Magnesium Disorders: Core Curriculum 2024.

Magnesium is ubiquitous in nature. It sits at the origin of the food chain, occupying the center of chlorophyl in plants. In humans, magnesium is critical to diverse molecular and catalytic processes, including energy transfer and maintenance of the genome. Despite its abundance, hypomagnesemia is common and often goes undiagnosed. This is in spite of epidemiologic data linking low magnesium with chronic diseases including diabetes mellitus. Clinically significant hypermagnesemia is encountered less frequently, but the presentation may be dramatic. Advances in molecular biology and the elucidation of the genetic causes of magnesium disorders have enhanced our understanding of their pathophysiology. Treatment approaches are also changing. The repurposing of newer medications, such as sodium/glucose cotransporter 2 inhibitors, offers new therapeutic options. In this review we integrate knowledge in this rapidly evolving field to provide clinicians and trainees with a resource for approaching common clinical scenarios involving magnesium disorders.

Hypermagnesemia in Clinical Practice.

Hypermagnesemia is a relatively uncommon but potentially life-threatening electrolyte disturbance characterized by elevated magnesium concentrations in the blood. Magnesium is a crucial mineral involved in various physiological functions, such as neuromuscular conduction, cardiac excitability, vasomotor tone, insulin metabolism, and muscular contraction. Hypomagnesemia is a prevalent electrolyte disturbance that can lead to several neuromuscular, cardiac, or nervous system disorders. Hypermagnesemia has been associated with adverse clinical outcomes, particularly in hospitalized patients. Prompt identification and management of hypermagnesemia are crucial to prevent complications, such as respiratory and cardiovascular negative outcomes, neuromuscular dysfunction, and coma. Preventing hypermagnesemia is crucial, particularly in high-risk populations, such as patients with impaired renal function or those receiving magnesium-containing medications or supplements. Clinical management of hypermagnesemia involves discontinuing magnesium-containing therapies, intravenous fluid therapy, or dialysis in severe cases. Furthermore, healthcare providers should monitor serum magnesium concentration in patients at risk of hypermagnesemia and promptly intervene if the concentration exceeds the normal range.

Correlation of Serum Magnesium Levels with Clinical Outcome: A Prospective Observational Study in Critically Ill Patients Admitted to a Tertiary Care ICU in India.

Background: We studied the incidence of magnesium (Mg) disturbances in patients admitted to a multidisciplinary intensive care unit (ICU) and correlated serum magnesium levels with clinical outcomes. Materials and methods: The study was conducted on 280 critically ill patients aged above 18 years and admitted to the ICU. Serum magnesium levels at admission were correlated with mortality, need for and duration of mechanical ventilation, duration of ICU stay, presence of comorbid conditions, and electrolyte disturbances. Result: There was a high incidence of Mg disturbances at admission among patients admitted to the ICU. The incidence of hypomagnesemia and hypermagnesemia was 40.9 and 13.9% respectively. The mean Mg level among patients who expired was 1.55 ± 0.68 mg/dL, and the association with outcome was found to be statistically significant (p = 0.001).Hypomagnesemia (HypoMg) was associated with significantly higher mortality (51.3%) as compared to normomagnesemia (NormoMg) (29.3%) and hypermagnesemia (HyperMg) (23.1%) (HypoMg vs NormoMg, HypoMg vs HyperMg, p = 0.001, 0.002 respectively). The need for mechanical ventilation was significantly higher in hypomagnesemic as compared to hypermagnesemia patients (p = 0.012). The association of baseline APACHE II and SOFA scores with serum Mg levels was statistically significant (p = 0.001 and 0.002 respectively).The incidence of gastrointestinal disorders was significantly higher among hypomagnesemia patients (HypoMg vs NormoMg, p = 0.023), while chronic kidney disease was significantly higher in hypermagnesemic patients (HypoMg vs HyperMg, p = 0.0009, NormoMg vs HyperMg, p = 0.0004). On comparing the incidence of electrolyte disorders between HypoMg, NormoMg, and HyperMg groups, it was found that hypokalemia and hypocalcemia (p = 0.0003 and 0.039 respectively) were associated with hypomagnesemia and hyperkalemia and hypercalcemia (p = 0.001 and 0.005 respectively) were associated with hypermagnesemia. Conclusion: Our study highlights the role of Mg monitoring in critically ill patients admitted to the ICU and its value for a favorable outcome. We found that hypomagnesemia was significantly associated with adverse outcomes and higher mortality in critically ill patients. Intensivists should maintain a high index of suspicion for Mg disturbances and evaluate patients appropriately. How to cite this article: Gonuguntla V, Talwar V, Krishna B, Srinivasan G. Correlation of Serum Magnesium Levels with Clinical Outcome: A Prospective Observational Study in Critically Ill Patients Admitted to a Tertiary Care ICU in India. Indian J Crit Care Med 2023;27(5):342-347.

