Magnesium Depletion Research Articles

Low plasma magnesium in type 2 diabetes.

Magnesium depletion has a negative impact on glucose homeostasis and insulin sensitivity in type 2 diabetic patients. Low plasma magnesium concentration is a highly specific indicator of poor magnesium status. In the USA and some European countries, plasma magnesium concentrations have been found to be decreased in diabetics. The aim of this study was to compare plasma magnesium concentrations of type 2 diabetics and healthy controls in Switzerland. Plasma magnesium concentrations were determined in 109 type 2 diabetics and 156 age- and sex-matched healthy controls. Mean (+/- SD) plasma magnesium concentrations of the diabetics and controls were 0.77 +/- 0.08 and 0.83 +/- 0.07 mmol/L, respectively (p <0.001). Plasma magnesium concentrations were below the normal reference range in 37.6% of the diabetic patients and 10.9% of the control subjects (p <0.001). Plasma magnesium was not correlated with glycemic control as measured by HbA1c. Lower plasma magnesium concentrations and poor magnesium status are common in type 2 diabetics in Zurich, Switzerland.

Analysis of virulence plasmid gene expression of intra-macrophage and in vitro grown Rhodococcus equi ATCC 33701

Rhodococcus equi is a soil organism that infects macrophages of foals and immunocompromised humans. Virulence in foal isolates is tightly associated with an 80 kb plasmid, which includes a pathogenicity island (PI) with a virulence-associated gene family, vap. A DNA microarray containing 66 of 69 putative open reading frames (ORFs) of the virulence plasmid was developed. Virulence plasmid gene expression of R. equi grown in macrophages or under different conditions in vitro was compared against in vitro growth at 30 °C, pH=7. When grown in macrophages, all seven vap family genes as well as six ORFs within, but not outside, the PI were induced. Cluster analysis of the gene expression matrix assembled from different growth conditions suggested that those genes that actively responded to environmental changes divided broadly into two groups. One group, orf1, 2, 5, 6–8, 12–15, 19, and 20 (which includes all the vap genes), was induced at 37 °C, mostly by low iron, and to a lesser extent by the synergy of low calcium and pH=5. The second group, orf3, 9, and 10, was induced at 37 °C by magnesium depletion (produced by EDTA treatment of growth medium). Temperature (37 °C) was the most important factor inducing gene expression for the both groups. Iron restriction led to down-regulation of Group II genes and magnesium restriction led to down-regulation of Group I genes. A putative consensus IdeR binding site was identified upstream of vapA, suggesting that vapA is a member of an IdeR regulon in R. equi. Expression of genes inside macrophages was most closely but not completely mimicked by growth of bacteria at 37 °C, pH=5, under conditions of restricted iron, calcium and magnesium; that is, similar to environmental factors found inside macrophages.

Effects of hypokalemia and hypomagnesemia on zidovudine (AZT) and didanosine (ddI) nephrotoxicity in rats.

Zidovudine (AZT) and didanosine (ddI) are antiretroviral drugs widely used in AIDS patients. Hypokalemia and hypomagnesemia are frequently encountered in AIDS patients using AZT and/or ddI. To verify the effects of AZT and ddI on rat renal function submitted to normal diet, low potassium diet and magnesium-free diet. Glomerular filtration rate and renal hemodynamic were measured in Wistar rats submitted to a normal or a potassium-depleted diet. The animals were given AZT, ddI for 15 days. Six groups of rats were studied: normal diet, normal diet + AZT, normal diet + ddI, low K diet, low K diet + AZT and low K diet + ddI. Three additional groups of rats submitted to magnesium depletion for 15 days were also studied: magnesium-free diet, magnesium-free diet + AZT and magnesium-free diet + ddI. AZT and didanosine did not modify renal function of rats on a normal diet. However, in hypokalemic rats, both drugs produced a decrease in glomerular filtration rate and in renal blood flow consequent to renal vasoconstriction and associated with alterations in tubular function (characterized by an increased fractional excretion of sodium). Hypomagnesemia induced a decrease in glomerular filtration rate and in renal blood flow only in AZT-treated rats. Our data suggest that hypokalemia predisposes to AZT and ddI nephrotoxicity, while hypomagnesemia predisposes only to AZT nephrotoxicity. Thus, chronic AZT and ddI administration may produce acute renal failure in AIDS patients with hypokalemia and/or hypomagnesemia. Serum K and Mg levels should be carefully monitored in these patients.

