Range of Normal Serum Magnesium Values

ABSTRACT Foscarnet (trisodium phosphonoformate hexahydrate) is an antiviral agent used to treat cytomegalovirus disease in immunocompromised patients. One common side effect is acute ionized hypocalcemia and hypomagnesemia following intravenous administration. Foscarnet-induced ionized hypomagnesemia might contribute to ionized hypocalcemia by impairing excretion of preformed parathyroid hormone (PTH) or by producing target organ resistance. Prevention of ionized hypomagnesemia following foscarnet administration could blunt the development of ionized hypocalcemia. To determine whether intravenous magnesium ameliorates the decline in ionized calcium and/or magnesium following foscarnet infusions, MgSO4 at doses of 1, 2, and 3 g was administered in a double-blind, placebo-controlled, randomized, crossover trial to 12 patients with AIDS and cytomegalovirus disease. Overall, increasing doses of MgSO4 reduced or eliminated foscarnet-induced acute ionized hypomagnesemia. Supplementation, however, had no discernible effect on foscarnet-induced ionized hypocalcemia despite significant increases in serum PTH levels. No dose-related, clinically significant adverse events were found, suggesting that intravenous supplementation with up to 3 g of MgSO4 was safe in this chronically ill population. Since parenteral MgSO4 did not alter foscarnet-induced ionized hypocalcemia or symptoms associated with foscarnet, routine intravenous supplementation for patients with normal serum magnesium levels is not recommended during treatment with foscarnet.

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Hospital-Acquired Dysmagnesemia and In-Hospital Mortality

Medical Sciences ◽

10.3390/medsci8030037 ◽

2020 ◽

Vol 8 (3) ◽

pp. 37 ◽

Cited By ~ 1

Author(s):

Wisit Cheungpasitporn ◽

Charat Thongprayoon ◽

Api Chewcharat ◽

Tananchai Petnak ◽

Michael A. Mao ◽

...

Keyword(s):

Logistic Regression ◽

Hospital Mortality ◽

Serum Magnesium ◽

Normal Serum ◽

Hospitalized Patients ◽

Normal Range ◽

Multivariable Logistic Regression ◽

Hospital Acquired

Background and Objectives: This study aimed to report the incidence of hospital-acquired dysmagnesemia and its association with in-hospital mortality in adult general hospitalized patients. Materials and Methods: We studied 26,020 adult hospitalized patients from 2009 to 2013 who had normal admission serum magnesium levels and at least two serum magnesium measurements during hospitalization. The normal range of serum magnesium was 1.7–2.3 mg/dL. We categorized in-hospital serum magnesium levels based on the occurrence of hospital-acquired hypomagnesemia and/or hypermagnesemia. We assessed the association between hospital-acquired dysmagnesemia and in-hospital mortality using multivariable logistic regression. Results: 28% of patients developed hospital-acquired dysmagnesemia. Fifteen per cent had hospital-acquired hypomagnesemia only, 10% had hospital-acquired hypermagnesemia only, and 3% had both hospital-acquired hypomagnesemia and hypermagnesemia. Compared with patients with persistently normal serum magnesium levels in hospital, those with hospital-acquired hypomagnesemia only (OR 1.77; p < 0.001), hospital-acquired hypermagnesemia only (OR 2.31; p < 0.001), and both hospital-acquired hypomagnesemia and hypermagnesemia (OR 2.14; p < 0.001) were significantly associated with higher in-hospital mortality. Conclusions: Hospital-acquired dysmagnesemia affected approximately one-fourth of hospitalized patients. Hospital-acquired hypomagnesemia and hypermagnesemia were significantly associated with increased in-hospital mortality.

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Serum Magnesium and Mortality in Maintenance Hemodialysis Patients

Blood Purification ◽

10.1159/000451052 ◽

2016 ◽

Vol 43 (1-3) ◽

pp. 31-36 ◽

Cited By ~ 19

Author(s):

Ling Yu ◽

Han Li ◽

Shi-xiang Wang

Keyword(s):

