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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 19 adult patients, with renal stones containing calcium and hypercalciuria, urinary calcium and magnesium excretion and urinary calcium/magnesium ratio was investigated before and during 4 days of treatment with sodium cellulose phosphate. Urinary magnesium excretion fell following sodium cellulose phosphate therapy in all but 1 patient investigated: in 9 patients by less than 50% and in 10 by more than 50% of the pretreatment values. In the latter group of patients urinary calcium/magnesium ratio increased significantly from the mean values ( +/- SD) 3.2 +/- 1.1 to 6.77 +/- 6.9. In 6 patients serum magnesium absorption is suggested, and routine serum and urinary magnesium analysis with the early treatment of magnesium deficiency in patients treated with sodium cellulose phosphate are recommended.
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PMID:Sodium cellulose phosphate-induced increment in urinary calcium/magnesium ratio. 123 99

Clinical or biochemical findings were reevaluated in 34 pediatric patients with primary renal tubular hypokalemic metabolic alkalosis. The patients were subdivided into two groups. Bartter syndrome (primary renal tubular hypokalemic metabolic alkalosis with normocalciuria or hypercalciuria) was diagnosed in 18 patients with molar urinary calcium/creatinine ratios greater than 0.20, and Gitelman syndrome (primary renal tubular hypokalemic metabolic alkalosis with magnesium deficiency and hypocalciuria) was diagnosed in 16 patients with molar urinary calcium/creatinine ratios less than or equal to 0.20 and plasma magnesium levels less than 0.75 mmol/L. Some clinically important differences between the groups were observed. Patients with Bartter syndrome were often born after pregnancies complicated by polyhydramnios (8/18) or premature delivery (7/18) and had short stature (11/18) or polyuria, polydipsia, and a tendency to dehydration (16/18) during infancy (12/18) or before school age (18/18). Patients with Gitelman syndrome had tetanic episodes (12/16) or short stature (3/16) at school age (14/16). We conclude that the Bartter and Gitelman syndromes represent two distinct variants of primary renal tubular hypokalemic metabolic alkalosis and are easily distinguished on the basis of urinary calcium levels.
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PMID:Use of calcium excretion values to distinguish two forms of primary renal tubular hypokalemic alkalosis: Bartter and Gitelman syndromes. 841 May 32

We have previously shown the synergistic interaction between fructose and magnesium (Mg) deficiency on renal calcification of female rats. The purpose of the present study was to determine whether the calcification formed in the kidneys of female rats fed an Mg-deficient fructose diet is due to phosphate or oxalate precipitates of calcium. The rats were divided into two dietary groups: fructose without Mg and starch with Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected for measuring urinary output, pH, Mg and calcium (Ca). The rats were then fasted overnight and after decapitation, blood was immediately collected for measuring plasma Ca and Mg, and the kidneys were removed. Left kidneys were used to determine their Mg and Ca contents, and right kidneys were dissected and fixed in neutral buffered formalin. Formalin-fixed specimens for microscopy were processed in paraffin using conventional procedures. Histochemical analysis was conducted by staining serial paraffin sections with haematoxylin, eosin, PAS-Schiff, alcian blue and trichrome. The sections were stained by the von Kossa method for calcium phosphate and by the silver hydroperoxide method for calcium oxalate. Only calcium phosphate was detected in the corticomedullary junction of the kidneys of female rats fed Mg-deficient fructose. The hypercalcaemia, hypercalciuria, and hypomagnesuria observed in the fructose group may cause calcium phosphate crystallization. A possible mechanism for the interaction between magnesium deficiency, fructose and oestrogen may be through parathyroid hormone which increases tubular fluid Ca and phosphorus (TF[Ca]x[P]). Further studies are required to prove the mechanism proposed here.
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PMID:Fructose precipitates calcium phosphate in the kidneys of female rats fed magnesium-deficient diets. 179 51