SCHIZOID NEUROCHEMICAL PATHOLOGY-INDUCED MEMBRANE NA+-K+ ATPASE INHIBITION IN RELATION TO NEUROLOGICAL DISORDERS

Psychiatric abnormalities have been described in primary neurological disorders like multiple sclerosis, primary generalized epilepsy, Parkinson's disease, subacute sclerosing panencephalitis (SSPE), central nervous system glioma, and syndrome X with vascular dementia. It was therefore considered pertinent to compare monoamine neurotransmitter pattern in schizophrenia with those in the disorders described above. The end result of neurotransmission is changes in membrane Na+-K+ ATPase activity. Membrane Na+-K+ ATPase inhibition can lead to magnesium depletion, which can lead to an upregulated isoprenoid pathway. The isoprenoid pathway produces three important metabolites--digoxin, an endogenous membrane Na+-K+ ATPase inhibitor; ubiquinone, a membrane antioxidant and component of mitochondrial electron transport chain; and dolichol, important in N-glycosylation of protein. The serum/plasma levels of digoxin, dolichol, ubiquinone, magnesium, HMG CoA reductase activity, and RBC Na+-K+ ATPase activity were estimated in all these disorders. The result showed that the concentration of serum tryptophan and serotonin was high and serum tyrosine, dopamine, adrenaline, and noradrenaline low in all the disorders studied. The plasma HMG CoA reductase activity, serum digoxin, and serum dolichol levels were high and serum ubiquinone levels, serum magnesium, and RBC Na+-K+ ATPase activity were low in all the disorders studied. The significance of these changes in the pathogenesis of syndrome X, multiple sclerosis, primary generalized epilepsy, schizophrenia, SSPE, and Parkinson's disease is discussed in the setting of the interrelationship between these disorders documented in literature

Magnesium depletion in chronic terminal liver cirrhosis.

Serum ionized magnesium represents less than 1% of the total body magnesium. The most reliable method to evaluate magnesium status is the magnesium loading test: In magnesium depletion its uptake is increased (20-50%) and is about 6% in normal magnesium status. There are no studies on magnesium status in chronic cirrhotics who may be in depletion. We performed magnesium loading test in 10 chronic cirrhotics listed for liver transplantation and in six healthy control patients. Magnesium sulphate 30 mmol was infused and urine magnesium was determined over 24 h. Serum ionized magnesium increased similarly in all patients. The uptake of magnesium was 8 +/- 8% in control patients and 34 +/- 26% in cirrhotics (p < 0.01). Chronic terminal cirrhotics are magnesium depleted which should be taken into account in case of liver transplantation and also in other interventions. Spot sampled serum ionized magnesium revealed magnesium depletion poorly.

Dietary Magnesium Depletion Affects Metabolic Responses during Submaximal Exercise in Postmenopausal Women

Magnesium is an essential mineral that is required for optimal biological function including energy metabolism. Although national nutritional surveys indicate that usual magnesium intakes do not meet recommendations, particularly among older women, diet-induced magnesium depletion is considered rare among humans without concurrent illness. We examined the effects of dietary magnesium restriction on biochemical measures of magnesium nutriture and physiologic responses during submaximal exercise in 10 postmenopausal women, 45-71 y old, not receiving hormone replacement therapy. The women consumed diets containing conventional foods with varying magnesium content totaling 112 mg/8.4 MJ (2000 kcal) supplemented with 200 mg magnesium daily for 35d (control), then 112 mg/8.4 MJ for 93d (depletion) followed by 112 mg/8.4 MJ supplemented with 200 mg magnesium/d for 49d (repletion) in a depletion-repletion experiment. RBC magnesium concentration (P < 0.05), magnesium retention (P < 0.05) and skeletal muscle magnesium concentration (P < 0.05) decreased when dietary magnesium was restricted. Peak oxygen uptake, total and cumulative net oxygen uptake determined by using indirect calorimetry and peak heart rate increased (P < 0.05) during standardized submaximal work with restricted compared with adequate dietary magnesium. These findings indicate that dietary magnesium depletion can be induced in otherwise healthy women; it results in increased energy needs and adversely affects cardiovascular function during submaximal work. This may also explain previous observations of increased energy cost during standardized exercise in physically active men and women considered to have reduced magnesium nutriture.

