Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Magnesium Deficiency”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1975

Bone composition and phosphatase activity in magnesium deficiency in rats.

The effect of magnesium deficiency on phosphatase activity and bone composition was determined in the femora of young rats. In the right distal metaphysis the acid and alkaline phosphatase activities were decreased in magnesium-deficient rats, and the activity of bone alkaline phosphatase in the incubation mixture after adding magnesium was significantly greater in the magnesium-deficient than in the control rats. In the left distal metaphysis the water content was significantly lower in the magnesium-deficient rats at the fifth week but not at the third week. Conversely, the ash content of metaphyseal bone was significantly increased in magnesium-deficient rats at the fifth week, but not at the third week. The magnesium and phosphorus contents were abnormally low in the deficient bone at both periods. The calcium content was increased in the deficient bone at the third week, but not at the fifth week.

Alkaline Phosphatase↗
PubMed1994

Role of dietary magnesium deficiency in the pressor and arrhythmogenic response to epinephrine in the intact dog.

The effect of dietary magnesium deficiency on the pressor and arrhythmogenic responses to epinephrine was investigated in 19 dogs maintained either on a normal diet (11 dogs) or a diet deficient in magnesium (8 dogs). Magnesium-deficient dogs had significantly lower serum magnesium levels than the control dogs on a normal diet. Magnesium-deficient dogs showed an increased pressor sensitivity to epinephrine as determined by the dose of epinephrine required to cause a maximal pressor response (3.4 micrograms/kg/min compared to 13.4 micrograms/kg/min, p < 0.05). Magnesium-deficient dogs also had a significantly lower threshold dose for ventricular premature beats (0.8 microgram/kg/min compared to 2.7 micrograms/kg/min, p < 0.05). Acute administration of magnesium sulfate restored pressor sensitivity and ventricular premature beat threshold to normal levels in the magnesium-deficient dogs. Threshold dose for ventricular tachycardia beat was similar in both normal and magnesium-deficient dogs, and threshold was raised significantly in both groups by acute administration of magnesium.

Animals↗
PubMed1989

Depression and magnesium deficiency.

The psychiatric symptoms of magnesium deficiency are unspecific, ranging from apathy to psychosis, and may be attributed to other disease processes associated with poor intake, defect absorption, or excretion of magnesium. Serum magnesium should be determined when there are symptoms consistent with magnesium deficiency and/or in conditions which can lead to a deficiency, e.g., malabsorption, malnutrition, alcoholism and diuretic treatment. A low serum value suggests magnesium deficiency, but the diagnosis is reinforced with analyses of magnesium in the urine and a loading test with magnesium. Magnesium can be given orally or intramuscular/intravenously.

Aged↗
PubMed1976

Magnesium, calcium and zinc levels of maternal and fetal tissues in magnesium deficient rats.

The interaction of magnesium with two other mineral elements, calcium and zinc, was studied in maternal tissues and fetuses of pregnant rats fed a magnesium deficient diet throughout gestation. Reduction in maternal femur magnesium and a trend for increased kidney calcium reflected the dietary magnesium deficiency. In fetuses, however, total magnesium content was reduced and , in addition, fetal zinc content was also lower than normal in the group most severly deficient in magnesium. The possible interpretation of this magnesium-zinc interaction is discussed.

Animals↗
PubMed1987

Tissue minerals of magnesium-deficient rats with thiamine deficiency and excess.

To clarify the influence of thiamine deficiency or a dietary excess of thiamine on the mineral balance in magnesium-deficient animals, the following six different synthetic diets were fed to Wistar rats. Group 1: thiamine and magnesium-deficient; group 2: thiamine-deficient, magnesium-deficient; group 3: thiamine-sufficient, magnesium-deficient; group 4: thiamine-sufficient, magnesium-sufficient; group 5: thiamine excess, magnesium-deficient; group 6: thiamine excess, magnesium-sufficient. Rats were sacrificed after 4 weeks of these dietary regimens. In the magnesium-deficient groups, magnesium levels in serum, bone and heart decreased; calcium levels in serum and heart increased and, in contrast, calcium levels in bone decreased. These changes in mineral concentration seen in magnesium-deficient animals, as well as kidney weight changes, were alleviated significantly when the animals were also deficient in thiamine. It can be presumed that thiamine deficiency inhibits magnesium depletion and, consequently, the influence of magnesium deficiency is less significant in the thiamine- and magnesium-deficient animals. In regard to trace elements, the significant changes seen in magnesium-deficient rats were as follows: zinc in liver, muscle and blood increased and that in bone decreased. Copper in blood, kidney, muscle and heart increased and that in liver decreased. Iron in serum, liver, spleen and kidney increased and that in whole blood decreased.