Serum Magnesium ◽

Multivariate Logistic Regression Analysis ◽

High Sensitivity ◽

Normal Serum ◽

Serum Phosphorus ◽

Maintenance Hemodialysis ◽

Related Factors ◽

Kaplan Meier ◽

Significant Difference ◽

Hs Crp

Background and Aim: The study aimed to investigate the potential contributing effect of serum magnesium on mortality in maintenance hemodialysis (MHD) patients. Methods: The patients receiving regular MHD in March 2013 were involved. Baseline data including clinical data, anthropometrics and biochemical measurement were collected. After being followed for 36 months, the time of death and reason were recorded. Results: One hundred and thirty-five MHD patients were enrolled in the study and analyzed, with mean serum magnesium of 1.11 ± 0.15 mmol/l. The level of serum magnesium in 64 patients was normal (47.4%), and it was elevated in 71 of the 135 patients (52.6%). And none of MHD patients had hypomagnesemia. The levels of serum albumin (Alb), urea nitrogen, creatinine (Cr), uric acid and phosphorus were significantly higher, but high-sensitivity C-reactive protein (Hs-CRP) and lipoprotein A were significantly lower in hypermagnesemia group compared to the normal serum magnesium group (p < 0.05). Serum Alb, serum Cr, serum phosphorus and Hs-CRP were related factors of hypermagnesemia by multivariate logistic regression analysis (p < 0.05). During the 36 months of follow-up, 27 patients died (20.0%), of whom 55.6% died of cardiovascular (CV) events. Kaplan-Meier curves showed that cumulative incidence of CV mortality were significantly higher in the normal serum magnesium group than in the hypermagnesemia group (p = 0.027); however, there was no significant difference in all-cause mortality (p > 0.05). Conclusions: Serum magnesium was elevated, which was related with nutrition and inflammation markers including serum Alb, serum Cr, serum phosphorus and Hs-CRP. Lower serum magnesium is a risk factor of CV mortality in MHD patients. Intervention studies are needed to clarify whether magnesium supplementation is beneficial for improving patient prognosis, when MHD patients had inflammatory and malnutrition.

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Serum Magnesium Concentration Is Inversely Associated with Albuminuria and Retinopathy among Patients with Diabetes

Journal of Diabetes Research ◽

10.1155/2016/1260141 ◽

2016 ◽

Vol 2016 ◽

pp. 1-6 ◽

Cited By ~ 5

Author(s):

Jun Lu ◽

Yuying Gu ◽

Meixiang Guo ◽

Peihong Chen ◽

Hongtao Wang ◽

...

Keyword(s):

Microvascular Complications ◽

Serum Magnesium ◽

Multiple Logistic Regression Analysis ◽

Albumin Excretion Rate ◽

Normal Serum ◽

Fundus Photography ◽

Magnesium Concentration ◽

Serum Magnesium Concentration ◽

Patients With Diabetes ◽

Diabetic Microvascular Complications

Aim. To investigate the association between serum magnesium levels and microvascular complications among patients with diabetes.Methods. Patients with diabetes were recruited between April 2012 and January 2015. All patients received an assay of serum magnesium concentration, were screened for 24 h albumin excretion rate, and underwent nonmydriatic fundus photography. Albuminuria and retinopathy were defined accordingly. A total of 3,100 patients with normal serum magnesium levels were included in this study.Results. Patients with albuminuria and/or retinopathy had lower levels of serum magnesium than patients without these complications (P<0.001). The prevalence of isolated albuminuria, isolated retinopathy, and combined albuminuria and retinopathy decreased as the concentration of serum magnesium increased. Multiple logistic regression analysis indicated that the odds ratio for isolated albuminuria, isolated retinopathy, and concomitant albuminuria and retinopathy decreased by approximately 20% for every 0.1 mmol/L increase in serum magnesium concentration.Conclusion. Serum magnesium levels were negatively associated with the risk of diabetic microvascular complications among patients with serum magnesium levels within the normal range.

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Calcium Unresponsive Hypocalcemic Tetany: Gitelman Syndrome with Hypocalcemia

Case Reports in Medicine ◽

10.1155/2013/197374 ◽

2013 ◽

Vol 2013 ◽

pp. 1-3 ◽

Cited By ~ 1

Author(s):

Madhav Desai ◽

Praveen Kumar Kolla ◽

P. L. Venkata Pakki Reddy

Keyword(s):