Abnormal magnesium levels and their impact on death and acute kidney injury in critically ill children.

BACKGROUND: The prevalence of magnesium imbalance in critically ill children is very high. However, its significance in the development of acute kidney injury (AKI) and mortality remains unknown. METHODS: In this retrospective observational study from 2010 to 2018, the pediatric-specific intensive care database was analyzed. We included critically ill children aged > 3 months and those without chronic kidney disease. Patients were diagnosed with AKI, according to the Kidney Disease Improving Global Outcomes (KDIGO) study. We calculated the initial corrected magnesium levels (cMg) within 24 h and used a spline regression model to evaluate the cut-off values for cMg. We analyzed 28-day mortality and its association with AKI. The interaction between AKI and magnesium imbalance was evaluated. RESULTS: The study included 3,669 children, of whom 105 died within 28 days, while 1,823 were diagnosed with AKI. The cut-off values for cMg were 0.72 and 0.94 mmol/L. Both hypermagnesemia and hypomagnesemia were associated with 28-day mortality (odds ratio [OR] = 2.99, 95% confidence interval [CI] = 1.89-4.71, p < 0.001; OR = 2.80, 95% CI = 1.60-4.89, p < 0.001). Hypermagnesemia was associated with AKI (OR = 1.52, 95% CI = 1.27-1.82, p < 0.001), while neither hypermagnesemia nor hypomagnesemia interacted with the AKI stage on the 28-day mortality. CONCLUSIONS: Abnormal magnesium levels were associated with 28-day mortality in critically ill children. AKI and hypermagnesemia had a strong association. "A higher resolution version of the Graphical abstract is available as Supplementary information".

Antenatal mgnesium sulfate and ritodrine increased potassium levels in preterm infants: A cohort study.

BACKGROUND: Ritodrine and magnesium sulfate are administered to prevent preterm labor. Magnesium sulfate is also administered to prevent preeclampsia. These drugs have been reported to increase potassium levels in pregnant women and neonates. The aim of this study was to investigate the relationship between potassium levels in preterm infants and antenatal treatment. METHODS: This prospective cohort study was conducted at Saiseikai Suita Hospital. Preterm infants born at <35 weeks' gestation between October 2012 and September 2014 were recruited and divided into four groups based on the antenatal treatment their mothers received. Serum and urine electrolyte levels at birth and serum potassium levels 1 day after birth were measured. RESULTS: The mothers of 16 infants received no antenatal treatment (condition C); the mothers of 29 infants received antenatal ritodrine (R); the mothers of seven infants received magnesium sulfate (M); and the mothers of 15 infants received both magnesium sulfate and ritodrine (M + R). At birth, potassium levels were similar among the four groups. However, potassium levels a day after birth were significantly higher in the M + R group than in the other groups: median (min.-max.) mEq/L 4.8 (3.8-6.2), 4.8 (3.6-6.0), and 4.4 (3.8-5.9) vs. 5.8 (4.9-7.2), in the C, R, and M groups versus the M + R group, respectively (P < 0.01). Significantly more infants in the M + R group exhibited a fractional excretion of potassium of <10% compared with those in the other groups. CONCLUSION: The increased potassium levels we observe in preterm infants of mothers who received antenatal magnesium sulfate and ritodrine administration on postnatal day 1 warrant monitoring by neonatologists.

