Effect of dietary magnesium supplementation on bone loss in rats fed a high phosphorus diet.

The purpose of this study was to investigate the effect of dietary magnesium (Mg) supplementation on bone loss in rats fed a high phosphorus (P) diet. Weanling Wistar strain rats were randomly divided into four dietary groups of 6 rats each and fed their respective diets; a diet containing 0.3% P and 0.05% Mg (C), a diet containing 1.5% P and 0.05% Mg (HP), a diet containing 0.3% P and 0.15% Mg (HMg), or a diet containing 1.5% P and 0.15% Mg (HPMg), for 21 days. Compared to the C and HMg groups, serum parathyroid hormone (PTH) concentration was significantly higher in the HP and HPMg groups. Serum osteocalcin concentration and urinary excretion of C-terminal telopeptides of type I collagen (CTx), markers of bone turnover, were significantly higher in the HP and HPMg groups than in the C and HMg groups. Dietary Mg supplementation had no significant effects on serum PTH and osteocalcin concentrations, while urinary excretion of CTx was significantly lower in the HPMg group than in the HP group. These results suggested that dietary Mg supplementation suppressed bone resorption due to high P diet.     

Urinary magnesium excretion in asthmatic children receiving magnesium supplementation: a randomized, placebo-controlled, double-blind study.

The aims of this study were to establish whether a magnesium (Mg) deficit indicated by a decreased urinary excretion exists and to determine whether 12-week oral Mg supplementation affects the Mg status and bronchodilator use in children with stable bronchial asthma. The effects of long-lasting Mg supplementation were investigated in 89 children 4 to 16 years of age with mild or moderate persistent bronchial asthma in a randomized, double-blind, placebo-controlled, prospective study. Each subject received one capsule of Mg citrate per day (= 7 years: 200 mg, > 7 years: 290 mg) or one capsule of placebo containing 260 mg glucose during 12 weeks. Evaluation was performed at 4-week intervals. Venous blood serum total and free Mg and urine Mg levels were determined at the beginning and end of the 12-week period. Parents recorded the number of bronchodilator doses twice daily. A urinary Mg loss (6.81 +/- 3.9 versus 2.79 +/- 1.39 mmol/day, p = 0.01) was observed in the placebo-treated persistent moderate asthmatics. Bronchodilator use was significantly higher after 8 and 12 weeks in the placebo-treated than in the Mg-treated patients with moderate asthma (31.1 +/- 1.8 versus 29.5 +/- 1.2 puffs per patient/4 weeks, p < 0.05, and 31.0 +/- 2.3 versus 29.3 +/- 0.9 puffs per patient/4 weeks, p < 0.05, respectively). Long-lasting Mg supplementation is clearly of benefit in mildly to moderately asthmatic children and is recommended as a concomitant drug in stable asthma.     

Recommended dietary amounts of magnesium: Mg RDA

In developed countries, the recommended dietary amounts of magnesium have been set at 6 mg/kg day. The magnesium requirements for optimal health in the adult population depend on mesological and constitutional conditioning factors. They may intervene at every stage of magnesium metabolism: absorption, circulation, storage and excretion. The influence of other nutrients is more significant on magnesium absorption than on urinary excretion. Among the multiple interactions it is important to emphasize the maintenance of a Ca/Mg ratio close to 2 in the intake. Magnesium deficit and stress reinforce each other in a pathogenic vicious circle. The Bw35 allele of HLA typing and behavioural type A discriminate two constitutional factors increasing magnesium requirements. The effective passive regulatory mechanism for magnesium overload, the lability of the active regulatory mechanisms for magnesium deficit and the considerable need for exchangeable magnesium are factors which attribute special importance to balance studies in determining the magnesium intake which prevents negative magnesium balance and magnesium deficiency. Marginal primary magnesium deficit affects a large proportion of the population (15 to 20%), in keeping with a daily mean magnesium intake slightly over 4 mg/kg day versus the Mg RDA of 6 mg/kg day. A physiological oral magnesium load test, evaluated through non-specific and specific clinical and paraclinical items, constitutes the best proof that the clinical pattern depends on an insufficient magnesium intake, confirmed after one month of supplementation. Further research appears necessary.(ABSTRACT TRUNCATED AT 250 WORDS)     

The alteration of magnesium, calcium and phosphorus metabolism by dietary magnesium deprivation in postmenopausal women is not affected by dietary boron deprivation.

