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Phuong T Pham - One of the best experts on this subject based on the ideXlab platform.
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Hypomagnesemia a clinical perspective
International Journal of Nephrology and Renovascular Disease, 2014Co-Authors: Phuong Chi T Pham, Phuong Anh T Pham, Son V Pham, Phuong T Pham, Phuong Mai T PhamAbstract:Although magnesium is involved in a wide spectrum of vital functions in normal human physiology, the significance of Hypomagnesemia and necessity for its treatment are under-recognized and underappreciated in clinical practice. In the current review, we first present an overview of the clinical significance of Hypomagnesemia and normal magnesium metabolism, with a focus on renal magnesium handling. Subsequently, we review the literature for both congenital and acquired hypomagnesemic conditions that affect the various steps in normal magnesium metabolism. Finally, we present an approach to the routine evaluation and suggested management of Hypomagnesemia.
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Hypomagnesemia in patients with type 2 diabetes
Clinical Journal of The American Society of Nephrology, 2007Co-Authors: Phuong Chi T Pham, Son V Pham, Phuong Mai T Pham, Jeffrey M Miller, Phuong T PhamAbstract:Hypomagnesemia has been reported to occur at an increased frequency among patients with type 2 diabetes compared with their counterparts without diabetes. Despite numerous reports linking Hypomagnesemia to chronic diabetic complications, attention to this issue is poor among clinicians. This article reviews the literature on the metabolism of magnesium, incidence of Hypomagnesemia in patients with type 2 diabetes, implicated contributing factors, and associated complications. Hypomagnesemia occurs at an incidence of 13.5 to 47.7% among patients with type 2 diabetes. Poor dietary intake, autonomic dysfunction, altered insulin metabolism, glomerular hyperfiltration, osmotic diuresis, recurrent metabolic acidosis, hypophosphatemia, and hypokalemia may be contributory. Hypomagnesemia has been linked to poor glycemic control, coronary artery diseases, hypertension, diabetic retinopathy, nephropathy, neuropathy, and foot ulcerations. The increased incidence of Hypomagnesemia among patients with type 2 diabetes presumably is multifactorial. Because current data suggest adverse outcomes in association with Hypomagnesemia, it is prudent to monitor magnesium routinely in this patient population and treat the condition whenever possible.
Joost G J Hoenderop - One of the best experts on this subject based on the ideXlab platform.
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common single nucleotide polymorphisms in transient receptor potential melastatin type 6 increase the risk for proton pump inhibitor induced Hypomagnesemia a case control study
Pharmacogenetics and Genomics, 2017Co-Authors: M W Hess, Jeroen H. F. Baaij, Joost G J Hoenderop, Rene J M Bindels, Mark M T J Broekman, Tanya M Bisseling, Bertram J T Haarhuis, Rene Te H M Morsche, Joost P H DrenthAbstract:OBJECTIVE: Proton pump inhibitors (PPIs) are effective drugs for the treatment of gastric acid-related disorders. Serious adverse events are rare for PPIs, but recent data suggest that PPIs cause Hypomagnesemia. The aim of this study was to estimate the frequency of PPI-induced Hypomagnesemia and to define the risk factors for its development. MATERIALS AND METHODS: A total of 133 chronic users of PPIs were enrolled and patients were distinguished on the basis of their serum Mg concentrations. Common single nucleotide polymorphisms (SNPs) in the candidate gene, transient receptor potential melastatin type 6 (TRPM6), were screened. RESULTS: Seventeen out of 133 patients had PPI-induced Hypomagnesemia. The duration of PPI use was longer in those with Hypomagnesemia (7.7 vs. 5.2 years). Two common SNPs in TRPM6 (rs3750425 and rs2274924) increased the risk for PPI-induced Hypomagnesemia by 5.8-fold. CONCLUSION: We found Hypomagnesemia in 13% of PPI users. SNPs in TRPM6 drive the risk of developing Hypomagnesemia during chronic PPI use.