Combination Antiviral Therapy for Ganciclovir‐Resistant Cytomegalovirus Infection in Solid‐Organ Transplant Recipients

The resistance of cytomegalovirus (CMV) to ganciclovir is a factor in therapeutic failure and disease progression. The clinical significance of such resistance in solid-organ transplantation has not been completely established. Six patients who developed persistent infection due to ganciclovir-resistant CMV were treated with a combination of ganciclovir (50% of the therapeutic dose) and a daily dose of intravenous foscarnet that gradually increased to a maximum of 125 mg/kg. All patients responded clinically within 72-96 hours. Magnesium depletion occurred in all patients. No clinical or laboratory relapses have been observed in 6-30 months of follow-up. Gradually increasing doses of foscarnet combined with half-dose regimens of ganciclovir are safe and can be beneficial in organ transplant recipients with ganciclovir-resistant CMV infection. Larger studies are needed to identify the patients who are most likely to benefit from this regimen.

Magnesium deposition and depletion in magnesium supplemented rats during and after hypokinesia and vivarium control.

Hypokinesia (diminished movement) induces significant magnesium (Mg) changes; however, little is known about Mg deposition and Mg depletion during HK. Measuring the Mg level in some tissues during HK and post-HK and Mg supplement, we aimed to establish Mg deposition and Mg depletion during prolonged HK. Studies were done on 408, 13-wk-old male Wistar rats (370-390 g) for a 15-d pre-HK period, a 98-d HK period, and a 15-d post-HK period. Rats were equally divided into four groups: unsupplemented vivarium control rats (UVCR), unsupplemented hypokinetic rats (UHKR), supplemented vivarium control rats (SVCR), and supplemented hypokinetic rats (SHKR). Both UHKR and SHKR were kept in small individual cages. The SVCR and SHKR took 53 mg Mg/d. During the HK period, plasma, urinary, and fecal Mg levels increased significantly (p < or = 0.05), whereas during the post-HK period Mg deposition, muscle and bone Mg content decreased significantly (p < or = 0.05) in UHKR and SHKR when compared with their pre-HK values and their respective vivarium controls (UVCR and SVCR). During the initial days of the post-HK period, plasma, urinary, and fecal Mg levels decreased significantly (p < or = 0.05), whereas during the post-HK period Mg deposition, muscle and bone Mg content remained significantly (p < or = 0.05) depressed in UHKR and SHKR when compared with UVCR and SVCR, respectively. However, during the HK period and post-HK period Mg deposition, bone, muscle, plasma, urinary, and fecal Mg levels changed significantly (p < or = 0.05) more in SHKR than UHKR. By contrast, during the HK period and post-HK period. Mg deposition, muscle, bone, plasma, urinary, and fecal Mg values change insignificantly (p > 0.05) in UVCR and SVCR when compared with their pre-HK values. It was concluded that reduced muscle, bone, plasma, urinary, and fecal Mg during post-HK and Mg supplement may demonstrate Mg depletion, whereas higher Mg loss during HK despite reduced muscle and bone Mg and Mg depletion might demonstrate Mg deposition incapacity during HK.

Long-term renal consequences of hypertension for normal and diseased kidneys.