A study with human volunteers was conducted to test the hypothesis that naturally occurring inadequate intakes of magnesium induce negative magnesium balance and undesirable changes in calcium metabolism variables, and that these changes are influenced by dietary boron. Diets composed of ordinary Western foods providing approximately 118 and 318 mg Mg/d and approximately 0.25 and 3.25 mg B/d were fed in a double-blind Latin square design to 13 healthy, post menopausal Caucasian women (aged 50-78 years) living in a metabolic unit. Magnesium balance, which was positive when dietary magnesium was 318 mg/d, became negative when dietary magnesium was 118 mg/d. Magnesium deprivation decreased urinary calcium excretion, and significantly increased calcium balance when balance data analyzed came from all collections during the 42-day periods. Urinary phosphorus excretion was increased, but fecal phosphorus excretion was decreased, thus phosphorus balance was not significantly affected by magnesium deprivation. Magnesium deprivation did not affect manganese or zinc balance. The balance data indicated that 700 mg of calcium, 1.0 mg of manganese, and 10 mg of zinc were adequate for post menopausal women. Magnesium deprivation increased serum 25-hydroxycholecalciferol and decreased serum total cholesterol concentrations. Boron deprivation increased but magnesium deprivation decreased urinary potassium excretion. Boron supplementation decreased serum 17beta-estradiol and progesterone when dietary magnesium was low. The dietary treatments did not affect serum calcitonin, parathyroid hormone, osteocalcin or alkaline phosphatase concentrations. One woman placed on consecutive magnesium-low dietary periods exhibited heart ventricular ectopy after consuming the magnesium-low diet for 72 days; the ectopy disappeared upon consuming the magnesium-adequate diet. The findings indicated that consuming an ordinary diet deficient in magnesium, resulting in negative magnesium balance, can affect calcium, potassium, and cholesterol metabolism. Dietary boron did not have an obvious effect on the response to magnesium deprivation.     

Comparative study of the efficacy of potassium magnesium L-, D- and DL-aspartate stereoisomers in overcoming digoxin- and furosemide-induced potassium and magnesium depletions.

Potassium and magnesium aspartate (K,Mg aspartate) is used in treating and preventing cardiac disruptions caused by electrolytic disturbances, primarily low potassium (K) and magnesium (Mg) levels (e.g. in the treatment with cardiac glycosides and diuretic drugs). Widely used, K,Mg aspartate is synthesized from aspartic acid representing a racemic mix of L- and D-stereoisomers. Differences in metabolism and utilisation of D- and L-amino acids probably have an effect on the pharmacological properties of K,Mg L- and D-aspartates, and what is more, pharmacological doses of magnesium and potassium salts may induce toxicity, which differs according to the nature of the anions. Therefore, the purpose of the present work was to study the effect of intravenously administered K,Mg L-aspartate in comparison with its D- and DL-stereoisomers on K and Mg restoration rates in plasma, erythrocytes and myocardium and to evaluate the urine excretion rate of amine nitrogen and Mg in digoxin and furosemide treated rats. To induce Mg depletion, male rats, weighing 180-200 g, were given furosemide and digoxin at doses of 30 mg/kg (i.p.) and 0.25 mg/kg (i.p.) daily for 14 days. After 14 days K,Mg L-, D- and DL-aspartates were administered with simultaneous furosemide and digoxin treating at dose of 100 mg/kg (i.v.), which corresponds to 46.95 mg of Mg aspartate (i.e. Mg = 3.96 mg) and 53.05 mg of K aspartate (i.e. K = 12.12 mg) per kg bodyweight. Erythrocyte, plasma and urine Mg levels were measured by colorimetric assay using the method based on the staining reaction of Mg and thiazole yellow. Myocardium Mg and K content and erythrocyte K levels were determined by flame atomic absorption spectroscopy. The level of amine nitrogen was measured by colorimetric assay using the method based on the staining reaction with ninhydrin. It was shown that K,Mg L-aspartate administration leads to higher compensation of K and Mg deficiency in rats with furosemide and digoxin induced K and Mg depletion, as compared with D- and DL-stereoisomers. According to the K and Mg deficiency correction rate, K,Mg aspartates may be ranged in the following order: K, Mg L-aspartate > K,Mg DL-aspartate > K,Mg D-aspartate. It was shown that after administration of K,Mg L-aspartate, daily urine excretion of amine nitrogen and Mg is less than after D- and DL-stereoisomer administration. According to the quantity of excreted amine nitrogen and Mg in urine, K,Mg aspartates may be ranged in the following order: K,Mg D-aspartate = K, Mg DL-aspartate > K,Mg L-aspartate. So, K,Mg L-aspartate is more beneficial in the treatment of several forms of primary Mg and K deficiency than K,Mg DL-aspartate and K, Mg D-aspartate.     