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determinants of Hypomagnesemia in patients with type 2 diabetes mellitus
European Journal of Endocrinology, 2017Co-Authors: Steef Kurstjens, Jeroen H. F. Baaij, Rene J M Bindels, Hacene Bouras, Cees J Tack, Joost G J HoenderopAbstract:BACKGROUND: Hypomagnesemia (plasma magnesium (Mg2+) concentration <0.7 mmol/L) has been described in patients with type 2 diabetes. Polypharmacy is inevitable when treating a complex disease such as type 2 diabetes and could explain disturbances in the plasma Mg2+ concentration. In this study, we aimed to establish the extent of Hypomagnesemia in a cohort of type 2 diabetes patients and to identify the determinants of plasma Mg2+ levels. METHODS: Patient data and samples of 395 type 2 diabetes patients were investigated. Plasma Mg2+ concentrations were measured using a spectrophotometric assay. Using Pearson correlation analyses, variables were correlated to plasma Mg2+ levels. After excluding confounding variables, all parameters correlating (P < 0.1) with plasma Mg2+ were included in a stepwise backward regression model. RESULTS: The mean plasma Mg2+ concentration in this cohort was 0.74 +/- 0.10 mmol/L. In total, 121 patients (30.6%) suffered from Hypomagnesemia. Both plasma triglyceride (r = -0.273, P < 0.001) and actual glucose levels (r = -0.231, P < 0.001) negatively correlated with the plasma Mg2+ concentration. Patients using metformin (n = 251, 62%), proton pump inhibitors (n = 179, 45%) or beta-adrenergic receptor agonists (n = 31, 8%) displayed reduced plasma Mg2+ levels. Insulin use (n = 299, 76%) positively correlated with plasma Mg2+ levels. The model predicted (R2) 20% of all variance in the plasma Mg2+ concentration. CONCLUSIONS: Hypomagnesemia is highly prevalent in type 2 diabetes patients. Plasma triglycerides and glucose levels are major determinants of the plasma Mg2+ concentration, whereas only a minor part (<10%) of Hypomagnesemia can be explained by drug intake, excluding polypharmacy as a major cause for Hypomagnesemia in type 2 diabetes.
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Hypomagnesemia as first clinical manifestation of adtkd hnf1b a case series and literature review
American Journal of Nephrology, 2015Co-Authors: Cas Van Der Made, Joost G J Hoenderop, Nine V. A. M. Knoers, Ewout J Hoorn, Renaud De La Faille, Huseyin Karaaslan, Rosa Vargas Poussou, Jeroen H. F. BaaijAbstract:Background: Autosomal dominant tubulointerstitial kidney disease subtype HNF1B (ADTKD-HNF1B) is caused by a mutation in hepatocyte nuclear factor 1 homeobox beta (HNF1B). Although 50-60% of ADTKD-HNF1B patients develop Hypomagnesemia, HNF1B mutations are mainly identified in patients with structural kidney defects or diabetes. Cases: The current case series describes 3 patients in whom Hypomagnesemia proved to be the first clinical manifestation of ADTKD-HNF1B. All patients presented with Hypomagnesemia with a high fractional excretion of Mg2+ and hypocalciuria. Exome sequencing performed for analysis of known and candidate hypomagnesaemia genes and subsequent multiplex ligation-dependent probe amplification analysis revealed a large deletion at the chromosome 17q12. Follow-up analysis showed increased blood glucose concentrations in all 3 patients and high hemoglobin A1c levels in 2 out of 3 patients, indicating diabetes mellitus. Although all patients suffered from mild renal insufficiency, only 1 of the 3 patients was shown to have renal cysts on CT. Conclusion: The prevalence of HNF1B mutations and the relative contribution of Hypomagnesemia to its symptoms are underestimated. Therefore, patients with primary renal magnesium wasting should be tested for HNF1B mutations to ensure early detection and optimal management of ADTKD-HNF1B.