Substantial evidence indicates that the adverse effects of hypertension on the kidney depend on the degree to which systemic blood pressure elevations are transmitted to the renal microvasculature. Such blood pressure transmission and consequent susceptibility to hypertensive renal damage is markedly exacerbated in states characterized by preglomerular vasodilation and an impairment of the normally protective renal autoregulatory mechanisms, e.g. diabetes or chronic renal disease. Moreover, this pathophysiology gives rise to the prediction that prevention of hypertension-induced barotrauma will require blood pressure to be reduced well into the normotensive range in such patients, as is being recognized in the currently recommended blood pressure goals. Agents that block the renin-angiotensin system should be preferred as initial therapy as they may provide additional risk reductions and minimize the potassium and magnesium depletion associated with the diuretic use usually necessary to achieve the lower blood pressure targets. The current failure to achieve optimal blood pressure reductions may be contributing not only to the still escalating incidence of end-stage renal disease in diabetic patients, but also to their greatly increased cardiovascular morbidity and mortality.

Assessing Magnesium Status: A Persisting Problem

AbstractMagnesium plays an essential role in a wide range of fundamental biological reactions. Although diets consumed by healthy Americans usually do not lead to clinically significant magnesium depletion, epidemiological and clinical studies have suggested an association between low magnesium status and increased risk of cardiovascular diseases, hypertension, osteoporosis, diabetes, and other chronic diseases. In acutely or chronically ill hospitalized patients, the prevalence of hypomagnesemia has been reported to be as high as 11%. Hypomagnesemia resulting from underlying disease can be due to decreased gastrointestinal absorption or increased renal magnesium losses. Magnesium is principally an intracellular cation. Tissue magnesium status is difficult to accurately estimate with non‐invasive measures due to poor correlations between serum or RBC or WBC magnesium levels and magnesium concentration in major tissue stores in muscle and the skeleton. At present, a comprehensive evaluation of a patient's risk of magnesium deficiency should include consideration of known risk factors and disease conditions possibly contributing to magnesium depletion, estimates of dietary magnesium intake, and clinical observations. The evaluation also should include laboratory measures of magnesium status, including analysis of both extracellular (serum magnesium) and intracellular (RBC, WBC or muscle magnesium) magnesium concentration, if available. Researchers should continue efforts to find a simple, reliable, and useful technique to accurately estimate magnesium status.

Isolation of Normal Epithelial Cells Adapted to Grow at Nonphysiological Concentration of Magnesium

Extracellular magnesium (Mg) depletion inhibits the growth of the HC11 normal mammary epithelial cells. In this study we found that an acute increase in extracellular Mg generally exerts a positive effect on the growth of these cells. We also isolated and characterized two derivatives adapted to grow and proliferate at nonphysiological concentration of Mg. The growth properties of the HC-LMg cells at 25 μM Mg were comparable to those of the parental HC11 cells in the regular medium (0.5 mM Mg) despite an increased expression of the CDK inhibitor p27Kip1. They also showed a reduced dependence from serum to grow. The HC-HMg cells have been adapted to grow and proliferate at an increased (45 mM) Mg concentration. Cell total Mg content was 19.6, 9.7, and 20.1 nmol/mg protein in the HC11, HC-LMg, and HC-HMg cells, respectively. Thus, we have isolated derivatives of normal epithelial cells which are able to maintain Mg content in a physiological range in the face of different extracellular concentration gradients and will be a valuable tool for further studies on the regulation of Mg homeostasis in eukaryotic cells.