Oral magnesium supplementation improves fetal circulation.

It is well known that pregnancy is a condition in which plasma magnesium falls because of accumulation of the ion in the placenta and fetus. Magnesium (Mg) is therefore widely given as a supplement during pregnancy, particularly in cases of preterm labour. In our experience, the combination of oral Mg (magnesium pyrrolidone carboxylic acid) at a dose of 360 mg/day with conventional ritodrine treatment allows a reduction in ritodrine dosage, accompanied by a significant reduction in side effects. We therefore evaluated changes in fetal blood flow, using pulsed Doppler, in women submitted to combined magnesium and ritodrine treatment compared to those treated with ritodrine plus placebo. The Mg-treated group showed a decrease in vessel resistance both in the umbilical artery and in the fetal middle cerebral artery, indicating that fetal vasculature is sensitive to exogenous Mg. Measurement of plasma and mononuclear cell Mg showed an intracellular increase in the cation of about 10 per cent. We conclude that oral magnesium supplementation in pregnancy is safe and that it has a positive effect on the fetal circulation.     

Changes in plasma, erythrocyte, and urinary magnesium with prolonged swimming exercise

Erythrocyte, plasma and urinary magnesium were observed in a group of 8 well-trained swimmers and in a group of 10 untrained subjects before, 2 minutes after and 30 minutes after a swimming test. After effort, plasma Mg (pMg) decreased significantly in both groups. Erythrocyte and urinary Mg variations were not significant in this study. PMg decrease after effort was more important in the swimmers group than in the untrained group (12% versus 6% after 2 minutes; 21% versus 4% after 30 minutes). The observed fall in plasma Mg concentration after exercise cannot be explained by a shift into erythrocytes during exercise, since the Mg content of these blood cells did not suffer significant alterations. The possible causes of the observed phenomena are discussed.     

Effect of parathyroid hormone on urinary acidification.

The effect of parathyroid hormone (PTH) administration on urinary acidification was studied in intact and thyroparathyroidectomized dogs. PTH administration resulted in a significant increase in urine pH and HCO3 excretion. In dogs with maximally acid urine caused by Na2SO4 infusion PTH administration also led to a significant increase in urine pH and to a decrease in ammonium excretion. To examine the effect of PTH on H+ secretion in the distal nephron we measured the urine-blood (U-B) PCO2 gradient in dogs with maximally alkaline urine (urine pH greater than 7.8) before and after PTH administration. After infusion of the hormone, HCO3 excretion increased significantly but the U-B PCO2 gradient remained unchanged. The effects of PTH infusion on urinary acidification in animals with distal renal tubular acidosis caused by LiCl administration were also studied. PTH administration to these dogs increased HCO3 excretion to the same level seen in normal dogs. These data suggest that PTH does not inhibit distal H+ secretion but increases HCO3 excretion by depressing proximal HCO3 reabsorption.     

Is magnesium a marker of disordered mineral metabolism in males with idiopathic recurrent calcium urolithiasis? Observations focussing on fasting magnesiuria and magnesiemia, protein and other substances in urine and plasma.