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evaluation of Hypomagnesemia lessons from disorders of tubular transport
American Journal of Kidney Diseases, 2013Co-Authors: Henrik Dimke, L A H Monnens, Joost G J Hoenderop, Rene J M BindelsAbstract:Hypomagnesemia is a highly prevalent clinical condition affecting a large number of hospitalized patients. A decrease in systemic magnesium concentration may lead to impaired function of both neurologic and cardiovascular systems. The kidney has a pivotal role in magnesium handling by adjusting the urinary excretion of this ion in order to maintain systemic concentrations within a narrow range. As such, the cause of Hypomagnesemia can be related to increments in the renal excretion of this cation. Many hypomagnesemic disorders also have characteristic changes in the renal reabsorptive capacity for other electrolytes, leading to symptoms that sometimes obscure the clinical presentation. For instance, changes in serum calcium concentration or its urinary excretion can aid in determining the underlying cause. Moreover, hypokalemia due to renal potassium losses often is associated with Hypomagnesemia. Genetic defects in pathways controlling renal electrolyte transport impose the hypomagnesemic condition by facilitating renal losses. The discovery of the causative genes has greatly increased our understanding of how magnesium is transported by the kidney. Such knowledge is integral for the continued improvement of patient care with respect to bettering therapies and diagnosis.
Jeroen H. F. Baaij - One of the best experts on this subject based on the ideXlab platform.
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Genetic causes of Hypomagnesemia, a clinical overview
Pediatric Nephrology, 2017Co-Authors: Daan H. H. M Viering, Jeroen H. F. Baaij, Stephen B. Walsh, Robert Kleta, Detlef BockenhauerAbstract:Magnesium is essential to the proper functioning of numerous cellular processes. Magnesium ion (Mg^2+) deficits, as reflected in Hypomagnesemia, can cause neuromuscular irritability, seizures and cardiac arrhythmias. With normal Mg^2+ intake, homeostasis is maintained primarily through the regulated reabsorption of Mg^2+ by the thick ascending limb of Henle’s loop and distal convoluted tubule of the kidney. Inadequate reabsorption results in renal Mg^2+ wasting, as evidenced by an inappropriately high fractional Mg^2+ excretion. Familial renal Mg^2+ wasting is suggestive of a genetic cause, and subsequent studies in these hypomagnesemic families have revealed over a dozen genes directly or indirectly involved in Mg^2+ transport. Those can be classified into four groups: hypercalciuric Hypomagnesemias (encompassing mutations in CLDN16 , CLDN19 , CASR , CLCNKB ), Gitelman-like Hypomagnesemias ( CLCNKB , SLC12A3 , BSND , KCNJ10 , FYXD2 , HNF1B , PCBD1 ), mitochondrial Hypomagnesemias ( SARS2 , MT-TI , Kearns–Sayre syndrome) and other Hypomagnesemias ( TRPM6 , CNMM2 , EGF , EGFR , KCNA1 , FAM111A ). Although identification of these genes has not yet changed treatment, which remains Mg^2+ supplementation, it has contributed enormously to our understanding of Mg^2+ transport and renal function. In this review, we discuss general mechanisms and symptoms of genetic causes of Hypomagnesemia as well as the specific molecular mechanisms and clinical phenotypes associated with each syndrome.