Animals↗
PubMed1996

Stability of free Mg2+ concentration and increased concentration of free Ca2+ in vascular smooth muscle cells during dietary magnesium deficiency in rat.

Intracellular free calcium and magnesium ion concentrations ([Ca2+]i and [Mg2+]i respectively) were estimated in thoracic aorta smooth muscle strips isolated from magnesium-deficient and control rats using fura-2/AM and mag-fura-2/AM, respectively. Adult male Wistar rats were fed a magnesium-deficient diet (10 mg Mg/kg diet) or a control diet (700 mg Mg/kg diet) for 30 days. Plasma magnesium level in magnesium-deficient rats was half of that in control rats at 30th day. Therefore, thoracic aorta strips, denuded of endothelium, were loaded with fura-2/AM or mag-fura-2/AM in the presence of 0.5 or 1.0 mM Mg2+, and [Ca2+]i or [Mg2+]i was measured under the same Mg2+ conditions. The [Ca2+]i in the aorta strips isolated from magnesium-deficient rats in the presence of 0.5 mM Mg2+ (254.9 +/- 13.1 nM) was approximately three times greater than in those from control rats in the presence of 1.0 mM Mg2+ (86.5 +/- 9.2 nM). The [Mg2+]i was not significantly different between the two groups at either Mg2+ level. The muscle tension and [Ca2+]i increased after [Mg2+]o was exchanged from 1.0 to 0.5 mM; however, [Mg2+]i showed no change. The total calcium content increased and total magnesium content decreased in thoracic aorta strips isolated from magnesium-deficient rats. These results suggest that [Mg2+]i is stable, but that [Ca2+]i increases in vascular smooth muscle cells of thoracic aortas isolated from dietary magnesium-deficient rats.

Animals↗
PubMed2002

Pro-fibrogenic effects of magnesium deficiency in the cardiovascular system.

Magnesium deficiency is known to produce cardiovascular injury. A large body of experimental evidence supports the postulation that an immuno-inflammatory reaction and increased oxidative stress may damage the myocardium and vasculature in magnesium deficiency. Reparative/reactive fibrosis in response to the injury has, however, received little attention. Recent evidence from a rodent model of acute magnesium deficiency suggests that humoral factors may activate cardiac fibroblasts by a free radical-mediated mechanism and contribute to cardiac fibrogenesis. A similar mechanism may also promote cellular hyperplasia and increased matrix synthesis in the vasculature.

Cardiomyopathies↗
PubMed1996

Integrins on joint cartilage chondrocytes and alterations by ofloxacin or magnesium deficiency in immature rats.

Recently, we showed that magnesium deficiency induces lesions in knee joint cartilage from 5-week-old rats that are very similar to ofloxacin-induced cartilage defects. We concluded that quinolone-induced arthropathy is probably due to chelation of magnesium and thus a deficit in functionally available magnesium in joint cartilage (Stahlmann et al. 1995). As magnesium deficiency in joint cartilage could impair chondrocyte-matrix interaction which is mediated by cation-dependent integrin receptors of the beta 1-subfamily, we investigated integrin expression in joint cartilage from untreated, ofloxacin-treated and magnesium-deficient Wistar rats. With immunohistochemical methods using monoclonal and polyclonal antibodies, we showed that the integrin pattern in joint cartilage from rats corresponded largely to integrin expression described for human cartilage tissue: beta 1, alpha 1, alpha 3 and alpha v subunits and the alpha 5 beta 1 and alpha v beta 3 heterodimers were consistently expressed. Joint cartilage lesions were detected in ofloxacin-treated and magnesium-deficient rats. Lesions were more pronounced in the quinolone-treated group. Expression of several integrins was reduced in the vicinity of lesions after oral treatment with 2 x 600 mg ofloxacin/kg for 1 day. Gross-structural lesions (e.g., cleft formation, unmasked collagen fibres) in magnesium-deficient rats were very similar but changes in integrin expression were less pronounced. On the other hand, changes in cartilage matrix composition showed similar alterations in ofloxacin-treated and magnesium-deficient rats: fibronectin deposition in the cartilage matrix increased in both groups while glycosaminoglycan content decreased. In summary, similar defects occur in ofloxacin-treated and magnesium-deficient rats and with immunohistochemical methods subtle differences are demonstrable.