Mg can theoretically play a role in renal calcium stone formation of IRCU patients, but the status of Mg is uncertain. The aim of this study was to investigate whether in IRCU variation of Mg in fasting urine and plasma is associated with altered urine Ca, Pi, oxalate, Ca/Pi ratio, supersaturation and other factors, the clinical severity of stone disease (metabolic activity; MA) included. This was a cross-sectional study (284 IRCU patients), comprising males with mean age in the fifth decade and unimpaired renal function. Patients had an unrestricted home diet, standardized laboratory procedures, including sample collection (daily and fasting urine, plasma), with classification of patients according to tertiles of fasting Mg-uria, keeping comparable age, the number of patients with renal stones present or absent, and normo- or idiopathic hypercalciuria. MA was scored. We found that the tertile I patients (= referent) exhibited sub-normal fasting Mg excretion (< 4 mg/2 h) and fractional excretion (< 3.5%), in daily urine the lowest Mg and oxalate, but highest Ca excretion rate; compared with tertile III, tertile I patients had significantly lower plasma total (not ultrafiltrable) Mg, blood bicarbonate and pH, and the lowest MA; fasting urinary excretion of Ca and citrate were also low, but urinary Pi, body weight, plasma glucose and insulin were increased. In tertile III not only was Mg-uria (excretion, FE) significantly elevated vs I, but so were urinary pH, excretion of sodium, Ca, potassium, protein (total and non-albumin) and citrate, FE sodium and Ca, the urinary molar ratios Ca/Pi and Mg/Potassium, hydroxyapatite supersaturation, bone resorption markers, and MA; in this environment urinary oxalate and Ca oxalate supersaturation were unchanged, plasma glucose, insulin and parathyroid hormone decreased. The tertile II patients, showing intermediate Mg excretion, also exhibited (vs. I) increase of FE Mg, urinary excretion and FE of sodium and Ca, excretion of protein, citrate and bone markers, the ratios Ca/Pi and Mg/Potassium, and MA. When urinary Ca/Pi was considered as the outcome of disordered metabolism, significant determinants (according to multiple regression analysis) were urinary Pi (negative), Ca and Mg/Potassium (positive); significant determinants of MA, the sum of stone-forming processes, were the urinary concentration of non-albumin protein, Mg/Potassium and sodium (all positive). Among IRCU patients 1) approx. one third is in need of Mg conservation by the kidney, associated with low plasma total Mg, modest metabolic acidosis, a trend towards overweight, high plasma insulin and glucose; 2) low Mg- or acidosis-induced increase of bone resorption may follow, attenuating glycemia and insulinemia but forcing the kidney to functional adaptation, manifesting as a rise of urinary sodium, Mg, Ca, Pi, Ca/Pi, pH and protein, together presumably aggravating MA; 3) larger controlled studies are justified, to decide whether Mg deficiency initiates renal Ca stones, and if urinary Mg loss exaggerates IRCU.     

Effects of acute cisplatin administration on renal ATPase activities and magnesium excretion of rats

Male Wistar rats were killed 1, 2, or 4 days after a single intraperitoneal injection of cisplatin (5 mg/kg). Functional renal indices, enzymatic activities, and morphological variables were studied. One day after the injection, the treated group showed an increase in the magnesium and phosphate fractional urinary excretion (FE) vs the control group (FE Mg = 5.2 +/- SEM 0.5% vs 13.0 +/- 1.7%; P less than 0.01; and FE P = 4.7 +/- 0.7% vs 14.0 +/- 1.9%; P less than 0.01). Two days after cisplatin administration, a decrease in creatinine clearance of treated animals was found, to 0.33 +/- 0.03 vs 0.51 +/- 0.03 ml/min; P less than 0.05. Na-K-ATPase and ouabain-insensitive ATPase activities were studied in the proximal convoluted tubule, the medullary thick ascending limb of the Henle's loop (mTAL), and the distal convoluted tubule. Only in mTAL one day after the cisplatin injection was there a decrease in Na-K-ATPase activity in the treated group vs controls (1103 +/- 145 vs 1734 +/- 189 pmol Pi/mm.h; P less than 0.05). Morphological studies showed a decrease in mTAL diameters on day 1, and an increase in proximal convoluted tuble diameters at day 2 of treated rats vs controls, at 27.8 +/- 0.6 vs 31.4 +/- 0.7 microns; P less than 0.05, and 50.4 +/- 1.2 vs 47.4 +/- 0.2 microns; P less than 0.05 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Histamine metabolism and pinnal hyperaemia during magnesium deficiency in rats