A novel claudin-10 mutation with a unique mechanism in two unrelated families with HELIX syndrome.

HELIX syndrome, characterized by hypohidrosis, electrolyte imbalance, lacrimal gland dysfunction, ichthyosis, and xerostomia due to claudin-10 (CLDN10) mutations, was recognized in 2017. Here we describe two unrelated Saudi families with this syndrome due to a novel CLDN10 mutation with a unique mechanism of CLDN10 inactivation. The two consanguineous families include 12 affected individuals (three siblings in family 1 and nine members in family 2). They presented with hypokalemia and the above-mentioned features of HELIX syndrome. The underlying mutation was detected by whole exome sequencing, confirmed by Sanger sequencing and functionally indicated by RT-PCR, electrophysiological studies and immunohistochemical staining of transfected HEK293 and MDCK C7 cells, and skin and kidney biopsy tissues. A novel biallelic single nucleotide deletion was identified in exon 5 of CLDN10 (NM_182848.3: c.647delC, p.P216Lfs∗19 for CLDN10a or NM_006984.4: c.653delC, p.P218Lfs∗21 for CLDN10b). The mutation led to frameshift and extension of the original termination codon by nine amino acids with loss of the C-terminus pdz-binding motif. Functional studies showed mRNA degradation and protein retention in intracellular compartments and that the pdz-binding motif is crucial for proper localization of claudin-10 in tight junctions. In the kidney, claudin-10 was replaced by translocation of claudin-2 (proximal tubule) and claudin-19 (thick ascending limb), and in the sweat gland by claudin-3 and occludin. However, these claudins did not functionally compensate for loss of claudin-10. Thus, this novel CLDN10 mutation identified in these two families disrupted the C-terminus pdz-binding motif of claudin-10 causing HELIX syndrome.

Continuous Observation of Serum Total Magnesium Level in Patients Undergoing Hemodialysis.

BACKGROUND: Magnesium is an indispensable cation and plays an important physiological role in the body. Most previous studies focused on the single measurement of serum magnesium in patients undergoing hemodialysis. However, scant studies focused on continuous observations of serum magnesium levels. OBJECTIVE: To provide continuous observations of serum magnesium levels in patients on maintenance hemodialysis (MHD). The levels of magnesium in patients initiating hemodialysis are also recorded and analyzed in the present study. METHODS: In this retrospective study, we serially investigated the measurements of serum total magnesium in MHD patients and patients initiating hemodialysis. Our data were followed up for one year. We provided real-time update on the levels of serum magnesium in patients on hemodialysis. RESULTS: On January 1, 2019, a total of 356 end-stage renal disease patients were receiving hemodialysis in our hospital. On December 31, 2019, the number had increased to 383. We found that serum total magnesium levels were in the normal range before initiating hemodialysis. With the initiation of hemodialysis, the levels of serum total magnesium increased. In patients on MHD, hypermagnesemia was very common. Hypomagnesemia was rare when 0.5 mmol/L magnesium dialysate was used. We did not find proton pump inhibitor associated hypomagnesemia. CONCLUSION: We find that serum total magnesium levels are in the normal range before initiating hemodialysis. However, in patients on MHD, hypermagnesemia is common when 0.5 mmol/L magnesium dialysate is used. Hypomagnesemia is very rare. Hypomagnesemia in patients on MHD is an indicator of poor condition.

Escalating the dose and downgrading the rhythm: the combination of prescribed and non-prescribed medications resulting in an abnormal heart rhythm.