Animals↗
PubMed1997

Functional magnesium deficiency in critically ill patients identified using a magnesium-loading test.

OBJECTIVE: To determine the feasibility of the magnesium-loading test in the critically ill and to validate serum ionized magnesium assay using the magnesium-loading test as a reference in this same patient population. DESIGN: Double-blind, randomized, controlled clinical investigation. SETTING: Tertiary level intensive care unit. PATIENTS: Forty-four consecutive critically ill patients without evidence of renal insufficiency. INTERVENTION: Patients were randomly allocated to receive 30 mmol (7.5 g) of magnesium sulfate daily for 3 days, or an equivalent amount of normal saline. MEASUREMENTS AND MAIN RESULTS: We recorded baseline characteristics, and serial serum biochemical measurements included creatinine, glucose, sodium, potassium, phosphate, total calcium, ionized calcium, total magnesium, and ionized magnesium. Serum assays were accompanied by 24-hr urine collections of creatinine and magnesium over the 3-day period. Baseline characteristics were comparable in both groups. In patients receiving magnesium, serum ionized magnesium and total magnesium concentrations were increased by 43% (p = .0001) and 59% (p = .0002), respectively, on day 1 as compared with the control group. Magnesium excretion in the control group averaged 4.8 +/- 2.3 mmol/day during the 3-day study period, while the magnesium excretion in the magnesium-loaded group was significantly increased to 22.7 +/- 10.9 mmol/day (p < .0001). Following day 1 magnesium loading, patients who excreted < 70% of the total magnesium (30 mmol infused magnesium plus 4.8 mmol basal excretion) were termed as functionally magnesium-deficient retainers (n = 12), and patients who excreted > 70% of the total magnesium were termed as nonretainers (n = 7). In addition, magnesium retainers on day 2 (nine of ten patients) and day 3 (five of six patients) excreted > 70% of the total magnesium, indicating a replenishment of body magnesium stores. In contrast, nonretainers on day 2 (four of five patients), and day 3 (four of four patients) continued to excrete excess amounts of magnesium. In the retainer group, only two patients had a low serum ionized magnesium concentration, while two other patients had low total serum magnesium values. In addition, magnesium retention was associated with low ionized calcium and high phosphate values. CONCLUSIONS: The magnesium-loading test is feasible and appears to be valid based on its performance during the 3-day evaluation. Using the magnesium-loading test as a reference, serum ionized magnesium appears to be an insensitive biochemical marker of functional hypomagnesemia. Larger cohort studies using the magnesium-loading test will help establish the true prevalence of magnesium deficiency and its associated risk factors in critically ill patients.

APACHE↗
PubMed1982

Plasma parathyroid hormone levels and intestinal calcium binding protein in magnesium deficient rats.

Rats were pair fed a magnesium deficient or control diet. Plasma parathyroid hormone (PTH) was estimated by radioimmunoassay using synthetic 1-34 PTH and intestinal calcium-binding protein (CaBP) was quantified directly by RIA in proximal duodenum, distal ileum and medium jejunum. In magnesium depleted rats, plasma magnesium levels were significantly decreased, a fall in plasma phosphate paralleled the decrease in plasma magnesium and plasma calcium levels were significantly increased after 14 days of magnesium deficiency. A significant rise in plasma PTH was observed on day 7 and 14 after magnesium deficiency. This increase disappeared on day 20. During the whole experimental period, no significant differences in CaBP levels were observed between the two groups of rats. Thus it is difficult to postulate an increase in vitamin D-dependent calcium absorption to explain the hypercalcemia found in magnesium deficient rats. Neither can the hypercalcemia be readily explained by an increased bone calcium mobilisation due to transient PTH increase since previous results have reported decreased bone resorption in magnesium deficient rats under similar experimental conditions.

Animals↗
PubMed2003

High fructose feeding of magnesium deficient rats is associated with increased plasma triglyceride concentration and increased oxidative stress.