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common single nucleotide polymorphisms in transient receptor potential melastatin type 6 increase the risk for proton pump inhibitor induced Hypomagnesemia a case control study
Pharmacogenetics and Genomics, 2017Co-Authors: M W Hess, Jeroen H. F. Baaij, Joost G J Hoenderop, Rene J M Bindels, Mark M T J Broekman, Tanya M Bisseling, Bertram J T Haarhuis, Rene Te H M Morsche, Joost P H DrenthAbstract:OBJECTIVE: Proton pump inhibitors (PPIs) are effective drugs for the treatment of gastric acid-related disorders. Serious adverse events are rare for PPIs, but recent data suggest that PPIs cause Hypomagnesemia. The aim of this study was to estimate the frequency of PPI-induced Hypomagnesemia and to define the risk factors for its development. MATERIALS AND METHODS: A total of 133 chronic users of PPIs were enrolled and patients were distinguished on the basis of their serum Mg concentrations. Common single nucleotide polymorphisms (SNPs) in the candidate gene, transient receptor potential melastatin type 6 (TRPM6), were screened. RESULTS: Seventeen out of 133 patients had PPI-induced Hypomagnesemia. The duration of PPI use was longer in those with Hypomagnesemia (7.7 vs. 5.2 years). Two common SNPs in TRPM6 (rs3750425 and rs2274924) increased the risk for PPI-induced Hypomagnesemia by 5.8-fold. CONCLUSION: We found Hypomagnesemia in 13% of PPI users. SNPs in TRPM6 drive the risk of developing Hypomagnesemia during chronic PPI use.
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determinants of Hypomagnesemia in patients with type 2 diabetes mellitus
European Journal of Endocrinology, 2017Co-Authors: Steef Kurstjens, Jeroen H. F. Baaij, Rene J M Bindels, Hacene Bouras, Cees J Tack, Joost G J HoenderopAbstract:BACKGROUND: Hypomagnesemia (plasma magnesium (Mg2+) concentration <0.7 mmol/L) has been described in patients with type 2 diabetes. Polypharmacy is inevitable when treating a complex disease such as type 2 diabetes and could explain disturbances in the plasma Mg2+ concentration. In this study, we aimed to establish the extent of Hypomagnesemia in a cohort of type 2 diabetes patients and to identify the determinants of plasma Mg2+ levels. METHODS: Patient data and samples of 395 type 2 diabetes patients were investigated. Plasma Mg2+ concentrations were measured using a spectrophotometric assay. Using Pearson correlation analyses, variables were correlated to plasma Mg2+ levels. After excluding confounding variables, all parameters correlating (P < 0.1) with plasma Mg2+ were included in a stepwise backward regression model. RESULTS: The mean plasma Mg2+ concentration in this cohort was 0.74 +/- 0.10 mmol/L. In total, 121 patients (30.6%) suffered from Hypomagnesemia. Both plasma triglyceride (r = -0.273, P < 0.001) and actual glucose levels (r = -0.231, P < 0.001) negatively correlated with the plasma Mg2+ concentration. Patients using metformin (n = 251, 62%), proton pump inhibitors (n = 179, 45%) or beta-adrenergic receptor agonists (n = 31, 8%) displayed reduced plasma Mg2+ levels. Insulin use (n = 299, 76%) positively correlated with plasma Mg2+ levels. The model predicted (R2) 20% of all variance in the plasma Mg2+ concentration. CONCLUSIONS: Hypomagnesemia is highly prevalent in type 2 diabetes patients. Plasma triglycerides and glucose levels are major determinants of the plasma Mg2+ concentration, whereas only a minor part (<10%) of Hypomagnesemia can be explained by drug intake, excluding polypharmacy as a major cause for Hypomagnesemia in type 2 diabetes.
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Hypomagnesemia as first clinical manifestation of adtkd hnf1b a case series and literature review
American Journal of Nephrology, 2015Co-Authors: Cas Van Der Made, Joost G J Hoenderop, Nine V. A. M. Knoers, Ewout J Hoorn, Renaud De La Faille, Huseyin Karaaslan, Rosa Vargas Poussou, Jeroen H. F. BaaijAbstract:Background: Autosomal dominant tubulointerstitial kidney disease subtype HNF1B (ADTKD-HNF1B) is caused by a mutation in hepatocyte nuclear factor 1 homeobox beta (HNF1B). Although 50-60% of ADTKD-HNF1B patients develop Hypomagnesemia, HNF1B mutations are mainly identified in patients with structural kidney defects or diabetes. Cases: The current case series describes 3 patients in whom Hypomagnesemia proved to be the first clinical manifestation of ADTKD-HNF1B. All patients presented with Hypomagnesemia with a high fractional excretion of Mg2+ and hypocalciuria. Exome sequencing performed for analysis of known and candidate hypomagnesaemia genes and subsequent multiplex ligation-dependent probe amplification analysis revealed a large deletion at the chromosome 17q12. Follow-up analysis showed increased blood glucose concentrations in all 3 patients and high hemoglobin A1c levels in 2 out of 3 patients, indicating diabetes mellitus. Although all patients suffered from mild renal insufficiency, only 1 of the 3 patients was shown to have renal cysts on CT. Conclusion: The prevalence of HNF1B mutations and the relative contribution of Hypomagnesemia to its symptoms are underestimated. Therefore, patients with primary renal magnesium wasting should be tested for HNF1B mutations to ensure early detection and optimal management of ADTKD-HNF1B.