Low Serum Magnesium Levels and Foot Ulcers in Subjects with Type 2 Diabetes

Background Hypomagnesemia is associated with the development of neuropathy and abnormal platelet activity, both of which are risk factors for the progression of ulcers of the feet. Thus, the aim of this study was to determine the relationship between low serum magnesium and foot ulcer in subjects with type 2 diabetes. Methods Thirty-three out-patients with type 2 diabetes and foot ulcers (16 women and 17 men) were compared with a control group of 66 out-patients with type 2 diabetes without foot ulcers (35 women and 31 men), matched by age, diabetes duration, HbA 1c, and glycemia. Patients with foot ulcers were included in the study only if a foot ulceration onset not exceeding 2 months was established. Patients diagnosed with reduced renal function, a history of alcohol intake, or as having received magnesium supplementation or diuretics were not included. Serum magnesium was measured by colorimetric method. The relationship between serum magnesium and foot ulcers was assessed by logistic regression. Results Hypomagnesemia was identified in 31 (93.9%) subjects with foot ulcers, and 49 (73.1%) control subjects, p = 0.02. Subjects with foot ulceration had lower serum magnesium levels (1.48 ± 0.33) than those in the control group (1.68 ± 0.32), p <0.001. Logistic regression analysis showed a significant relationship between low serum magnesium levels and foot ulcers (odds ratio [OR] 2.9, CI 95% 1.7–6.8; p = 0.01). Conclusions Serum magnesium depletion is present and shows a strong relationship with foot ulcers in subjects with type 2 diabetes and foot ulcers, a relationship not previously reported.

Bone mineral content reduction in youth with surgical form of Schistosomiasis mansoni: factors involved in the pathogenesis

Thirty two children and adolescents from 14 to 20 years of age, suffering from hepatosplenic schistosomiasis mansoni and bleeding esophageal varicose veins, were evaluated for bone mineral density (BMD), before undergoing medical and surgical treatment. The surgical protocol was splenectomy, autoimplantation of spleen tissue into a pouch of the major omentum and ligature of the left gastric vein. Follow up of these patients’ ranges from one to ten years with a mean of five years. The BMD was measured at the lumbar spine (L2 - L4) through the dual energy absorptionmetry X-ray (DEXA), using a LUNAR DPX-L densitometer. The degree of Symmers´ fibrosis was assessed by semiautomatic hystomorphometry. In eleven patients, the serum magnesium was measured before an intravenous overload of this ion and subsequently after eight and twenty four hours. Urine was collected 24 hours before and 24 hours after the magnesium overload. Deficiency of magnesium was considered when the uptake of this ion was greater than 40%. There was a significant trend of association between the status of bone mineral content and the Symmers´ fibrosis degree (c² = 6.606 R = 0.01017). There was also a moderate agreement between the greater fibrosis densities ( &gt; the mean percentage) and bone mineral deficits. Although the normal bone mineral content was more found among the patients with better hepatic functional reserve, the results did not reach statistical significance. There was a marked magnesium retention (&gt;95%) in one patient who had severe osteoporosis and a slight depletion (&lt;5%) in another patient, who presented no bone mineral deficit. It was concluded that the patients included in this series, showed an important BMD deficit, specially among the females which has had a significant improvement after medical and surgical treatment. Bone mineral deficit was associated with the degree of Symmers´ fibrosis. Magnesium depletion was present in two out of eleven patients. It is speculated that magnesium supplementation may be warranted to forestall the progression of bone mineral deficit in patients with more impaired hepatic functional reserve.

Alteration in glycoconjugate metabolism in CNS disorders ‐ role of isoprenoid pathway

AbstractThe isoprenoid pathway which is upregulated in neuropsychiatric disorders produces two metabolites which can regulate glycoconjugate metabolism ‐ dolichol (required for N‐glycosylation) and digoxin (endogenous membrane sodium‐potassium ATPase inhibitor producing magnesium depletion). It is known that Mg++ deficiency can influence glycoconjugate metabolism. The results showed an increase in the concentration of serum total glycosaminoglycan (GAG), glycolipids and carbohydrate component of glycoproteins and a decrease in the total GAG and carbohydrate component of glycoproteins in the Red blood cell (RBC) membrane suggesting their reduced incorporation into the membrane. The pattern of change in individual GAG in the serum was different, however heparan sulphate (HS) and chondroitin sulphate (ChS) increased in most of the disorders studied. The activity of GAG degrading enzymes and glycohydrolases showed significant increase in the serum in all the groups suggesting reduced lysosomal stability consequent to defective lysosomal membrane formation. The importance of altered glycoconjugate metabolism in the pathogenesis of multiple sclerosis, Parkinson's disease, schizophrenia, epilepsy and CNS gliomas is stressed.