The purpose of this study was to assess whether dietary carbohydrate could differentially influence the consequences of magnesium deficiency with particular emphasis on lipid metabolism and oxidative stress. Rats were fed a sucrose based or starch based diet either adequate or deficient in magnesium for two weeks. Magnesium deficient rats, as compared with rats fed magnesium adequate diets, displayed the usual decrease in plasma magnesium concentration. The classic symptoms of inflammation including hyperaemia, increased number of blood leukocytes and enlarged spleen weight were observed in these rats. Plasma TG and plasma apo B concentrations were also significantly increased. In addition, magnesium-deficient animals presented an increased susceptibility to lipid peroxidation of heart and liver tissues as shown by TBARS concentration. Regardless of magnesium status, sucrose feeding did not affect the magnesium plasma level and inflammatory parameters. Feeding rats the sucrose diets induced hypertriglyceridaemia and increased plasma apo B concentration. Heart and liver susceptibility to lipid peroxidation were significantly increased in rats fed the sucrose diets as compared with those fed the starch diets. Sucrose feeding in magnesium deficient rats was associated with higher plasma triglycerides concentration and higher tissue susceptibility to peroxidation as compared with magnesium deficient rats fed the starch diet. The results emphasised the potential detrimental and additional effect of sucrose feeding and magnesium deficiency on cardiovascular risk. Since the intake of magnesium has been reduced appreciably in industrialised countries while fructose consumption has been rapidly increased, the impact of this eating pattern should be clarified in humans.

Animals↗
PubMed1977

Magnesium deficiency anemia in the rat fetus.

Magnesium-deficient fetuses exhibited malformations (44%), anemia, and edema. Maternal plasma magnesium levels at day 21 of pregnancy reflected the level of dietary magnesium (2.43 +/- 0.09 mg Mg/100 ml, control; 0.74 +/- 0.02 mg Mg/100 ml, deficient). Plasma magnesium levels of deficient fetuses showed similar decreases although all fetal magnesium values at term were hihger than maternal values from the same group (3.29 +/- 0.22 mg Mg/100 ml, control; 1.78 +/- 0.07 mg Mg/100 ml, deficient). Magnesium deficiency did not appear to affect the maternal blood parameters. However, when fetal blood was examined, all of the parameters measured were altered in magnesum-deficient fetuses (Table 2). No abnormalities in hemoglobin bands or plasma proteins were seen between any groups by electrophoresis. Measurement of total protein contents showed no differences between maternal blood protein contents, but total plasma protein from magnesium-deficient fetuses was significantly lower than controls (2.00 +/- 0.14 versus 2.62 +/- 0.13 g/100 ml), thus establishing a factor in fetal edema production. Morphologic data showed that in magnesium-deficient fetuses, fetal erythropoiesis was significantly greater in liver, adrenal glands, and spleen than in controls and that maturation was normoblastic. Stained and unstained peripheral blood smears of magnesium-deficient fetuses showed and obvious macrocytosis and at least 50% of the red cells stained abnormally, exhibiting pale areas. Erythrocytic morphology seen in fetal magnesium deficiency is consistent with inadequate filling of the cell by hemoglobin as suggested by Cohlan et al. (5), a probable cause of membrane collapse. The inadequate filling of magnesium-deficient red blood cells (RBC) with hemoglobin might be explained by a reduction in hemoglobin synthesis which is consistent with the reduced mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) of the deficient fetal red cells. The role of magnesium in protein synthesis is also compatible with a reduction in hemoglobin synthesis, yet may not completely explain the abnormalities and resultant shortened lifespan of the red cells.

Anemia↗
PubMed1977

Erythrocyte membrane plaques from rats with magnesium deficiency.

This study investigated the anemia of dietary magnesium deficiency in inbred Fisher white rats using freeze-fracture electron microscopy. The plasma membranes of erythrocytes from animals receiving two different magnesium-deficient and control diets were observed at weekly or biweekly intervals for 6 wk. The earliest changes were small plaques on the external surface (ES) and fracture face (PF) of erythrocyte plasma membranes, which occurred after 2 wk of either magnesium-deficient diet. These plaques persisted and increased in size with progressive magnesium deficiency. When fully developed, the plaques consisted of round or oval elevations approximately 30-50 nm in diameter outlined by a narrow raised border. The surface of the plaques was smooth and devoid of intramembranous particles. Incubation of erythrocytes from magnesium-deficient rats in a physiologic solution containing 2 meq/liter magnesium for 1 hr at 37degrees C did not alter the appearance of the plaques. Erythrocytes from control rats, obtained during the same time periods, showed no plaques. Thus, a deficiency of magnesium in rats altered erythrocyte membrane structure.