Robert Zietse - One of the best experts on this subject based on the ideXlab platform.
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a case series of proton pump inhibitor induced Hypomagnesemia
American Journal of Kidney Diseases, 2010Co-Authors: Ewout J Hoorn, Joost Van Der Hoek, Ernst J Kuipers, Clemens J M Bolwerk, Robert ZietseAbstract:Proton pump inhibitor (PPI)-induced Hypomagnesemia has been recognized since 2006. Our aim was to further characterize the clinical consequences and possible mechanisms of this electrolyte disorder using 4 cases. Two men (aged 63 and 81 years) and 2 women (aged 73 and 62 years) had been using a PPI (esomeprazole, pantoprazole, omeprazole, and rabeprazole, 20-40 mg) for 1-13 years. They developed severe Hypomagnesemia (magnesium, 0.30 ± 0.28 mEq/L; reference, 1.40-2.10 mEq/L) with hypocalcemia (calcium, 6.4 ± 1.8 mg/dL), relative hypoparathyroidism (parathyroid hormone, 43 ± 6 pg/mL), and extremely low urinary calcium and magnesium excretion. One patient was admitted with postanoxic encephalopathy after a collapse likely caused by arrhythmia. The others had electrocardiogram abnormalities (prolonged QT interval, ST depression, and U waves). Concomitant hypokalemia (potassium, 2.8 ± 0.1 mEq/L) was considered the trigger for these arrhythmias. Hypomagnesemia-induced kaliuresis (potassium excretion, 65 ± 24 mEq/L) was identified as the cause of hypokalemia. This series of PPI-induced Hypomagnesemia shows that this is a generic effect. It also indicates that Hypomagnesemia may occur within 1 year of PPI therapy initiation and can have serious clinical consequences, likely triggered by the associated hypokalemia. A high index of suspicion is required in PPI users for unexplained Hypomagnesemia, hypocalcemia, hypokalemia, or associated symptoms.
Rene J M Bindels - One of the best experts on this subject based on the ideXlab platform.
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common single nucleotide polymorphisms in transient receptor potential melastatin type 6 increase the risk for proton pump inhibitor induced Hypomagnesemia a case control study
Pharmacogenetics and Genomics, 2017Co-Authors: M W Hess, Jeroen H. F. Baaij, Joost G J Hoenderop, Rene J M Bindels, Mark M T J Broekman, Tanya M Bisseling, Bertram J T Haarhuis, Rene Te H M Morsche, Joost P H DrenthAbstract:OBJECTIVE: Proton pump inhibitors (PPIs) are effective drugs for the treatment of gastric acid-related disorders. Serious adverse events are rare for PPIs, but recent data suggest that PPIs cause Hypomagnesemia. The aim of this study was to estimate the frequency of PPI-induced Hypomagnesemia and to define the risk factors for its development. MATERIALS AND METHODS: A total of 133 chronic users of PPIs were enrolled and patients were distinguished on the basis of their serum Mg concentrations. Common single nucleotide polymorphisms (SNPs) in the candidate gene, transient receptor potential melastatin type 6 (TRPM6), were screened. RESULTS: Seventeen out of 133 patients had PPI-induced Hypomagnesemia. The duration of PPI use was longer in those with Hypomagnesemia (7.7 vs. 5.2 years). Two common SNPs in TRPM6 (rs3750425 and rs2274924) increased the risk for PPI-induced Hypomagnesemia by 5.8-fold. CONCLUSION: We found Hypomagnesemia in 13% of PPI users. SNPs in TRPM6 drive the risk of developing Hypomagnesemia during chronic PPI use.