Management of patients with a short bowel.

There are two common types of adult patient with a short bowel, those with jejunum in continuity with a functioning colon and those with a jejunostomy. Both groups have potential problems of undernutrition, but this is a greater problem in those without a colon, as they do not derive energy from anaerobic bacterial fermentation of carbohydrate to short chain fatty acids in the colon. Patients with a jejunostomy have major problems of dehydration, sodium and magnesium depletion all due to a large volume of stomal output. Both types of patient have lost at least 60 cm of terminal ileum and so will become deficient of vitamin B(12). Both groups have a high prevalence of gallstones (45%) resulting from periods of biliary stasis. Patients with a retained colon have a 25% chance of developing calcium oxalate renal stones and they may have problems with D(-) lactic acidosis. The survival of patients with a short bowel, even if they need long-term parenteral nutrition, is good.

EVIDENCE FOR GLUCAN COMPONENTS IN THE PRIMARY ZYGOTE WALL OF CHLAMYDOMONAS MONOICA

The primary zygote wall of C. monoica is transient and is released from mature zygospores. The fluorochromes aniline blue and primulin, used in other systems to detect β‐1,3 glucans, stain the primary wall intensely. Two β‐1,3 glucan synthases have been identified in higher plants: a calcium‐dependent synthase produced in response to wounding and induced by chitosan, and a magnesium‐dependent enzyme, associated with pollen development and unresponsive to chitosan. Chitosan has no effect on C. monoica primary wall synthesis or staining properties. We are presently testing for the effect of magnesium and/or calcium depletion on primary wall synthesis. Aniline blue and primulin do not stain purified cellulose fibers, while the fluorochrome Calcofluor does. Calcofluor also stains the primary wall intensely. For all fluorochormes tested, fluorescence is first detected in motile quadriflagellate zygotes. Aniline blue staining maximizes quickly, while Calcofluor staining continues to intensify until primary wall release. Dinitrobenzonitrile, a specific inhibitor of cellulose synthesis in plants, has no effect on primary wall synthesis in C. monoica. Addition of glucanase or cellulase to partially purified primary walls results in wall thinning and loss of staining. Using electron microscopy, we are evaluating the effects of these enzymes on primary wall ultrastructure. Further studies are needed to determine whether all three fluorochromes are recognizing the same polysaccharide component (a β‐1,3 glucan or a β‐1,3; β‐1,4 mixed glucan), or whether Calcofluor staining indicates the presence of a distinct component containing β‐1,4 linkages, such as cellulose or a xyloglucan.

The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis

Multiple sclerosis (MS) has a much higher incidence among caucasians that in any other race. Furthermore: females are much more susceptible than males and white females living in colder, wetter areas are much more susceptible than those living in warmer areas. On the other hand, menstruating women have increased copper (Cu) absorption and half-life, so they tend to accumulate more Cu than males. Moreover, rapidly growing girls have an increased demand for zinc (Zn), but their rapidly decreasing production of melatonin results in impaired Zn absorption, which is exacerbated by the high Cu levels. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. Menstruating females also often present with low magnesium (Mg) and vitamin B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd) accumulation also increase superoxide production. Which explains MS in males, who tend to accumulate Fe much faster and Cu much less rapidly than females. Since vitamin D is paramount for Mg absorption, the much reduced exposure to sunlight in the higher latitudes may account for the higher incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine oxidase, and its deficiency exacerbates the low levels of uric acid caused by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD. Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 μg Se, 180 mg EPA and 120 mg DHA per day between 14 and 16 years of age may prevent MS.