Animals↗
PubMed1981

Magnesium deficiency. Role in arrhythmias complicating acute myocardial infarction?

Magnesium deficiency is likely to occur in certain patients prone to developing acute myocardial infarction, such as hypertensive patients being treated with diuretics, alcoholics, diabetics and patients with ischaemic cardiomyopathy taking diuretics and digitalis. Magnesium deficiency commonly accompanies potassium deficiency, can also cause it, and can prevent correction of potassium deficiency if potassium supplements alone are used. The results of analysis of plasma magnesium and potassium levels in 25 patients presenting with acute myocardial infarction are presented. Three patients were hypomagnesaemic and all exhibited serious ventricular arrhythmias (two patients exhibited early ventricular fibrillation and the third exhibited ventricular trigeminy and multifocal ventricular ectopy). Two of the three hypomagnesaemic patients were hypokalaemic. Two other patients in the series exhibited ventricular tachycardia and both were hypokalaemic. Magnesium therapy should be considered in hypokalaemic patients during the early stages of acute myocardial infarction, as the body distribution kinetics of magnesium and potassium are interlinked and magnesium deficiency may be the crucial factor in hypokalaemia-associated arrhythmias. In addition, consideration should be given to magnesium supplementation in patients prone to acute myocardial infarction if there is a likelihood of magnesium deficiency developing, as magnesium-deficient patients may be more susceptible to developing potentially fatal ventricular tachyarrhythmias during the early stages of infarction.

Adult↗
PubMed2002

Magnesium deficiency increases oxidative stress in rats.

Magnesium deficiency has been implicated in the development of atherosclerosis and late diabetic complications, diseases often associated with increased oxidative stress. Present study was carried out to examine the effect of magnesium deficiency on oxidative stress and total radical trapping antioxidant parameter (calculated) in rats and correlate it with the development of free radical mediated diseases. Male Wistar rats were divided into two groups and pair fed for six weeks with low magnesium diet (70 mg/kg) and control diet (990 mg/kg) prepared synthetically. Deionized water was given ad libitum. Low magnesium diet caused a significant decrease in plasma and red blood cell magnesium levels. A marked increase in plasma malondialdehyde and corresponding decrease in total radical trapping antioxidant parameters (calculated) were observed in the low magnesium diet group than control group. The level of plasma glucose increased moderately in the low magnesium diet group. Hypertriglyceridemia and significantly decreased plasma HDL (high density lipoprotein)-cholesterol levels were observed in the low magnesium diet group. The results clearly demonstrate that magnesium deficiency is associated with increased oxidative stress through reduction in plasma antioxidants and increased lipid peroxidation suggesting that the increased oxidative stress may be due to increased susceptibility of body organs to free radical injury.

Animals↗
PubMed1993

Magnesium deficiency produces insulin resistance and increased thromboxane synthesis.

Evidence suggests that magnesium deficiency may play an important role in cardiovascular disease. In this study, we evaluated the effects of a magnesium infusion and dietary-induced isolated magnesium deficiency on the production of thromboxane and on angiotensin II-mediated aldosterone synthesis in normal human subjects. Because insulin resistance may be associated with altered blood pressure, we also measured insulin sensitivity using an intravenous glucose tolerance test with minimal model analysis in six subjects. The magnesium infusion reduced urinary thromboxane concentration and angiotensin II-induced plasma aldosterone levels. The low magnesium diet reduced both serum magnesium and intracellular free magnesium in red blood cells as determined by nuclear magnetic resonance (186 +/- 10 [SEM] to 127 +/- 9 mM, p < 0.01). Urinary thromboxane concentration measured by radioimmunoassay increased after magnesium deficiency. Similarly, angiotensin II-induced plasma aldosterone concentration increased after magnesium deficiency. Analysis showed that all subjects studied had a decrease in insulin sensitivity after magnesium deficiency (3.69 +/- 0.6 to 2.75 +/- 0.5 min-1 per microunit per milliliter x 10(-4), p < 0.03). We conclude that dietary-induced magnesium deficiency 1) increases thromboxane urinary concentration and 2) enhances angiotensin-induced aldosterone synthesis. These effects are associated with a decrease in insulin action, suggesting that magnesium deficiency may be a common factor associated with insulin resistance and vascular disease.

