An approximate estimate of the ion-activity product of calcium oxalate in rat urine

Tiselius, Hans‐Göran; Ferraz, Renato Ribeiro Nogueira; Heilberg, Ita Pfeferman

doi:10.1007/s00240-003-0363-9

Cited by 21 publications

(17 citation statements)

References 8 publications

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“…The CaOx SS can be assessed by a computer program named EQUIL 2, or by the equation proposed by Tiselius et al (43). In a preliminary analysis, the calculated AP(CaOx)index RAT was observed to correlate with the CaOx SS obtained from EQUIL 2 (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…However, a large number of variables have to be analyzed for these calculations, particularly in animal models when the urine volume is limited. Here, the ion activity product was determined by an equation validated by Tiselius et al (43) specifically for rat urine, which gave a simple estimation of CaOx SS. The ion activity product of CaOx (APCaOx) in rat [AP(CaOx)indexRAT], as an index of CaOx SS, was calculated as follows AP ϭ 4,067 ϫ Ca 0.93 ϫ Ox 0.96 ͑Citrate ϩ 0.015͒ 0.60 ϫ Mg 0.55 ϫ Volume 0.99 This equation was designed specifically for a 24-h collection period and the total excretions of Ca 2ϩ , Ox, Mg 2ϩ , and citrate were expressed in millimoles.…”

Section: Methodsmentioning

confidence: 99%

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Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

McMartin²

2009

American Journal of Physiology-Renal Physiology

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Ethylene glycol (EG)-induced hyperoxaluria is the most commonly employed experimental regimen as an animal model of calcium oxalate (CaOx) stone formation. The variant sensitivity to CaOx among different rat strains has not been fully explored, although the Wistar rat is known to accumulate more CaOx in kidney tissue after low-dose EG exposure than in the Fischer 344 (F344) rats. Supersaturation of CaOx in tubular fluid contributes to the amount of CaOx crystal formation in the kidney. We hypothesized that the urinary supersaturation of CaOx in Wistar rats is higher than that of F344 rats, thereby allowing for greater CaOx crystal deposition in the Wistar rat. Age-matched male Wistar and F344 rats were treated with 0.75% EG or drinking water for 8 wk. Twenty-four-hour urine was collected at 0, 2, 4, 6, and 8 wk for analysis of key electrolytes to calculate the CaOx supersaturation. Plasma oxalate level was also measured. Our data confirmed the different sensitivity to renal toxicity from EG between the two rat strains (Wistar > F344). After EG treatment, the plasma oxalate level and urine oxalate excretion were markedly greater in the Wistar rats than in the F344 rats, while urine calcium was slightly decreased in Wistars. Thus, the CaOx supersaturation in urine of Wistar rats was higher, which led to a greater crystal deposition in kidney in Wistar rats. These studies suggest that during EG treatment, changes in urine electrolytes and in CaOx supersaturation occur to a greater extent in the Wistar rat, in agreement with its greater sensitivity to EG toxicity.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

McMartin²

2009

American Journal of Physiology-Renal Physiology

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“…All assays were performed in duplicate for each sample and expressed per gram or milligram of urinary Cr. Urinary supersaturation with respect to CaOx was assessed with the index proposed previously (14,30).…”