The relation between histamine metabolism and an appearance of pinnal hyperaemia during magnesium (Mg) deficiency, and the effects of some factors on these were studied in 3-week-old Wistar rats. On a Mg-deficient diet (Mg 0.001%), the histamine concentrations in plasma and urine increased after 4-5 d, and reached a maximum after 6-12 d. Pinnal hyperaemia appeared during the same time course. The hyperaemia was reduced by the administration of antihistamines (cimetidine and diphenhydramine). These results indicate that pinnal hyperaemia during Mg deficiency is mediated by histamine. The administration of oestradiol benzoate (0.08 mg/100g body weight subcutaneously once a day for 8 d) and/or gamma-ray irradiation (600 rad/d before experiments) reduced the appearance of pinnal hyperaemia and the increment in the urinary histamine during Mg deficiency. The histamine content increased in the spleen and some tissues after 8 d, but not in the skin, with increasing the activity of histamine synthesis. The treatments mentioned above depressed the increment of histamine content. These results suggest that the pinnal hyperaemia and the increment of the urinary histamine in the Mg-deficient rat are related to the increment of both the histamine synthesis and release.     

Renal potassium wasting and hypocalciuria ameliorated with magnesium repletion in Gitelman's syndrome.

A woman aged 45 years was presented with hypokalemic metabolic alkalosis and hypomagnesemia associated with renal potassium and magnesium wasting. Her 24-hour urinary calcium excretion was strikingly low despite normocalcemia and normal creatinine clearance, which is one of characteristic findings of Gitelman''s syndrome (GS). She was evaluated for the responses following Mg supplementation for 10 days, which showed marked increments in serum potassium and magnesium as well as improvements of the degree of renal potassium wasting and hypocalciuria. This amelioration of abnormal biochemical pictures in this patient after Mg supplementation proposes that the hypokalemia with renal potassium wasting and hypocalciuria may be caused by abnormal Mg metabolism.     

Metabolic studies in primary tubular hypomagnesaemia-hypokalaemia

13 1/2 year old boy with short stature and pubertal delay had infrequent episodes of tetany. Biochemical determinations demonstrated low plasma and high urinary magnesium and potassium levels, hypocalciuria, slightly increased plasma bicarbonate, slightly reduced fractional distal reabsorption of chloride and sodium, high plasma renin activity and high urinary excretion of prostaglandins (E2, F2 alpha). The other parameters of renal functions were normal. Endocrine evaluation of short stature and pubertal delay was normal. Intracellular magnesium and potassium levels in lymphocytes and erythrocytes were within normal limits. Cyclooxygenase blockade with Indomethacin 2.5 mg/kg daily during 4 weeks normalized urinary excretion of prostaglandins and corrected in part low plasma and high urinary potassium levels, but had no effect on magnesium, calcium, sodium and chloride handling. These data raise the possibility that tubular hypomagnesaemia-hypokalaemia could be solely explained by a low renal threshold for magnesium.     

Effect of glucagon on magnesium renal reabsorption in the rat

The recent localization, in the rat, of a glucagon-sensitive adenylate cyclase in these segments where the bulk of calcium and magnesium is reabsorbed suggests an effect of this hormone on calcium and magnesium tubular transport. Renal tubular handling of calcium and magnesium as well as of sodium and phosphate was therefore studied by clearance methods in anesthetized rats, either intact or thyroparathyroidectomized (TPTX), infused with glucagon at a rate of 25 ng·min^–1/100 g bw just after a priming dose of 2.5 g. The hormone administration resulted in a significant decrease of absolute and fractional magnesium excretion (from 16.3±0.7% to 9.7±1.7% for intact rats and from 20.9±1.8% to 6.9±1.0% for TPTX rats), associated with the well-known increase in sodium and phosphate fractional excretion. Moreover, a small and transient decrease of calcium fractional excretion was observed concomitantly with a decrease of plasma calcium concentration. The significant increase in magnesium absolute reabsorption, observed whatever the filtered load and independently of PTH and calcitonin, may be an evidence for a direct tubular effect of glucagon.     

