Effects of Mineral Composition of Drinking Water on Risk for Stone Formation and Bone Metabolism in Idiopathic Calcium Nephrolithiasis

1996 ◽  
Vol 91 (3) ◽  
pp. 313-318 ◽  
Author(s):  
Martino Marangella ◽  
Corrado Vitale ◽  
Michele Petrarulo ◽  
Lidia Rovera ◽  
Franca Dutto

1. To assess whether the mineral content of drinking water influences both risk of stone formation and bone metabolism in idiopathic calcium nephrolithiasis, 21 patients were switched from their usual home diets to a 10 mmol calcium, low-oxalate, protein-controlled diet, supplemented with 21 of three different types of mineral water. Drinking water added 1, 6 and 20 mmol of calcium and 0.5, 10 and 50 mmol of bicarbonate respectively to the controlled diet. 2. The three controlled study periods lasted 1 month each and were separated by a 20 day washout interval. Blood and urine chemistries, including intact parathyroid hormone, calcitriol and two markers of bone resorption, were performed at the end of each study period. The stone-forming risk was assessed by calculating urine saturation with calcium oxalate (βCaOx), calcium phosphate (βbsh) and uric acid (βUA). 3. The addition of any mineral water produced the expected increase in urine output and was associated with similar decreases in βCaOx and βUA, whereas βbsh varied marginally. These equal decreases in βCaOx, however, resulted from peculiar changes in calcium, oxalate and citrate excretion during each study period. The increase in overall calcium intake due to different drinking water induced modest increases in calcium excretion, whereas oxalate excretion tended to decrease. The changes in oxalate excretion during any one study period compared with another were significantly related to those in calcium intake. Citrate excretion was significantly higher with the high-calcium, alkaline water. 4. Parathyroid hormone, calcitriol and markers of bone resorption increased when patients were changed from the high-calcium, alkaline to the low-calcium drinking water. 5. We suggest that overall calcium intake may be tailored by supplying calcium in drinking water. Adverse effects on bone turnover with low-calcium diets can be prevented by giving high-calcium, alkaline drinking water, and the stone-forming risk can be decreased as effectively as with low-calcium drinking water.

2005 ◽  
Vol 16 (10) ◽  
pp. 1203-1209 ◽  
Author(s):  
Pierre J. Meunier ◽  
Cecile Jenvrin ◽  
Françoise Munoz ◽  
Viviane de la Gueronnière ◽  
Patrick Garnero ◽  
...  

1988 ◽  
Vol 254 (1) ◽  
pp. E63-E70 ◽  
Author(s):  
J. J. Morrissey

The influence of phorbol myristate acetate (PMA), an activator of protein kinase c, on the secretion of parathyroid hormone from collagenase-dispersed bovine parathyroid cells was tested. The cells were incubated at low (0.5 mM) or high (2.0 mM) concentrations of calcium in the medium, and the hormone secreted into the medium was measured by a radioimmunoassay that recognizes both intact and C-terminal fragments of hormone. At low calcium, the secretory rate averaged 32 +/- 3.8 ng.h-1.(10(5) cells)-1. The addition of 1.6 microM PMA did not affect secretion. At high calcium there was a significant suppression of secretion by 38% to 19.8 +/- 3 ng.h-1.(10(5) cells)-1. The addition of 1.6 microM PMA significantly stimulated hormone secretion to 35.8 +/- 8 ng.h-1.(10(5) cells)-1, a rate indistinguishable from low calcium. This stimulatory effect of PMA at high calcium was seen at PMA concentrations as low as 1.6 nM, did not occur with a biologically inactive 4 alpha-isomer of phorbol ester, and was independent of changes in cellular adenosine 3',5'-cyclic monophosphate levels. Examination of 32P-labeled phosphoproteins by two-dimensional gel electrophoresis revealed acidic proteins of approximately 20,000 and 100,000 Da that were phosphorylated at low and high calcium + 1.6 microM PMA but not at high calcium alone. The protein kinase c activity associated with the membrane fraction of parathyroid cells significantly decreased 40% when the cells were incubated at high vs. low calcium. The data suggest that calcium may regulate parathyroid hormone secretion through changes in protein kinase c activity of the membrane fraction of the cell and protein phosphorylation.