In order to determine the effects of hypoinsulinaemia or hyperinsulinaemia on nephrocalcinosis induced by the interaction between fructose and magnesium (Mg) deficiency, we compared kidney calcification in obese versus lean, and non-diabetic versus diabetic female Zucker rats fed a magnesium-deficient fructose diet. One half of the obese and lean animals, respectively, was injected with streptozotocin to produce diabetes, and the other half was injected with citrate buffer alone. Diabetic, non-diabetic, obese, and lean animals were divided into two dietary groups, consisting of high starch or high fructose without added Mg. After a four week period, 24 hour urine was collected for urinary output, protein, oxalate, citrate, MG, and calcium (Ca) measurements. The animals were then decapitated, and blood was collected for glucose, Mg, and Ca determinations, and kidneys were removed to determine their Mg and Ca contents. All fructose-fed animals exhibited significantly more kidney Ca then the starch-fed animals. Lean non-diabetic rats fed fructose showed the greatest kidney Ca along with the greatest urinary protein excretion among all experimental groups. The significant finding in the present study is that diabetes or obesity reduced nephrocalcinosis regardless of the insulin status of the rats. Diuresis and hypercitraturia in diabetic and/or obese animals may cause a reduction in nephrocalcinosis induced by the interaction between fructose and magnesium deficiency. Hyperproteinuria (uromucoid) in combination with hypercalciuria and hypomagnesuria may be responsible for greater nephrocalcinosis in the fructose than the starch group. The possible mechanisms for this interaction on nephrocalcinosis have been discussed.
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PMID:Comparison of renal calcium concentration in obese, lean, diabetic, and non-diabetic Zucker rats fed a magnesium-deficient fructose diet. 183 14

The synergistic interaction of fructose and magnesium (Mg) deficiency on kidney calcification was compared in male and female rats. Male and female weanling rats were divided into four dietary groups: fructose or starch, with or without Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected to measure urinary output, pH, Mg, calcium (Ca), and oxalic acid. Rats were fasted overnight. After decapitation, blood was collected immediately, and kidneys were removed to determine their Mg and Ca content. Dietary fructose significantly increased kidney Ca in female rats fed deficient or adequate Mg diet and in male rats fed Mg-deficient diet only; the greatest kidney calcification occurred in female rats fed Mg-deficient diet (P less than 0.0001). Even in starch groups female rats fed the Mg-deficient diet showed some kidney Ca accumulation. The synergistic interaction of fructose and magnesium deficiency on nephrocalcinosis was significantly greater in female than in male rats. Low urinary output, optimal pH 6.8 for calcium phosphate precipitation, hypercalcaemia, hypercalciuria, hypomagnesuria, and low ratio of urinary Mg to Ca may independently or multifactorially contribute to nephrocalcinosis. The possible mechanism of this interaction is discussed.
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PMID:Dietary fructose produces greater nephrocalcinosis in female than in male magnesium-deficient rats. 191 Oct 97

Metabolic disorders are the most frequent risk factor for the development of urolithiasis. They are manigenic substances or deficiency of inhibitors of crystalgenic substances or deficiency of inhibitors of crystallization and aggregation. The authors use for their diagnosis a modification of Pak's procedure. It involves examination of 24-hour urine with the patient on a low-calcium diet, supplemented by urine examination on fasting and after a 1000 mg calcium load. The procedure includes also examination of serum and bacteriological examination of urine. A total of 93% of patients with calcium lithiasis had a metabolic disorder, 42% suffered from idiopathic hypercalciuria, 32% from hyperuricosuria, 19% from hyperoxaluria, 15% from magnesium deficiency and 38% from hypocitraturia. On the other hand, patients with uric acid lithiasis had a detectable metabolic disorder only in 62%. Active detection of metabolic disorders is essential for the introduction of effective, specific metaphylaxis of urolithiasis.
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PMID:[Detection of metabolic disorders as a cause of urolithiasis in clinical practice]. 272 Jul 28

One hundred fifty-five recurrent noninfectious calcium oxalate stone formers were evaluated in an effort to assess the importance of magnesium excretion on calcium oxalate stone formation. All patients evaluated had normal urinary magnesium excretion, and any elevation of the calcium/magnesium ratio was related to the presence of hypercalciuria. The findings indicate that magnesium deficiency does not appear to be a significant cause of calcium oxalate urolithiasis. If magnesium supplement is of value in some patients, it is likely related to its inhibitory effect on calcium oxalate crystallization.
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PMID:Magnesium excretion and calcium oxalate urolithiasis. 714 7