Adenosine 3',5' cyclic monophosphate, calcium and magnesium excretion in ethanol intoxication and hangover.

Effect of ethanol on adenosine 3', 5' cyclic monophosphate (cAMP), calcium (Ca) and magnesium (Mg) excretion was studied in controlled clinical conditions in man. Seven male volunteers served as their own controls. In 5 subjects cAMP excretion was primarily suppressed by ethanol. Ethanol appeared to have a biphasic effect on Ca excretion, an initial stimulation followed by a conservation phase. Mg excretion was stimulated by ethanol in 5 subjects. Subjects having nausea and vomitus and the most severe hangover symptoms had the lowest urinary Ca excretion and the lowest imitial cAMP excretion. Ca and Mg metabolism and the susceptibility of the body to the toxic effects of ethanol appeared to be interrelated.     

肾局部内皮素、一氧化氮在尿蛋白产生中的作用

目的:为明确肾局部内皮素(ET)和一氧化氮(NO)在蛋白尿产生中的作用,作者观察了阿霉素肾病鼠血浆及肾皮质ET、NO含量在蛋白尿发生发展过程中的变化及其与尿蛋白含量的关系。方法:(1)一次性注射法复制大鼠阿霉素肾病综合征模型,并隔日留24 h尿测取尿蛋白含量;(2)分别于蛋白尿前期、上升期、高峰期及下降期取血浆及肾皮质匀浆,用放射免疫法检测ET含量,用Griess法检测NO代谢产物NO^-₂代表NO水平;(3)分别研究了血浆及肾皮质中ET 、NO与尿蛋白量两两间的相关性。结果: 正常鼠尿蛋白排泌量4-7(mg/d),肾病鼠4个时间点尿蛋白排泌量分别为5、10、241和201 mg/d,于蛋白尿上升期始有显著意义的增加,32 d为高峰期,56 d有所下降。蛋白尿前期、上升期、高峰期和下降期的血浆ET值分别为134、 150、 538、 445 ng/L,自上升期始明显高于同期对照组(126-129 ng/L);肾皮质ET分别为364.6、 653.3、 1 526.8、 1 393.6 pg/g肾皮质,自蛋白尿前期始均明显高于对照组(235.9-246.1 pg/g,P＜0.05);4个时点血浆NO^-₂值分别为40、36、8、11 μmol/L,自上升期始明显低于对照组(42-46 μmol/L);肾皮质NO^-₂值分别为80、69、8、25 nmol/g肾皮质,自蛋白尿前期始明显低于对照组(114-124 nmol/g,P＜0.05)。上升期血浆ET和下降期血浆NO^-₂与尿蛋白含量密切相关,而肾皮质ET和NO均自蛋白尿前期始便密切相关于尿蛋白排泌量(P＜0.05)。结论: 在蛋白尿发生发展过程中血浆和肾皮质ET、NO均有显著改变,而肾皮质ET、NO含量的改变在蛋白尿的发生发展中起重要作用。     

Adenosine 3‘, 5’ cyclic monophosphate,calcium and magnesium excretion in ethanol intoxication and hangover

Effect of ethanol on adenosine 3′, 5′ cyclic monophosphate (cAMP), calcium (Ca) and magnesium (Mg) excretion was studied in controlled clinical conditions in man. Seven male volunteers served as their own controls. In 5 subjects cAMP excretion was primarily suppressed by ethanol. Ethanol appeared to have a biphasic effect on Ca excretion, an initial stimulation followed by a conservation phase. Mg excretion was stimulated by ethanol in 5 subjects. Subjects having nausea and vomitus and the most severe hangover symptoms had the lowest urinary Ca excretion and the lowest initial cAMP excretion. Ca and Mg metabolism and the susceptibility of the body to the toxic effects of ethanol appeared to be interrelated.     

Decreased absorption and retention rates of magnesium in the rats fed on spinach-supplemented diets: possible explanations.