Older patients often have multiple medical issues which predisposes them to complications of polypharmacy and medication interactions. We present a case of an 89-year-old female who presented to the emergency department after a fall. An electrocardiogram (ECG) showed a junctional bradycardia with a ventricular rate of 50 beats per minute (BPM). Her magnesium was 3.5 mg/dl (1.7-2.3 mg/dl). She had recently increased her milk of magnesia use for constipation. Pertinent other medications included verapamil 280 mg daily. On admission 2 grams of calcium gluconate IV were administered and the verapamil was held. An ECG the next morning showed sinus rhythm with a ventricular rate of 76 BPM.

Epsom Salt Ingestion Leading to Severe Hypermagnesemia Necessitating Dialysis.

BACKGROUND: Hypermagnesemia is an often overlooked electrolyte abnormality that has a myriad of presenting symptoms. It has been observed after both accidental and intentional ingestions of magnesium-containing compounds, and as in the case presented, Epsom salts, which are primarily magnesium sulfate. CASE REPORT: A 56-year-old man presented to the emergency department reporting weakness after an ingestion of Epsom salts used as a laxative and was found to be bradycardic and hypotensive. He subsequently developed altered mental status and respiratory depression necessitating intubation. His magnesium level was found to be > 3.91 mmol/L (> 9.5 mg/dL). He was given multiple doses of calcium gluconate and generous i.v. fluids with furosemide, with minimal improvement. However, his magnesium level corrected rapidly after initiation of dialysis, and 3 days later he was discharged home in good condition with normal neurologic function. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Keeping a high level of suspicion for, and quickly recognizing, hypermagnesemia allows for prompt initiation of treatment, which can avoid significant hemodynamic or respiratory compromise. Mainstays of treatment are i.v. calcium and i.v. fluids. Loop diuretics may be given as an adjunct as well. Dialysis should be considered in cases of severe hypermagnesemia because it results in rapid correction of magnesium levels.

Pharmacokinetics of magnesium and its effects on clinical variables following experimentally induced hypermagnesemia.

The objectives of this study were to describe pharmacokinetic and pharmacodynamic changes as a result of a single intravenous administration of magnesium sulfate (MgSO4 ) to healthy horses. MgSO4 is a magnesium salt that has been used to calm horses in equestrian competition and is difficult to regulate because magnesium is an essential constituent of all mammals. Six healthy adult female horses were administered a single intravenous dose of MgSO4 at 60 mg/kg of body weight over 5 min. Blood, urine, and cerebrospinal fluid (CSF) samples were collected, and cardiovascular parameters were monitored and echocardiograms performed at predetermined times. Noncompartmental pharmacokinetic analysis was applied to plasma concentrations of ionized magnesium (Mg2+ ). Objective data were analyzed using the Wilcoxon rank-sum test with p < .05 used as a determination for significance. Plasma concentrations of Mg2+ increased nearly fivefold, ionized calcium (Ca2+ ) decreased by nearly 10%, and the Ca2+ to Mg2+ ratio declined more than 3.5-fold and remained different than baseline until 24 hr (p < .05). Significant changes were seen with urinary fractional excretion of electrolytes, cardiovascular parameters, and echocardiographic measurements. No changes were detected in CSF electrolyte concentrations. The decrease in Ca2+ result of hypermagnesemia supports the interaction between these cations. Alterations detected in plasma electrolyte concentrations and urinary fractional excretion of electrolytes may serve as biomarkers for regulatory control for the nefarious administration of MgSO4 .

Hypokalemia Associated With a Claudin 10 Mutation: A Case Report.