Interfacial reactions and mechanical properties of 6061Al matrix composites reinforced with alumina-coated Al 18B 4O 33 whiskers

Sol–gel γ-Al 2O 3 and α-Al 2O 3 ceramic coatings were deposited onto surfaces of aluminum borate whiskers to control the spinel reactions between whiskers and matrix alloys. Interface observations, tensile experiments and hardness measurements of the composites were conducted to evaluate the coating effect. By comparison with γ-Al 2O 3 coating, the α-Al 2O 3 coating was found to be more effective in controlling the interfacial reactions, and it helped to enhance the elastic modulus of the composite. The introduction of alumina coatings to the composite postponed the peak-aging process, due to a smaller depletion of magnesium in the matrix of the coated composites.

Serum Ionized Magnesium Levels in Type 2 Diabetic Patients with Microalbuminuria or Clinical Proteinuria

Background/Aims: The association between microalbuminuria and magnesium depletion is a controversial issue, and serum ionized magnesium levels have not been previously studied in patients with different grades of diabetic nephropathy. Therefore, the aim of this study was to evaluate circulating ionized magnesium concentrations in patients with non-insulin-dependent diabetes mellitus (NIDDM) and incipient or overt diabetic nephropathy. Methods: We measured fasting plasma glucose, creatinine, creatinine clearance estimate, total cholesterol and triglycerides, and serum ionized magnesium (ion-selective electrodes, ISE) in 30 NIDDM patients with urinary albumin excretion rate (UAER) <20 μg/min (normoalbuminuria), 30 NIDDM patients with microalbuminuria (20 < UAER < 200 μg/min), 30 NIDDM patients with clinical proteinuria (UAER >200 μg/min), and 20 healthy subjects. Results: Serum ionized magnesium levels were significantly reduced in diabetic patients when compared to control subjects (0.39 ± 0.06 vs. 0.58 ± 0.05 mmol/l, p < 0.001). Moreover, diabetic patients with microalbuminuria or clinical proteinuria showed a significant decrease in serum ionized magnesium with respect to normoalbuminuria group (normoalbuminuria: 0.45 ± 0.02 mmol/l; microalbuminuria: 0.36 ± 0.05 mmol/l, p < 0.001; clinical proteinuria: 0.35 ± 0.04 mmol/l, p < 0.001). Serum ionized magnesium showed a significant negative correlation with plasma HbA1c and triglycerides in both microalbuminuria and clinical proteinuria groups. Multiple linear regression analysis showed that circulating ionized magnesium levels decrease together with the increase of plasma HbA1c and triglycerides in NIDDM patients with incipient or overt nephropathy, also after adjusting for age, sex, BMI, diabetes duration, systolic and diastolic blood pressure, hypoglycemic therapy, plasma creatinine, creatinine clearance, plasma cholesterol and fasting glucose. Conclusions: Microalbuminuria and clinical proteinuria, as well as poor glycometabolic control and hypertriglyceridemia, are associated to relevant alterations in magnesium metabolism, and the measurement of serum ionized magnesium seems to represent a useful biochemical tool for the study of magnesium disturbances in patients with different grades of diabetic nephropathy.

Metabolic and clinical effects of oral magnesium supplementation in furosemide-treated patients with severe congestive heart failure.

Magnesium depletion and hypomagnesemia are common among furosemide-treated patients with chronic congestive heart failure. This investigation evaluated clinical and metabolic effects of oral magnesium supplementation. Ten patients with severe congestive heart failure maintained on high dose furosemide (> or = 80 mg/day) received a supplement of oral magnesium citrate 300 mg/daily for 30 days. Clinical parameters were followed, and peripheral blood mononuclear cell magnesium and zinc content, serum and urine magnesium, potassium, zinc, calcium, phosphorus, and creatinine were assessed. Peripheral blood mononuclear cell magnesium content and serum potassium rose significantly at the end of the study (2.09 +/- 1.89 to 3.99 +/- 2.26 micrograms/mg cell protein, p < 0.05, and 4.17 +/- 0.38 to 4.39 +/- 0.27 mEq/l, p < 0.05, respectively), while the other parameters remained unchanged. In some of these patients, oral magnesium supplementation is effective in achieving substantial increments in intracellular magnesium and serum potassium which, in turn, may have cardioprotective effects.