Aldosterone↗
PubMed1999

Effect of magnesium deficiency on autonomic circulatory regulation in conscious rats.

A close relationship between magnesium and cardiovascular function has been reported; however, the effect of magnesium deficiency on autonomic cardiovascular regulation has not been clarified. We investigated the effect of magnesium deficiency on the autonomic regulation of oscillations of the R-R interval, arterial blood pressure (BP), and renal sympathetic nerve activity (RSNA) by using the maximum entropy method in conscious rats. Its effect on baroreflex control of RSNA and heart rate were also investigated with a logistic function curve. Mean BP in magnesium-deficient rats was higher than that in control rats (mean+/-SE, 114.0+/-4.3 versus 101.6+/-3.4 mm Hg; P<0.05), and urinary excretion of catecholamine was increased by 2.4-fold. The fraction of low-frequency oscillation of RSNA was reduced (31.7+/-0.9% versus 36.2+/-1.5%, P<0.05) and the correlation between low-frequency oscillations of BP and RSNA was weakened in magnesium-deficient rats. There was no difference in high-frequency oscillation of the R-R interval, which is related to vagal tone, whereas sympathetic tone became dominant (square root of low-frequency/high-frequency ratio of R-R interval, 1.00+/-0.05 versus 0.67+/-0.05, P<0.0001) in magnesium-deficient rats. The maximal gain in the BP-RSNA relation tended to be reduced in magnesium-deficient rats (-7.7+/-1.1% versus -12.2+/-1.9%/mm Hg, P=0. 07); however, that in the BP-heart rate relation was increased (-8. 1+/-0.7 versus -4.5+/-0.5 bpm/mm Hg, P<0.01). These results suggest that magnesium deficiency induces sympathetic excitation, which results in hypertension but attenuates the baroreflex-related response of sympathetic nerves, whereas magnesium deficiency enhances the sensitivity of the sinus node to autonomic regulation.

Animals↗
PubMed1999

Can one really measure magnesium deficiency using the short-term magnesium loading test?

OBJECTIVE: To compare a 1-h-version of a magnesium-loading-test (MLT) designed for outpatients in healthy controls with the 8-h standard; to establish the test in patients after renal transplantation prone to develop magnesium (Mg) deficiency; to correlate femur Mg-concentration and percentage retention of the given load. DESIGN: Comparison of mean values from healthy controls with respective from the literature; a prospective, randomized, controlled 4-month study; an intra-individual correlation of Mg-serum values and loading-test data with femur-Mg concentrations. SETTING: One centre study in a medical university; outpatients from the transplant unit; inpatients from the orthopedic unit. SUBJECTS: Twenty-four healthy controls aged 36.7 +/- 7.4 years; 34 patients after renal transplantation (46.5 +/- 14.3 years); 41 patients with hip replacement therapy (63.9 +/- 18.6 years). INTERVENTION: Baseline Mg values were measured by atomic absorption spectroscopy (AAS) in serum and urine. An intravenous Mg load with 0.1 mmol Mg-aspartate hydrochloride per kilogram bodyweight was given during 1 h. In 24 h-urine, the amount of excreted Mg was measured by AAS and the percentage retention of the given load calculated according to the formula: 1 - [Mg 24 h-urine/Mg test dose] x 100. Femur Mg was measured by AAS in a peace of the femur neck. Patients after renal transplantation were randomized after the first Mg load to either obtain daily 5 mmol Mg-aspartate hydrochloride per kilogram bodyweight, or placebo. Four months later a second loading-procedure was performed. MAIN OUTCOME MEASURE: Serum Mg, percentage retention of the given Mg load (%Ret) and femur Mg concentration. RESULTS: Mean serum Mg values were within the normal range. In controls, %Ret was -18 +/- 21 and not different from the literature. In the first MLT after renal transplantation, %Ret was 47 +/- 43. In patients under Mg medication it decreased significantly to 16 +/- 26, but was 58 +/- 27 in the placebo group. Femur Mg concentration was 62.6 +/- 20.9 mmol kg-1 dry substance and the corresponding %Ret was 14 +/- 28 with r = - 0.7093. CONCLUSION: The short-term version of the MLT is as good as the standard and was easily applied in outpatients. The indication from the good correlation between bone-Mg and %Ret and a marked decrease in %Ret in patients after Mg medication was that one can really measure magnesium deficiency.

Adolescent↗