Section: Methodsmentioning

confidence: 99%

Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney

Huang¹,

Chieh²

2009

American Journal of Physiology-Renal Physiology

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Huang HS, Ma MC, Chen J. Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney. Am J Physiol Renal Physiol 295: F34-F45, 2008. First published September 17, 2008 doi:10.1152/ajprenal.90309.2008.-Vitamin E was previously reported to reduce calcium oxalate (CaOx) crystal formation. This study explored whether vitamin E deficiency affects intrarenal oxidative stress and accelerates crystal deposition in hyperoxaluria. The control (C) group of rats received a standard diet and drinking water, while the experimental groups received 0.75% ethylene glycol (EG) in drinking water for 42 days. Of the latter, one group received a standard diet (EG group), one received a low-vitamin E (LE) diet (EGϩLE group), and the last received an LE diet with vitamin E supplement (4 mg) (EGϩLEϩE group). The CϩLE and CϩLEϩE groups were the specific controls for the last two experimental groups, respectively. In a separate experiment, EG and EGϩLE rats were studied on days 3-42 to examine the temporal relationship between oxidative change and crystal formation. Urinary biochemistry and activity/levels of antioxidative and oxidative enzymes in glomeruli and tubulointerstitial specimens (TIS) were examined. In EG rats, CaOx crystal accumulation was associated with low antioxidative enzyme activity in TIS and with increased oxidative enzyme expression in glomeruli. In the EGϩLE group, marked changes in antioxidative and oxidative enzyme levels were seen and correlated with massive CaOx deposition and tubular damage. The increased oxidative stress seen with EGϩLE treatment was largely reversed by vitamin E supplementation. A temporal study showed that decrease in antioxidative defense and increased free radical formation in the EGϩLE group occurred before crystal deposition. This study shows that low vitamin E disrupts the redox balance and causes cell death, thereby favoring crystal formation. antioxidative proteins; free radicals; hyperoxaluria CALCIUM OXALATE (CaOx) crystal formation is a multifaceted and complex process that involves a series of chemical, physical, biochemical, and physiological events (6, 10, 16). The principal causative agent for the formation of calcium salt crystals is thought to be supersaturation that causes the precipitation of salts in urine. However, even though urine is supersaturated with calcium and oxalate ions in normal subjects, stones do not form because of the presence of inhibitors and other unknown mechanisms (22).Membrane injury is suggested to be the primary event in CaOx crystal binding, and oxalate-induced free radicals are significant causative factors in membrane injury (11,12,25). This injury leads to lipid and protein peroxidation and altered biochemical reactions, including depletion of the antioxidant defense system (25). On the basis of these findings, we hypothesized that if renal tubular injury due to increased oxidative stress caused by hyperoxaluria can be prevented, CaOx crystal accumulation in the kidneys can also be ...

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“…In previously formulated indices [1,[6][7][8][9], the total excretion of urine variables during defined periods of time was used together with measurements of the urine volume during the same period. In the indices given in this article we used the concentration of each variable and information on the duration of the collection period is thus not necessary, neither is any correction factor for that.…”

Section: Discussionmentioning

confidence: 99%

“…Simplified estimates therefore previously were derived for the ion-activity products of CaOx [6][7][8] and CaP in human urine [1] as well as for these ion-activity products in rat urine [9]. In this article we report the corresponding calculations for mouse urine and present approximate estimates of these ion-activity products.…”

Section: Introductionmentioning

confidence: 96%

Simplified estimates of ion-activity products of calcium oxalate and calcium phosphate in mouse urine

2011

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This study aimed at formulating simplified estimates of ion-activity products of calcium oxalate (AP(CaOx)) and calcium phosphate (AP(CaP)) in mouse urineto find the most important determinants in order to limit the analytical work-up. Literature data on mouse urine composition was used to determine the relative effect of each urine variable on the two ion-activity products. AP(CaOx) and AP(CaP) were calculated by iterative approximation with the EQUIL2 computerized program. The most important determinants for AP(CaOx) were calcium, oxalate and citrate and for AP(CaP) calcium, phosphate, citrate, magnesium and pH. Urine concentrations of the variables were used. A simplified estimate of AP(CaOx) (AP(CaOx)-index(MOUSE)) that numerically approximately corresponded to 10(8) × AP(CaOx) was given the following expression:[Formula: see text]For a series of urine samples with various composition the coefficient of correlation between AP(CaOx)-index(MOUSE) and 10(8) × AP(CaOx) was 0.99 (p = 0.00000). A similar estimate of AP(CaP) (AP(CaP)-index(MOUSE)) was formulated so that it approximately would correspond numerically to 10(14) × AP(CaP) taking the following form:[Formula: see text]For a series of variations in urine composition the coefficient of correlation was 0.95 (p = 0.00000). The two approximate estimates shown in this article are simplified expressions of AP(CaOx) and AP(CaP). The intention of these theoretical calculations was not to get methods for accurate information on the saturation levels in urine, but to have mathematical tools useful for rough conclusions on the outcome of different experimental situations in mice. It needs to be emphasized that the accuracy will be negatively influenced if urine variables not included in the formulas differ very much from basic concentrations.

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An approximate estimate of the ion-activity product of calcium oxalate in rat urine

Cited by 21 publications

References 8 publications

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney

Simplified estimates of ion-activity products of calcium oxalate and calcium phosphate in mouse urine

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