Enzymic determination of serum oxalate

Sugiura, Masahiro; Yamamura, Hirohiko; Hirano, Kazuyuki; Ito, Yoshimasa; Sasaki, Masahiro; Morikawa, Masako; Inoue, Michiko; Tsuboi, Masahiro

doi:10.1016/0009-8981(80)90121-7

Cited by 24 publications

(6 citation statements)

References 12 publications

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“…Oxalate was analysed on the Fusion analyser (Ortho Clinical Diagnostics, Buckinghamshire, UK) by an established oxidase/peroxidase laboratory method linked to formation of an indamine dye. 14 Between-batch CV was 2.6% at 0.29 mmol/L. GAGs were measured by an established laboratory method involving binding of dimethylmethylene blue at alkaline pH.…”

Section: Methodsmentioning

confidence: 99%

Biochemical risk factors for stone formation in a Scottish paediatric hospital population

MacDougall¹,

Taheri

Crofton³

2010

Ann Clin Biochem

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Background: Renal stones in children, although rare, may be associated with morbidity and renal damage. Scottish children have a different ethnic composition and diet compared with paediatric populations previously studied. Urinary stone promoters include calcium, oxalate and urate. Postulated inhibitors include citrate and glycosaminoglycans (GAGs). We tested the hypothesis that Scottish paediatric stone-formers have higher excretion of urinary stone promoters (calcium/ oxalate/urate) and/or lower excretion of stone inhibitors (citrate/GAGs) than children with isolated haematuria and controls. Methods: In this case-controlled study, we measured creatinine, calcium, oxalate, urate, citrate and GAGs in random urine samples from 24 stone-formers (excluding inherited metabolic disorders), median age 10.2 (range 1.0 -17.2) y; 25 patients with isolated haematuria, 6.3 (0.6-13.7) y; and 32 controls, 7.5 (0.8-14.7) y. Results: Excretion of urinary promoters and inhibitors differed among stone-formers, haematuria and control groups for (median (range)): calcium (0.82 (0.02 -2.19), 0.43 (0.08 -2.65), 0.31 (0.04-2.12) mmol/mmol creatinine, respectively, P ¼ 0.005), citrate (0.42 (0.13 -0.72), 0.33 (0.05-0.84), 0.61 (0.11 -1.75) mmol/mmol creatinine, P ¼ 0.001), calcium:citrate ratio (1.68 (0.19 -4.81), 1.30 (0.19-9.57), 0.54 (0.10 -2.27) mmol/mmol, P , 0.0001) and the promoter:inhibitor ratio (calcium Â oxalate)/ (citrate Â GAGs) (8.3 (1.0-82.5), 4.3 (1.2-69.5), 2.8 (0.3-13.2) mmol/g, P , 0.0001). Conclusions: Scottish paediatric stone-formers had lower urinary citrate excretion and higher urinary calcium excretion, calcium:citrate ratio and promoter:inhibitor ratio compared with controls. Urinary calcium excretion and promoter:inhibitor ratio was also higher than children with isolated haematuria. Nevertheless, marked overlap between the stone-former and haematuria groups for promoter:inhibitor and calcium:citrate ratios suggests that some patients with isolated haematuria may be at future risk of urolithiasis.

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Section: Methodsmentioning

confidence: 99%

Biochemical risk factors for stone formation in a Scottish paediatric hospital population

MacDougall¹,

Taheri

Crofton³

2010

Ann Clin Biochem

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“…Oxalic acid was measured using oxalate oxidase, which oxidizes oxalate to hydrogen peroxide and carbon dioxide. The hydrogen peroxide then reacts with 3-methyl-2-benzothiazolinone hydrozone and 3-(dimethyl)benzoic acid to form an indamine dye that is monitored photometrically (45). Citric acid was determined using citrate lyase, which catalyzes the conversion citrate to oxaloacetic acid, which then is converted to malic acid, in the presence of malate dehydrogenase.…”

Section: Chemical Determinationsmentioning

confidence: 99%

Thiazides Reduce Brushite, but not Calcium Oxalate, Supersaturation, and Stone Formation in Genetic Hypercalciuric Stone–Forming Rats

Bushinsky¹,

Asplin²

2005

Journal of the American Society of Nephrology

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Over 59 generations, a strain of rats has been inbred to maximize urine calcium excretion. The rats now excrete eight to 10 times as much calcium as controls. These rats uniformly form calcium phosphate (apatite) kidney stones and have been termed genetic hypercalciuric stone-forming (GHS) rats. The addition of a common amino acid and oxalate precursor, hydroxyproline, to the diet of the GHS rats leads to formation of calcium oxalate (CaOx) kidney stones. Hydroxyproline-supplemented GHS rats were used to test the hypothesis that the thiazide diuretic chlorthalidone would decrease urine calcium excretion, supersaturation, and perhaps stone formation. All GHS rats received a fixed amount of a standard 1.2% calcium diet with 5% trans-4-hydroxy-L-proline (hydroxyproline) so that the rats would exclusively form CaOx stones. Half of the rats had chlorthalidone (Thz; 4 to 5 mg/kg per d) added to their diets. Urine was collected weekly, and at the conclusion of the study, the kidneys, ureters, and bladders were radiographed for the presence of stones. Compared with control, the addition of Thz led to a significant reduction of urine calcium and phosphorus excretion, whereas urine oxalate excretion increased. Supersaturation with respect to the calcium hydrogen phosphate fell, whereas supersaturation with respect to CaOx was unchanged. Rats that were fed Thz had fewer stones. As calcium phosphate seems to be the preferred initial solid phase in patients with CaOx kidney stones, the reduction in supersaturation with respect to the calcium phosphate solid phase may be the mechanism by which thiazides reduce CaOx stone formation.

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“…Tests of sigide and carbon dioxide. The hydrogen peroxide then nificance were calculated by analysis of variance with reacts with 3-methyl-2-benzothiazolinone hydrozone the Bonferroni correction for multiple comparisons and and 3-(dimethyl)benzoic acid to form an indamine dye regression analysis using conventional computer pro- [29]. Citric acid was determined using citrate lyase, which grams (BMDP; University of California, Los Angeles, catalyzes the conversion citrate to oxaloacetic acid, CA, USA) on a digital computer.…”

Section: Establishment Of Hypercalciuric Ratsmentioning

confidence: 99%

Calcium phosphate supersaturation regulates stone formation in genetic hypercalciuric stone-forming rats

Bushinsky¹,

Parker²,

Asplin³

2000

Kidney Int

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Enzymic determination of serum oxalate

Cited by 24 publications

References 12 publications

Biochemical risk factors for stone formation in a Scottish paediatric hospital population

Biochemical risk factors for stone formation in a Scottish paediatric hospital population

Thiazides Reduce Brushite, but not Calcium Oxalate, Supersaturation, and Stone Formation in Genetic Hypercalciuric Stone–Forming Rats

Calcium phosphate supersaturation regulates stone formation in genetic hypercalciuric stone-forming rats

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