Nucleation and growth of brushite and calcium oxalate in urine of stone-formers

Pak, Charles Y.C.; Holt, Karen

doi:10.1016/0026-0495(76)90064-0

Cited by 209 publications

(52 citation statements)

References 15 publications

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“…There are some other factors associated with stone formation. Pak and Holt reported that the urine of patients with hyperparathyroidism was significantly more supersaturated with calcium oxalate and brushite [20]. These stone forming constituents may increase the propensity for crystallization of stone forming calcium salts, whereas pyrophosphate, citrate and magnesium are known as inhibitors of crystallization of calcium salts.…”

Section: Methodsmentioning

confidence: 99%

Clinical and Biochemical Presentation of Primary Hyperparathyroidism in Kansai District of Japan.

1997

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Abstract. Although the number of patients with primary hyperparathyroidism (pHPT) has increased since biochemical screening came to be widely employed, few data are available concerning the clinical analysis of Japanese patients. We therefore tried to determine the recent clinical and biochemical state of Japanese patients with pHPT. Clinical and biochemical data were analyzed in a series of 103 pHPT patients who had been hospitalized in Kobe University Hospital during a 17 year period from 1979 to 1995. The data were obtained from the hospital records and additionally from information through questionnaires performed in 1995. Patients were 29 males and 74 females. The average ages at diagnosis were 53.4 ± 16.0 (SD) year-old and 53.9 ± 15.2 year-old, respectively. The major clinical symptoms were nephrolithiasis (35.9%), thirst/polyuria (33.0%), easy fatigability (20.4%) and back pain/lumbago (16.5%), but 19.4% of the patients were asymptomatic. Out of 87 cases who received parathyroidectomy, 10 (11.5%) were diagnosed with parathyroid carcinoma. Age-and sex-corrected bone mineral density (BMD) of the radius was significantly lower in the group with back pain/lumbago than in the group without the symptom. Similarly, radial BMD was lower in the group with a high serum alkaline phosphatase value. Patients with nephrolithiasis had a lower urinary calcium/creatinine ratio (UCa/ UCr; 0.305 ± 0.188 mg/mg) than the patients without nephrolithiasis (0.400 ± 0.160 mg/mg). This inconsistent result suggests that some important factors except urinary calcium would contribute to urinary stone formation in pHPT. Our data mostly agreed with previous reports on a Caucasian population except for a relatively high prevalence of parathyroid carcinoma, but the negative correlation between nephrolithiasis and urinary calcium was not easily explicable. This finding should be confirmed by analyzing a larger number of cases.

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Section: Methodsmentioning

confidence: 99%

Clinical and Biochemical Presentation of Primary Hyperparathyroidism in Kansai District of Japan.

1997

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“…We have measured serum supersaturation with respect to calcium oxalate monohydrate using two independent methods, both of which have been used to estimate supersaturation in urine (25,27,28). One method (25) uses an iterative computer model of the polyelectrolyte equilibria of serum ultrafiltrates to calculate the calcium oxalate free-ion activity product, from which the solution activity of dissolved calcium oxalate complex [CaOx] is calculated.…”

Section: Introductionmentioning

confidence: 99%

“…This value, divided by the known solubility of [CaOx] in aqueous solution (6.16 X 10-6 M) (25), is the relative supersaturation ofthe serum with respect to calcium oxalate. In the other method (27,28), serum ultrafiltrates are incubated with preformed crystals of calcium oxalate monohydrate for a period long enough to permit the attainment ofthermodynamic equilibrium; the ratio of the calcium oxalate chemical product before to that at the end of the incubation, the concentration product ratio (CPR),' gives a direct estimate of supersaturation.…”

Section: Introductionmentioning

confidence: 99%

Evidence that serum calcium oxalate supersaturation is a consequence of oxalate retention in patients with chronic renal failure.

Worcester¹,

Nakagawa²,

Bushinsky³

et al. 1986

J. Clin. Invest.

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Serum oxalate rises in uremia because of decreased renal clearance, and crystals ofcalcium oxalate occur in the tissues of uremic patients. Crystal formation suggests that either uremic serum is supersaturated with calcium oxalate, or local oxalate production or accumulation causes regional supersaturation. To test the first alternative, we ultrafiltered uremic serum and measured supersaturation with two different methods previously used to study supersaturation in urine. First, the relative saturation ratio (RSR), the ratio of the dissolved calcium oxalate complex to the thermodynamic calcium oxalate solubility product, was estimated for 11 uremic (before and after dialysis) and 4 normal serum samples using a computer program. Mean ultrafiltrate oxalate predialysis was 89±8 ,uM/liter (±SEM), 31±4 postdialysis, and 10±3 in normals. Mean RSR was 1.7±0.1 (predialysis), 0.7±0.1 (postdialysis), and 0.2±0.1 (normal), where values >1 denote supersaturation, <1, undersaturation. Second, the concentration product ratio (CPR), the ratio of the measured calcium oxalate concentration product before to that after incubation of the sample with calcium oxalate monohydrate crystal, was measured in seven uremic and seven normal serum ultrafiltrates. Mean oxalate was 91±11 (uremic) and 8±3 (normal). Mean CPR was 1.4±0.2 (uremic) and 0.2±0.1 (normal). Predialysis, 17 of 18 uremic ultrafiltrates were supersaturated with respect to calcium oxalate. The degree of supersaturation was correlated with ultrafiltrate oxalate (RSR, r = 0.99, n = 29, P < 0.001; CPR, r = 0.75, n = 11, P < 0.001). A value of ultrafiltrate oxalate of 50 AM/liter separated undersaturated from supersaturated samples and occurred at a creatinine of -9.0 mg/dl.

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“…6 11 High urinary calcium concentrations lead to increased urinary saturation of salts. 12 Additionally, citrate, which is the common urinary inhibitor is reduced by the way of complication in hypercalciuric statement of urine. 13 Intestine, bone and kidney are the main sites regulating calcium transport and any dysregulation of these sites result in hypercalciuria.…”

Section: Calcium-hypercalciuriamentioning

confidence: 99%

Calcium-sensing receptor gene polymorphisms in patients with calcium urolithiasis: a systematic review

et al. 2014

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Background: Calcium-sensing receptor gene (CaSR) might be a strong component of the complex genetic background regulating calcium excretion and stone formation in kidney. The polymorphisms in different parts of the gene could be associated with calcium stone formation. Objective: The individual studies indicate a correlation between CaSR gene polymorphisms and urolithiasis but not sufficient to draw a precise result. We aimed to search literature to come to a reliable conclusion through a systematic review. Materials and methods: We have serached individiual studies regarding the issue and high quality reviews. We assessed all the studies to draw a conclusion. Conclusion: The genetic background of the neprolithiasis is an interesting issue deserving to be disscussed on. Regading genes of which, CaSR gene polymorphisms is the leading one, are studied in many individual studies but they are not sufficient to have a precise conclusion. Well-oriented and documented, phenotypically homogenous large cohort studies are needed for further evaluation.

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Nucleation and growth of brushite and calcium oxalate in urine of stone-formers

Cited by 209 publications

References 15 publications

Clinical and Biochemical Presentation of Primary Hyperparathyroidism in Kansai District of Japan.

Clinical and Biochemical Presentation of Primary Hyperparathyroidism in Kansai District of Japan.

Evidence that serum calcium oxalate supersaturation is a consequence of oxalate retention in patients with chronic renal failure.

Calcium-sensing receptor gene polymorphisms in patients with calcium urolithiasis: a systematic review

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