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determinants of Hypomagnesemia in patients with type 2 diabetes mellitus
European Journal of Endocrinology, 2017Co-Authors: Steef Kurstjens, Jeroen H. F. Baaij, Rene J M Bindels, Hacene Bouras, Cees J Tack, Joost G J HoenderopAbstract:BACKGROUND: Hypomagnesemia (plasma magnesium (Mg2+) concentration <0.7 mmol/L) has been described in patients with type 2 diabetes. Polypharmacy is inevitable when treating a complex disease such as type 2 diabetes and could explain disturbances in the plasma Mg2+ concentration. In this study, we aimed to establish the extent of Hypomagnesemia in a cohort of type 2 diabetes patients and to identify the determinants of plasma Mg2+ levels. METHODS: Patient data and samples of 395 type 2 diabetes patients were investigated. Plasma Mg2+ concentrations were measured using a spectrophotometric assay. Using Pearson correlation analyses, variables were correlated to plasma Mg2+ levels. After excluding confounding variables, all parameters correlating (P < 0.1) with plasma Mg2+ were included in a stepwise backward regression model. RESULTS: The mean plasma Mg2+ concentration in this cohort was 0.74 +/- 0.10 mmol/L. In total, 121 patients (30.6%) suffered from Hypomagnesemia. Both plasma triglyceride (r = -0.273, P < 0.001) and actual glucose levels (r = -0.231, P < 0.001) negatively correlated with the plasma Mg2+ concentration. Patients using metformin (n = 251, 62%), proton pump inhibitors (n = 179, 45%) or beta-adrenergic receptor agonists (n = 31, 8%) displayed reduced plasma Mg2+ levels. Insulin use (n = 299, 76%) positively correlated with plasma Mg2+ levels. The model predicted (R2) 20% of all variance in the plasma Mg2+ concentration. CONCLUSIONS: Hypomagnesemia is highly prevalent in type 2 diabetes patients. Plasma triglycerides and glucose levels are major determinants of the plasma Mg2+ concentration, whereas only a minor part (<10%) of Hypomagnesemia can be explained by drug intake, excluding polypharmacy as a major cause for Hypomagnesemia in type 2 diabetes.
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evaluation of Hypomagnesemia lessons from disorders of tubular transport
American Journal of Kidney Diseases, 2013Co-Authors: Henrik Dimke, L A H Monnens, Joost G J Hoenderop, Rene J M BindelsAbstract:Hypomagnesemia is a highly prevalent clinical condition affecting a large number of hospitalized patients. A decrease in systemic magnesium concentration may lead to impaired function of both neurologic and cardiovascular systems. The kidney has a pivotal role in magnesium handling by adjusting the urinary excretion of this ion in order to maintain systemic concentrations within a narrow range. As such, the cause of Hypomagnesemia can be related to increments in the renal excretion of this cation. Many hypomagnesemic disorders also have characteristic changes in the renal reabsorptive capacity for other electrolytes, leading to symptoms that sometimes obscure the clinical presentation. For instance, changes in serum calcium concentration or its urinary excretion can aid in determining the underlying cause. Moreover, hypokalemia due to renal potassium losses often is associated with Hypomagnesemia. Genetic defects in pathways controlling renal electrolyte transport impose the hypomagnesemic condition by facilitating renal losses. The discovery of the causative genes has greatly increased our understanding of how magnesium is transported by the kidney. Such knowledge is integral for the continued improvement of patient care with respect to bettering therapies and diagnosis.