Hypokalemia of renal origin can arise from genetic abnormalities in a variety of transporters or channel proteins that mediate tubular handling of potassium. Recently, mutations in claudin 10 have been documented in patients with hypokalemia in association with a range of other electrolyte abnormalities and skin and sweat gland manifestations. We report a 12-year-old Hispanic boy who presented with anhydrosis, aptyalism, alacrima, hypokalemia, and hypocalciuria, in whom we detected a homozygous mutation in the claudin 10 gene. During the 4-year follow-up period, he developed hypermagnesemia and a decline in estimated glomerular filtration rate to 59mL/min/1.73m2. His unaffected parents and siblings were heterozygous for the mutation. We summarize the clinical phenotype encountered in patients with claudin 10 mutations. It is characterized by significant heterogeneity in electrolyte and extrarenal abnormalities and is associated with a risk for progressive loss of kidney function in up to 33% of cases. Awareness of this association between claudin 10 mutations and electrolyte abnormalities, namely hypokalemia and hypermagnesemia, sheds new light on the physiology of potassium and magnesium handling along the nephron and increases the likelihood of identifying the underlying tubular mechanism in patients with newly diagnosed hypokalemia with or without concomitant hypermagnesemia.

A Novel Claudinopathy Based on Claudin-10 Mutations.

Claudins are key components of the tight junction, sealing the paracellular cleft or composing size-, charge- and water-selective paracellular channels. Claudin-10 occurs in two major isoforms, claudin-10a and claudin-10b, which constitute paracellular anion or cation channels, respectively. For several years after the discovery of claudin-10, its functional relevance in men has remained elusive. Within the past two years, several studies appeared, describing patients with different pathogenic variants of the CLDN10 gene. Patients presented with dysfunction of kidney, exocrine glands and skin. This review summarizes and compares the recently published studies reporting on a novel autosomal-recessive disorder based on claudin-10 mutations.

Clinical features of hypermagnesemia in patients with functional constipation taking daily magnesium oxide.

Although magnesium oxide is widely used as a laxative, alterations in serum magnesium concentrations among patients taking daily magnesium oxide have not been clarified. The present retrospective, cross-sectional study investigated the risk factors for hypermagnesemia in patients taking daily oral magnesium oxide. Of 2,176 patients administered daily magnesium oxide, 193 (8.9%) underwent assays of serum magnesium concentrations and were evaluated. High serum magnesium concentration and hypermagnesemia were defined as serum magnesium concentrations ≥2.5 mg/dl and ≥3.0 mg/dl, respectively. Of the 193 patients taking daily magnesium oxide, 32 (16.6%) had high serum magnesium concentration and 10 (5.2%) had hypermagnesemia. Factors associated with hypermagnesemia included chronic kidney disease (CKD) grade 4 (p = 0.014) and magnesium oxide dosage (p = 0.009). Factors associated with high serum magnesium concentration included magnesium oxide dosage >1,000 mg/day (p = 0.004), CKD grades 4 (p = 0.000) and concomitant use of stimulant laxatives (p = 0.035). Age, however, was not associated with hypermagnesemia or high serum magnesium concentration. In conclusion, renal function and magnesium oxide dosage, but not age, were associated with hypermagnesemia and high serum magnesium concentration in patients with functional constipation taking daily magnesium oxide.

The association between serum magnesium levels and community-acquired pneumonia 30-day mortality.

BACKGROUND: Community acquired pneumonia (CAP) is a common illness affecting hundreds of millions worldwide. Few studies have investigated the relationship between serum magnesium levels and outcomes of these patients. We aimed to study the association between serum magnesium levels and 30-day mortality among patients with CAP. METHODS: Retrospective overview of patients hospitalized with CAP between January 1, 2010 and December 31, 2016. Participants were analyzed retrospectively in order to identify the risk factors for a primary endpoint of 30-day mortality. Normal levels of magnesium levels in our laboratory varies between 1.35 and 2.4 mg/dl. RESULTS: 3851 patients were included in our cohort. Age > 75 years, blood urea nitrogen (BUN) > 20 mg/dl, hypoalbuminemia, and abnormal levels of magnesium were all associated with increased risk of 30-day mortality. Normal magnesium levels were associated with the lowest mortality rate (14.7%). Notably, within the normal levels, high normal magnesium levels (2-2.4 mg/dl) were correlated with higher mortality rates (30.3%) as compared to levels that ranged between 1.35-2 mg/dl (12.9%). Hypomagnesemia and hypermagnesemia were both associated with excess of 30-day mortality, 18.4 and 50%, respectively. CONCLUSION: Hypomagnesemia and hypermagnesemia on admission were associated with an increased rate of 30-day mortality among adult patients hospitalized with CAP. Interestingly, magnesium levels within the upper normal limits were associated with higher mortality.