Hypertension ◽  
2000 ◽  
Vol 35 (5) ◽  
pp. 1154-1159 ◽  
Author(s):  
Rolf Jorde ◽  
Johan Sundsfjord ◽  
Egil Haug ◽  
Kaare H. Bønaa

2021 ◽  
pp. 29-30
Author(s):  
Harshawardhan V Tanwar ◽  
Uttam Wadavkar

Introduction: Metabolic abnormalities are common cause of urolithiasis in pediatric age group. Children with urolithiasis are associated with considerable morbidity. By treating these abnormalities stone formation is prevented. Objectives: Prospective study to nd the metabolic risk factors of urolithiasis in children and compare them with literature. Materials and Methods: In open, prospective and observational study, 85 children were evaluated from August 2019 to June 2020. In all patients' dietary history, water intake and results of laboratory ndings were recorded. All urine samples obtained from patients were without dietary restrictions. Reference pediatric 24 hour urinary parameter was used according to western literature. Results: We investigated 85 patients with urolithiasis. Low urine volume was found in 52 patients which is comparable with previous studies indicating simple intervention as to increase water intake. Low calcium intake was found in 48 patients suggesting that low calcium intake is associated with higher incidence of urolithiasis due to increased intestinal oxalate absorption. Hypocalcaemia was found in 34 patients and 24 hour urinary abnormality was found in only 18 patients'. Both these nding does not support previous literature. Stone analysis nding does not correlate with urinary nding. Conclusions: Hypocalcaemia is major metabolic abnormality in contradiction to western literature. Low urine volume secondary to low water intake is predominant nding .There are no nomograms for urinary excretion of Calcium, uric acid, oxalate and citrate in Indian children. Keeping the optimum blood calcium level & increased uid intake can prevent stone formation in children.


1988 ◽  
Vol 6 (3) ◽  
pp. 253-256 ◽  
Author(s):  
Alfonso Siani ◽  
Pasquale Strazzullo ◽  
Sergio Guglielmi ◽  
Delia Pacioni ◽  
Angela Giacco ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1112 ◽  
Author(s):  
Cecilia Villa-Etchegoyen ◽  
Mercedes Lombarte ◽  
Natalia Matamoros ◽  
José M. Belizán ◽  
Gabriela Cormick

There is increasing epidemiologic and animal evidence that a low calcium diet increases blood pressure. The aim of this review is to compile the information on the link between low calcium intake and blood pressure. Calcium intake may regulate blood pressure by modifying intracellular calcium in vascular smooth muscle cells and by varying vascular volume through the renin–angiotensin–aldosterone system. Low calcium intake produces a rise of parathyroid gland activity. The parathyroid hormone increases intracellular calcium in vascular smooth muscles resulting in vasoconstriction. Parathyroidectomized animals did not show an increase in blood pressure when fed a low calcium diet as did sham-operated animals. Low calcium intake also increases the synthesis of calcitriol in a direct manner or mediated by parathyroid hormone (PTH). Calcitriol increases intracellular calcium in vascular smooth muscle cells. Both low calcium intake and PTH may stimulate renin release and consequently angiotensin II and aldosterone synthesis. We are willing with this review to promote discussions and contributions to achieve a better understanding of these mechanisms, and if required, the design of future studies.


2001 ◽  
Vol 86 (2) ◽  
pp. 307-307
Author(s):  
D. Bonofiglio ◽  
S. Catalano ◽  
M. Maggiolini ◽  
S. Andò

1997 ◽  
Vol 93 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Piergiorgio Messa ◽  
Martino Marangella ◽  
Luisa Paganin ◽  
Mara Codardini ◽  
Aldo Cruciatti ◽  
...  