Serum Calcium ◽

Metabolic Alkalosis ◽

Serum Magnesium ◽

Normal Serum ◽

Gitelman Syndrome ◽

Self Medication ◽

Loading Test ◽

Gitelman's Syndrome ◽

Arterial Blood ◽

Renal Tubular Disorder

Introduction. Gitelman’s syndrome (GS) is autosomal recessive renal tubular disorder characterized by hypokalemia, hypomagnesemia, hypocalciuria, metabolic alkalosis, and hyperreninemic hyperaldosteronism. It is usually associated with normal serum calcium. We report a patient presented with hypocalcemic tetany, and evaluation showed Gitelman’s syndrome with hypocalcemia.Case Report. A 28-year-old woman presented with cramps of the arms, legs, fatigue, and carpal spasms of one week duration. She has history of similar episodes on and off for the past two years. Her blood pressure was 98/66 mmHg. Chvostek’s sign and Trousseau’s sign were positive. Evaluation showed hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Self-medication, diuretic use, laxative abuse, persistent vomiting, and diarrhoea were ruled out. Urinary prostaglandins and genetic testing could not be done because of nonavailability. To differentiate Gitelman syndrome from Bartter’s syndrome (BS), thiazide loading test was done. It showed blunted fractional chloride excretion. GS was confirmed and patient was treated with spironolactone along with magnesium, calcium, and potassium supplementation. Symptomatically, she improved and did not develop episodes of tetany again.Conclusion. In tetany patient along with serum calcium measurement, serum magnesium, serum potassium, and arterial blood gases should be measured. Even though hypocalcemia in Gitelman syndrome is rare, it still can occur.

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High-Normal Serum Magnesium and Hypermagnesemia Are Associated With Increased 30-Day In-Hospital Mortality: A Retrospective Cohort Study

Frontiers in Cardiovascular Medicine ◽

10.3389/fcvm.2021.625133 ◽

2021 ◽

Vol 8 ◽

Author(s):

Liao Tan ◽

Qian Xu ◽

Chan Li ◽

Jie Liu ◽

Ruizheng Shi

Keyword(s):

Logistic Regression ◽

Regression Analysis ◽

Hospital Mortality ◽

Critically Ill ◽

Critically Ill Patients ◽

Cox Regression ◽

Serum Magnesium ◽

Normal Serum ◽

Magnesium Level ◽

Serum Magnesium Level

Background: Magnesium, the fourth most abundant mineral nutrient in our body, plays a critical role in regulating ion channels and energy generation, intracardiac conduction, and myocardial contraction. In this study, we assessed the association of admission serum magnesium level with all-cause in-hospital mortality in critically ill patients with acute myocardial infarction (AMI).Methods: Clinical data were extracted from the eICU Collaborative Research Database (eICU-CRD). Only the data for the first intensive care unit (ICU) admission of each patient were used, and baseline data were extracted within 24 h after ICU admission. Logistic regression, Cox regression, and subgroup analyses were conducted to determine the relationship between admission serum magnesium level and 30-day in-hospital mortality in ICU patients with AMI.Results: A total of 9,005 eligible patients were included. In the logistic regression analysis, serum magnesium at 2.2 to ≤2.4 and >2.4 mg/dl levels were both significant predictors of all-cause in-hospital mortality in AMI patients. Moreover, serum magnesium of 2.2 to ≤2.4 mg/dl showed higher risk of in-hospital mortality than magnesium of >2.4 mg/dl (adjusted odds ratio, 1.63 vs. 1.39). The Cox regression analysis yielded similar results (adjusted hazard ratio, 1.36 vs. 1.25).Conclusions: High-normal serum magnesium and hypermagnesemia may be useful and easier predictors for 30-day in-hospital mortality in critically ill patients with AMI.

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Hyperaldosteronism in a Patient With Gastrointestinal Potassium Wasting

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.270 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A134-A134

Author(s):

Samuel Amankwah ◽

Henry G Fein

Keyword(s):

Differential Diagnosis ◽

Serum Potassium ◽

Serum Magnesium ◽

Elevated Serum ◽

Bowel Function ◽

The United States ◽

Bartter Syndrome ◽

Normal Serum ◽

Primary Hyperaldosteronism ◽

Urinary Potassium

Abstract Background: Medical conditions causing hypokalemia can be masked by a diet very rich in potassium. The following case presents a patient who developed new onset symptoms of hypokalemia after immigrating to the United States. Clinical Case: A 35 year old man, native of Mali, had a history of intermittent muscle spasms and serum potassium of 3.0 mmol/L first recognized elsewhere in 2019. He was not on any home medications. He was admitted with postprandial generalized abdominal pain, diarrhea, and bright blood in his stools. Serum potassium was 2.7 (nl 3.5–5.1mmol/L). He required at least 120 mEq of intravenous and oral potassium chloride per day while hospitalized to achieve and maintain serum potassium in the normal range. Colonoscopy found segmental colitis and it was thought that his hypokalemia was due to gastrointestinal losses. However, studies demonstrated urinary potassium wasting. A 1.9 cm nodular mass of the left adrenal gland was found on CT of the abdomen, and the differential diagnosis was expanded to include hypokalemia secondary to primary hyperaldosteronism or renal tubulopathies such as Bartter and Gitleman syndromes. The patient was normotensive and had biochemical findings that were consistent with Bartter syndrome including metabolic alkalosis, hypercalciuria, elevated urine sodium and chloride, and normal serum magnesium levels. However, he had low plasma rennin activity with an elevated serum aldosterone on three tests over two months (the last test was more than one month after normalization of bowel function). On all of these, the aldosterone to renin ratio was greater than 20 ng/mL/hour. The persistent suppression of plasma rennin with elevated aldosterone in the setting of left adrenal mass narrowed the differential diagnosis to primary hyperaldosteronism, as elevated rennin would be expected in Bartter syndrome. Since discharge, he has received 80 meq of daily oral potassium in divided doses, which has kept serum potassium at or below the lower limit of normal. Further management will consist of either pharmacologic or surgical treatment with or without adrenal venous sampling. Conclusion: The patient had hypokalemia for which an endocrine etiology could have been easily overlooked and attributed to gastrointestinal losses. This case demonstrates the very close clinical similarities between primary hyperaldosteronism and renal tubulopathies. However, there are biochemical patterns that can be relied on to help differentiate amongst these disorders. This patient with primary hyperaldosteronism may not have been hypokalemic in his native country due to consuming a diet rich in potassium.