Serum Magnesium Abnormality and Influencing Factors of Serum Magnesium Level in Peritoneal Dialysis Patients: A Single-Center Study in Northern China.

BACKGROUND/AIMS: Both hypomagnesemia and hypermagnesemia have been associated with cardiovascular diseases, bone diseases, and mortality in dialysis patients. We aimed to investigate the prevalence of and influencing factors for abnormal serum Mg levels in patients on peritoneal dialysis (PD). METHODS: A cross-sectional study in Peking University People's Hospital recorded the demographic information, clinical characteristics, and laboratory data. Data were assessed and compared with the results from 2 other studies in China. RESULTS: Of 180 enrolled PD patients, the primary diseases were glomerulonephritis (38.3%) and diabetic nephropathy (38.3%). Mean serum Mg concentration was 1.02 ± 0.16 mmol/L; 67% had normal serum Mg concentrations, and 33% had hypermagnesemia. CONCLUSIONS: Hypermagnesemia is likely to occur in patients with higher serum phosphate, lower intact parathyroid hormone, and lower high-sensitivity C-reactive protein levels. Serum Mg level distributions in PD patients vary throughout China, may have different potential causes (such as geographical location and dietary habits) and should be further studied.

Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report.

BACKGROUND: Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium (Na+)/potassium (K+) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. CASE PRESENTATION: A neonate born at 32 weeks of gestation developed hyperkalemia (K+ 6.4 mmol/L) 2 h after birth. The neonate's blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. CONCLUSION: The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the Na+/K+ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery.

Magnesium: An Overlooked Electrolyte.

BACKGROUND: Hypermagnesemia is rare and usually iatrogenic. Due to decreased renal function, older patients are generally more susceptible to hypermagnesemia than are younger patients. Because it is not one of the commonly assessed electrolytes in the blood work panel of patients, high levels are usually missed. CASE REPORT: An elderly gentleman with history of leukemia presented with complaints of shortness of breath and extreme weakness while walking. He was diagnosed with severe hypermagnesemia, but unfortunately succumbed to cardiorespiratory arrest. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Thorough history taking is crucial in evaluating weakness in elderly patients because the differential diagnosis is vast. Prompt consultation for emergent dialysis is critical to avoiding unfavorable outcomes due to electrolyte abnormalities.

Serum Magnesium and Mortality in Hemodialysis Patients in the United States: A Cohort Study.

