gender [43,[45][46][47].…”

Section: Discussionmentioning

confidence: 98%

Reference values of plasma oxalate in children and adolescents

et al. 2008

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Oxalate homeostasis is a derivative of absorption and transportation in the digestive system and renal/intestinal excretion of oxalate. The objective of this cross-sectional study was to determine normative values of plasma oxalate in relation to age, gender, and body size. A group of 1,260 healthy Caucasian children and adolescents aged 3 months to 18 years [mean +/- standard deviation (SD) 10.5 +/- 4.3] was studied. Each 1-year group comprised 70 subjects. Oxalate levels were assessed in blood plasma samples obtained from fasted individuals using the precipitation-enzymatic method with oxalate oxidase. Median oxalate levels in healthy infants was 3.20 micromol/L (5th-95th percentiles: 1.56-5.58) and was higher compared with older children [2.50 micromol/L (5th-95th percentiles: 0.95-5.74); p < 0.01]. No differences were found in plasma oxalate levels between boys and girls. There were no associations between plasma oxalate levels and anthropometric traits. In the healthy population aged 1-18 years, plasma oxalate concentration is independent of age, gender, and body size. Infants demonstrate higher plasma oxalate levels compared with older children, which suggests possible immature mechanisms of renal excretion. This study appears to be the first extensive report providing normative data for plasma oxalate in children and adolescents.

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The Determination of Oxalate in Urine and Plasma by High Performance Liquid Chromatography

Cited by 41 publications

References 24 publications

Effect of formate and oxalate on fluid reabsorption from the proximal convoluted tubule of the anaesthetized rat.

Effect of formate and oxalate on fluid reabsorption from the proximal convoluted tubule of the anaesthetized rat.

Oxalate, inflammasome, and progression of kidney disease

Reference values of plasma oxalate in children and adolescents

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