We studied the bioavailability of magnesium (Mg) in spinach after boiling with distilled water, using Mg-deficient growing male rats. The rats were fed a semipurified diet (Mg:0.063 per cent (w/w)) for 3 days. then a Mg-deficient diet (Mg:0.001 per cent (w/w)) for 5 days. They were then divided randomly into 7 groups of 6 rats each, and fed the semipurified diet (Mg: 0.063, 0.045 or 0.027 per cent (w/w)), or the spinach-supplemented diet (10 per cent (w/w) dried and powdered spinach after boiling with distilled water for 3 min at 100 degrees C). The Mg content of the diets supplemented with spinach grown on chemical nutrients, and on manure from pigs, cattle and fowl, was 0.069, 0.051, 0.043 and 0.036 per cent (w/w), respectively. Water intake and volumes of urine and faeces were significantly greater in the rats fed the spinach-supplemented diets than in those fed the semipurified diets. Apparent absorption of Mg, and urinary and faecal excretions of Mg were directly related to Mg intake: no significant difference was observed amongst the groups. Both the ratios of Mg absorption and retention were significantly lower in the rats fed diets supplemented with spinach than in those fed semipurified diets. The plasma Mg level was directly related to Mg intake in the rats fed the semipurified diets and the spinach-supplemented diets. However, the plasma Mg level in the rats fed spinach grown organically on manure from fowl tended to be higher than in the other groups. From these results, it was concluded that bound Mg in spinach was effectively utilized by Mg-deficient rats, however, the absorption and retention rates of Mg in rats fed diets supplemented with spinach were decreased. Possible explanations were discussed.     

Nephrocalcinosis without functional renal impairment in rats subjected to subacute moderate magnesium deficiency, and intervention studies on the mobilization of calcium deposits

Female Sprague-Dawley rats (100-120 g) were kept for 12 d on diets containing 250, 1500, or 9000 ppm Mg. Then subgroups were loaded with water, frusemide or magnesium and urine was collected over 6 h. Moderately Mg-deficient diet (250 ppm) induced moderate hypomagnesaemia (62.3% of controls), but did not result in hypercalcaemia or the formation of typical erythema. Nevertheless, pronounced nephrocalcinosis developed, as shown by increased renal wet and dry weight and elevated tissue concentrations of Ca, P and Mg, the calculous deposits probably consisting to a large extent of Ca3 (PO4)2. Despite these alterations, renal function remained unimpaired in Mg-deficient rats, as shown by normal urinary creatinine excretion and the unaffected ability of the kidneys to concentrate urine. Loading with water, frusemide or Mg increased urinary excretion of calcium in all three diet groups to a similar extent; hence no significant proof can be given that calculous deposits are mobilized under these conditions. Since comparable conditions may also be present under clinical conditions in man, special care should be given to maintain optimal Mg balance.     

Effects of simultaneous increases in dietary phosphorus and magnesium concentrations on nephrocalcinosis and kidney function in female rats.

The effects of simultaneous increases in dietary phosphorus (P) and magnesium (Mg) concentrations while maintaining a constant P:Mg ratio on nephrocalcinosis and kidney function in female rats was investigated. Female Wistar rats were fed a control diet (3.12 g P, 0.51 g Mg per kg diet) or a diet having either 3 times the control P and Mg concentrations (3-fold diet; 9.25 g P and 1.42 g Mg per kg diet) or 5 times the control concentrations (5-fold diet; 14.97 g P and 2.37 g Mg per kg diet) for 21 d. The three experimental diets all had same P:Mg molar ratios (control diet; 4.81, 3-fold diet; 5.11, 5-fold diet; 4.96). The 3-fold diet had no significant influence on kidney calcium (Ca), Mg or P concentrations. However, kidney Ca, Mg and P concentrations were significantly higher in rats fed the 5-fold diet than in rats fed the control or 3-fold diets. No significant differences in creatinine clearance were observed among the three groups. Urinary albumin and beta 2-microglobulin excretion were higher in rats fed the 5-fold diet than in rats fed the control or 3-fold diets, while the 3-fold diet had no significant influence on the urinary albumin and beta 2-microglobulin excretion. These results suggest that absolute concentrations of dietary P and Mg are important factors with regard to the development of nephrocalcinosis and diminished kidney function.