BACKGROUND: Low serum magnesium levels in patients with kidney disease have been linked to increased mortality. This study investigated whether similar associations existed in maintenance hemodialysis (HD) patients. STUDY DESIGN: Cohort study. SETTING & PARTICIPANTS: All Fresenius Medical Care North America in-center HD patients with available serum magnesium measurements were studied. The initial exploratory study in 21,534 HD patients evaluated associations among serum magnesium level, dialysate magnesium concentration, and mortality from April 2007 through June 2008. The follow-up study in 27,544 HD patients evaluated associations between serum magnesium levels and mortality over 1 year (January through December 2008). PREDICTORS: The primary predictor was serum magnesium level, with adjustment for case-mix (age, sex, race, diabetes, and dialysis vintage and additionally for follow-up study: body surface area and vascular access) and laboratory variables (albumin, hemoglobin, phosphorus, equilibrated Kt/V, potassium, calcium, and intact parathyroid hormone values). OUTCOME: Primary outcome variable was 1-year mortality risk, evaluated using Cox proportional hazards models. RESULTS: Among 21,534 HD patients in the exploratory study, there were 3,682 deaths. Higher dialysate magnesium level was associated with higher serum magnesium level (R=0.22; P<0.001). Patients with the lowest serum magnesium levels (<1.30 mEq/L) were at highest risk for death (HR, 1.63; 95% CI, 1.30-1.96; reference serum magnesium, 1.60-<1.90 mEq/L). Among 27,544 HD patients in the follow-up study, there were 4,531 deaths. In Cox proportional hazards models, there was a linear decline in death risk from the lowest to the highest serum magnesium category, with the best survival at serum magnesium levels ≥ 2.50 mEq/L (HR, 0.68; 95% CI, 0.56-0.82). However, risk estimates were attenuated with case-mix and lab adjustment. This pattern was consistent within diabetes subgroups and for cardiovascular or noncardiovascular causes of death. LIMITATIONS: Observational study with cross-sectional serum magnesium measurements and no information for oral magnesium intake. CONCLUSIONS: Elevated serum magnesium levels > 2.10 mEq/L were associated with better survival than low serum magnesium levels < 1.30 mEq/L in HD patients. Prospective studies may determine whether manipulation of low serum magnesium levels affects survival.

Magnesium and Dialysis: The Neglected Cation.

Disorders of magnesium homeostasis are very common in dialysis patients but have received scant attention. In this review, we address measurement of plasma magnesium, magnesium balance and the factors that affect magnesium flux during dialysis, the prevalence of hypo- and hypermagnesemia in dialysis patients, and the potential clinical significance of hypo- and hypermagnesemia in dialysis patients. Many factors can affect plasma magnesium concentration, including diet, nutritional status (including plasma albumin level), medications (such as proton pump inhibitors), and dialysis prescription. Further interventional studies to determine the effect of normalization of plasma magnesium concentration on clinical outcomes are needed. At the present time, we recommend that predialysis plasma magnesium be measured on a regular basis, with the dialysate magnesium concentration adjusted to maintain plasma magnesium concentration within the normal range.

Admission hypomagnesemia and hypermagnesemia increase the risk of acute kidney injury.

BACKGROUND: The association between admission serum magnesium (Mg) levels and risk of in-hospital acute kidney injury (AKI) is limited. The aim of this study was to assess the risk of developing AKI in all hospitalized patients with various admission Mg levels. METHODS: This is a single-center retrospective study conducted at a tertiary referral hospital. All hospitalized adult patients who had admission Mg available from January to December 2013 were analyzed in this study. Admission Mg was categorized based on its distribution into six groups (less than 1.5, 1.5-1.7, 1.7-1.9, 1.9-2.1, 2.1-2.3 and greater than 2.3 mg/dL). The primary outcome was in-hospital AKI occurring after hospital admission. Logistic regression analysis was performed to obtain the odds ratio of AKI of various admission Mg levels using Mg with lowest AKI incidence (1.9-2.1 mg/dL) as the reference group. RESULTS: Of 9241 patients enrolled, AKI occurred in 1124 patients (12.2%). The lowest incidence of AKI was when serum Mg was within 1.7-1.9 and 1.9-2.1 mg/dL. A U-shaped curve emerged demonstrating higher incidences of AKI associated with both hypoMg (<1.7) and hyperMg (>2.1). After adjusting for potential confounders, both hypoMg (<1.5 mg/dL) and hyperMg (>2.3 mg/dL) were associated with an increased risk of developing AKI with odds ratios of 1.70 (95% CI 1.31-2.18) and 1.42 (95% CI 1.11-1.81), respectively. CONCLUSION: Both admission hypoMg and hyperMg were associated with an increased risk for in-hospital AKI.