The normal fractional urinary excretion of filtered magnesium is about 5%. In magnesium deficiency in man, the kidneys can normally reduce the 24-hour urinary magnesium excretion to less than 1 mmol (24 mg) via unknown mechanisms, and initially without a fall in plasma magnesium concentration. Renal magnesium wasting may be defined as a urinary excretion greater than 1 mmol/day in the presence of hypomagnesemia (plasma magnesium < 0.7 mmol/l). Congenital renal magnesium wasting occurs in several syndromes including Bartter's syndrome in which it is associated with hypercalciuria, and the defect may be in the thick ascending limb of Henle's loop, and Gitelman's syndrome in which there is hypocalciuria, and the defect may be in the distal convoluted tubule. Other causes of renal magnesium wasting include diabetes mellitus, hypercalcemia and diuretics. Magnesium wasting may also result from various toxicities including those of cis-platinum, in which the biochemical features resemble Gitelman's syndrome, and those of aminoglycosides, pentamidine and cyclosporin. Calcitriol deficiency may also contribute to renal magnesium wasting in some circumstances. Mild hypermagnesemia may occur in familial hypocalciuric hypercalcemia and may reflect abnormal sensitivity of the loop of Henle to calcium and magnesium ions. By contrast, the hypermagnesemia that occurs in chronic renal failure results from the reduced glomerular filtration of magnesium.
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PMID:Abnormal renal magnesium handling. 826 9

Hypomagnesemia in childhood is relatively frequently noted in the neonatal period due to maternal causes, such as decreased intake due to vomiting, overuse of laxatives, and neonatal causes such as intrauterine growth retardation, birth asphyxia and exchange transfusion. A very rare cause of neonatal magnesium deficiency is called primary hypomagnesemia caused by impaired intestinal absorption of magnesium. Reference values of serum magnesium in cord blood are slightly lowered. Erythrocyte magnesium content is also lowered in cord blood and during the first month after birth. Mononuclear magnesium content shows no differences with age. Renal magnesium loss is diagnosed by the presence of hypomagnesemia with an inappropriately high 24-hour urinary magnesium excretion. In isolated familial hypomagnesemia an autosomal dominant as well as an autosomal recessive mode of inheritance was found. The renal magnesium threshold is lowered in both forms but the tubular maximum is only lowered in the dominant form. In familial hypomagnesemia-hypokalemia (Gitelman syndrome) the renal magnesium threshold is lowered but the tubular maximum is in the normal range. In this syndrome, with probably an autosomal recessive mode of inheritance, the renal defect might be located in the distal nephron after the medullary part of the ascending limb of the loop of Henle. The magnesium content of mononuclear cells and erythrocytes is in the normal and lower normal range, respectively. In the familial hypomagnesemia-hypercalciuria syndrome, hypomagnesemia is always combined with hyperuricemia and nephrocalcinosis. Myopia and horizontal nystagmus are often present.
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PMID:Magnesium metabolism in childhood. 826 18

To investigate interactions between sex hormones, dietary fructose, and a severe magnesium deficiency on calcium metabolism, 10 week old ovariectomized (OVX) female, and orchiectomized (ORX) males rats were studied. The OVX and ORX animals were divided into two groups: one half of the animals in each group was injected with beta-oestradiol-3-benzoate dissolved in sesame oil twice a week; the other half was injected with testosterone cypionate in sesame oil twice a week. All animals were pari-fed a severely magnesium-deficient fructose diet. After a 4 week experimental period, a 24 h urine sample was collected for measurements of cAMP, calcium, magnesium, and phosphorus. Blood was collected for determination of calcium, magnesium, phosphorus, 25-hydroxy- and 1.25-dihydroxycholecalciferol [25(OH)D, 1.25(OH)2D], and parathyroid hormone (PTH). Femurs were used for measurements of bone mineral content (BMC) and density (BMD). Oestrogen treatment produced hypercalcaemia and hypercalciuria, and, further, this was higher in female than in male rats. In contrast, testosterone treatment produced hypocalcaemia and hypocalciuria. Hypocalcaemia in testosterone-treated animals may stimulate secretion of PTH. Testosterone-treated animals had significantly lower BMD than oestrogen-treated animals. High circulating PTH seemed to cause bone loss in the testosterone group. High PTH may stimulate hydroxylation of 25(OH) D to 1.25(OH)2D in the kidneys, and high circulating 1.25(OH)2D would antagonize bone formation. Either endogenous or exogenous oestrogen increased kidney calcification. The study indicates that oestrogen-fructose-magnesium interaction on calcium metabolism was significantly different from that of testosterone.
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PMID:Exogenous oestrogen affects calcium metabolism differently from exogenous testosterone in ovariectomized or orchiectomized rats fed a high fructose diet severely deficient in magnesium. 881 91


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