1. Dietary calcium restriction, an efficient practice in reducing urinary calcium excretion, has been reported to induce either an increase or no change in oxalate excretion, questioning its use in hypercalciuric stone-forming patients. In addition, calcium restriction has been previously demonstrated to induce other urinary changes which might influence the relative supersaturation of calcium oxalate. So the overall effect of calcium deprivation on the relative supersaturation of calcium oxalate is unpredictable. 2. The aim of the study was to evaluate the effect of dietary calcium restriction on the relative supersaturation of calcium oxalate in the urine of stone-forming patients utilizing a computer methodology which takes into account the main soluble complex species of oxalate. 3. We studied 34 stone-forming patients on both a free-choice diet, whose Ca and oxalate content (24 and 1.2 mmol respectively) was assessed by dietary inquiry, and after 30 days on a prescribed low-calcium and normal oxalate diet (11 and 1.1 mmol respectively). Under both conditions, the excretion of the main urinary parameters related to dietary composition, electrolytes, oxalate and daily citrate urinary excretion, were measured. The relative supersaturation of calcium oxalate was calculated by means of an iterative computer method which takes into account the main soluble complex species on which the solubility of calcium oxalate is dependent. In addition, intact parathyroid hormone and 1,25-dihydroxyvitamin D blood levels were also evaluated. In 13 of the patients intestinal calcium absorption was evaluated during both a free- and a low-calcium diet, utilizing kinetics methodology. 4. The low-calcium diet induced, together with an expected reduction of calcium excretion, a marked increase in oxalate urinary output. This finding was independent of the presence or otherwise of hypercalciuria and of the serum levels of parathyroid hormone and vitamin D. Intestinal calcium absorption was also stimulated by calcium deprivation and its levels were well correlated with oxalate excretion. Minor changes in magnesium and citrate excretion were also observed. The overall effect on the relative supersaturation of calcium oxalate consisted in a substantial increase in this parameter during the low-calcium diet. 5. In conclusion, our data reinforce the concept that dietary calcium restriction has potentially deleterious effects on lithogenesis, by increasing the relative supersaturation of calcium oxalate.


2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Mousa Al-Reza Hadjzadeh ◽  
Parichehr Hayatdavoudi ◽  
Reza Karim Keshteh ◽  
Nazanin Entezari Entezari ◽  
Roghayeh Pakdel ◽  
...  

Background: There is a folk belief that drinking Ramsar spring mineral water (RSW) is a remedy for renal stones. Objectives: This study aimed to evaluate the effect of RSW on prevention or treatment of nephrolithiasis in male Wistar rats and identify the constituents of the water. Methods: Nephrolithiasis was induced by providing drinking water containing 1% ethylene glycol (EG) for two weeks in male Wistar rats. The animals were divided into prevention and treatment groups, each contained five sub-groups (10 rats for each). Prevention groups were treated for two weeks: control group (without treatment), EG group (1% ethylene glycol in drinking water), RSW 5, 10, and 15% groups (1% ethylene glycol + RSW 5, 10, and 15% in drinking water). The treatment groups received 1% EG for two weeks, then it was discontinued, and the RSW (10, 15, and 20%) was added to the drinking water for the next two weeks. The calcium oxalate (CaOx) depositions in the kidneys' tubules were evaluated by Hematoxylin and Eosin staining. The spring water was analyzed for its constituents. Results: Calcium oxalate crystals were significantly increased in EG group as compared to the control group (P < 0.05). Moreover, RSW did not significantly prevent CaOx crystals but alleviated CaOx crystals at 15 and 20% concentrations in the treatment protocol (P < 0.001). Conclusions: The hard water of Ramsar spring reduced CaOx crystals in nephrolithiatic rats, which may be due to its high calcium and magnesium content.


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