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Gitelman Syndrome with Normal Serum Magnesium

Journal of the Korean Society of Pediatric Nephrology ◽

10.3339/jkspn.2012.16.2.121 ◽

2012 ◽

Vol 16 (2) ◽

pp. 121

Author(s):

Younghee Cheon ◽

Ji Hye Seo ◽

Hae Il Cheong ◽

Yong Hoon Park

Keyword(s):

Serum Magnesium ◽

Normal Serum ◽

Gitelman Syndrome

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Disorders of plasma magnesium

10.1093/med/9780199568741.003.0177 ◽

2018 ◽

Author(s):

Aron Chakera ◽

William G. Herrington ◽

Christopher A. O’Callaghan

Keyword(s):

Normal Cell ◽

Soft Tissues ◽

Cell Metabolism ◽

Serum Magnesium ◽

Normal Serum ◽

Hormone Release ◽

Neuronal Function ◽

Total Body ◽

Plasma Magnesium ◽

Parathyroid Hormone Release

Normal serum magnesium levels are in the range of 0.7–1.0 mmol/l and, as for calcium, most of the total body magnesium is found in bone and soft tissues. Magnesium is essential for normal cell metabolism (as a cofactor for numerous enzymes) and for neuronal function, and regulates parathyroid hormone release. Alterations in serum magnesium levels are usually asymptomatic unless severe. As there are large tissue reserves of magnesium, hypomagnesaemia usually only develops with chronic gastrointestinal or renal losses, or prolonged dietary insufficiency. Hypermagnesaemia is almost always iatrogenic, due to excessive supplementation. This chapter reviews the causes and management of derangements of plasma magnesium.

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Gitelman Syndrome: A Rare Cause of Seizure Disorder and a Systematic Review

Case Reports in Medicine ◽

10.1155/2019/4204907 ◽

2019 ◽

Vol 2019 ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

Muhammad Asim Shahzad ◽

Maryam Mukhtar ◽

Asrar Ahmed ◽

Waqas Ullah ◽

Rehan Saeed ◽

...

Keyword(s):

Clinical Presentation ◽

Brain Activity ◽

Serum Magnesium ◽

Normal Serum ◽

Gitelman Syndrome ◽

Low Magnesium ◽

Depth Analysis ◽

Biochemical Variability ◽

Convoluted Tubules ◽

Main Complication

Gitelman syndrome is one of the few inherited causes of metabolic alkalosis due to salt losing tubulopathy. It is caused by tubular defects at the level of distal convoluted tubules, mimicking a thiazide-like tumor. It usually presents in late childhood or in teenage as nonspecific weakness, fatigability, polyuria, and polydipsia but very rarely with seizures. It is classically associated with hypokalemia, hypomagnesemia, hypocalciuria, hyperreninemia, and hyperaldosteronism. However, less frequently, it can present with normal magnesium levels. It is even rarer to find normomagnesemic patients of GS who develop seizures as the main complication since hypomagnesemia is considered the principal etiology of abnormal foci of seizure-related brain activity in GS cases. Interestingly, patients with GS are oftentimes diagnosed during pregnancy when the classic electrolyte pattern consistent with GS is noticed. Our case presents GS with normal serum magnesium in a patient, with seizures being the main clinical presentation. We also did a comprehensive literature review of 122 reported cases to show the prevalence of normal magnesium in GS cases and an overview of clinical and biochemical variability in GS. We suggest that further studies and in-depth analysis are required to understand the pathophysiology of seizures in GS patients with both normal and low magnesium levels.

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