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1.
Clin Biochem ; 133-134: 110815, 2024 Sep 04.
Article in English | MEDLINE | ID: mdl-39241903

ABSTRACT

OBJECTIVES: The objective of this study was to determine the in vivo correlation of ionized magnesium (iMg) with ionized calcium (iCa), total calcium, albumin and pH. In addition, the analytical interference of iCa on iMg measurement on the Stat Profile Prime Plus (Nova Biomedical) and vice versa was defined. METHODS: In vivo correlation of iCa, iMg and pH was studied in 238 paired blood gas samples of 109 different patients admitted to the intensive care unit. Albumin and total magnesium (tMg) were measured in heparinized plasma samples. Measurement of iMg was performed with the ion selective magnesium electrode (ISE) of the Stat Profile Prime Plus (Nova Biomedical) and iCa and pH were measured with a Rapid Point 500 blood gas analyzer (Siemens). Albumin, total calcium and total magnesium were analyzed with a Siemens Atellica CH. Analytical interference of iCa with iMg and vice versa was investigated using unbuffered saline solutions. RESULTS: In the studied patient population, no significant correlations were observed between iMg and iCa, albumin, and pH. An inverse relationship was observed between iCa and Mg-ISE. For every 0.1 mmol/L change in iCa concentration, the iMg concentration deviated by 0.01 mmol/L at an iMg concentration of 0.5 mmol/L and by 0.013 mmol/L at an iMg concentration of 1.0 mmol/L. The measurement of iCa was not affected by iMg. CONCLUSIONS: In vivo, no correlation was observed between iMg with iCa, albumin and pH. Interference of iCa on iMg measurement was noted, with a maximum deviation of ±0.02 mmol/L iMg across the reference range of iCa (1.15-1.32 mmol/L). Additionally, the iCa measurement was not affected by the iMg concentration.

3.
Am J Physiol Regul Integr Comp Physiol ; 294(6): R2001-7, 2008 Jun.
Article in English | MEDLINE | ID: mdl-18385471

ABSTRACT

The body maintains Mg(2+) homeostasis by renal and intestinal (re)absorption. However, the molecular mechanisms that mediate transepithelial Mg(2+) transport are largely unknown. Transient receptor potential melastatin 6 (TRPM6) was recently identified and shown to function in active epithelial Mg(2+) transport in intestine and kidney. To define the relationship between Mg(2+) status and TRPM6 expression, we used two models of hypomagnesemia: 1) C57BL/6J mice fed a mildly or severely Mg(2+)-deficient diet, and 2) mice selected for either low (MgL) or high (MgH) erythrocyte and plasma Mg(2+) status. In addition, the mice were subjected to a severely Mg(2+)-deficient diet. Our results show that C57BL/6J mice fed a severely Mg(2+)-deficient diet developed hypomagnesemia and hypomagnesuria and showed increased TRPM6 expression in kidney and intestine. When fed a Mg(2+)-adequate diet, MgL mice presented hypomagnesemia and hypermagnesuria, and lower kidney and intestinal TRPM6 expression, compared with MgH mice. A severely Mg(2+)-deficient diet led to hypomagnesemia and hypomagnesuria in both strains. Furthermore, this diet induced kidney TRPM6 expression in MgL mice, but not in MgH mice. In conclusion, as shown in C57BL/6J mice, dietary Mg(2+)-restriction results in increased Mg(2+) (re)absorption, which is correlated with increased TRPM6 expression. In MgL and MgH mice, the inherited Mg(2+) status is linked to different TRPM6 expression. The MgL and MgH mice respond differently to a low-Mg(2+) diet with regard to TRPM6 expression in the kidney, consistent with genetic factors contributing to the regulation of cellular Mg(2+) levels. Further studies of these mice strains could improve our understanding of the genetics of Mg(2+) homeostasis.


Subject(s)
Intestine, Large/metabolism , Kidney/metabolism , Magnesium Deficiency/metabolism , Magnesium/metabolism , TRPM Cation Channels/metabolism , Animals , Erythrocytes/metabolism , Female , Homeostasis/physiology , Intestinal Absorption/physiology , Mice , Mice, Inbred C57BL , TRPM Cation Channels/genetics
4.
J Clin Invest ; 117(8): 2260-7, 2007 Aug.
Article in English | MEDLINE | ID: mdl-17671655

ABSTRACT

Primary hypomagnesemia constitutes a rare heterogeneous group of disorders characterized by renal or intestinal magnesium (Mg(2+)) wasting resulting in generally shared symptoms of Mg(2+) depletion, such as tetany and generalized convulsions, and often including associated disturbances in calcium excretion. However, most of the genes involved in the physiology of Mg(2+) handling are unknown. Through the discovery of a mutation in the EGF gene in isolated autosomal recessive renal hypomagnesemia, we have, for what we believe is the first time, identified a magnesiotropic hormone crucial for total body Mg(2+) balance. The mutation leads to impaired basolateral sorting of pro-EGF. As a consequence, the renal EGFR is inadequately stimulated, resulting in insufficient activation of the epithelial Mg(2+) channel TRPM6 (transient receptor potential cation channel, subfamily M, member 6) and thereby Mg(2+) loss. Furthermore, we show that colorectal cancer patients treated with cetuximab, an antagonist of the EGFR, develop hypomagnesemia, emphasizing the significance of EGF in maintaining Mg(2+) balance.


Subject(s)
Epidermal Growth Factor/genetics , Epidermal Growth Factor/metabolism , Magnesium/metabolism , Mutation , Protein Precursors/genetics , Protein Precursors/metabolism , Protein Processing, Post-Translational/genetics , Renal Tubular Transport, Inborn Errors/genetics , Renal Tubular Transport, Inborn Errors/metabolism , Animals , Antibodies, Monoclonal/adverse effects , Antibodies, Monoclonal/therapeutic use , Antibodies, Monoclonal, Humanized , Antineoplastic Agents/adverse effects , Antineoplastic Agents/therapeutic use , Cetuximab , Colorectal Neoplasms/complications , Colorectal Neoplasms/drug therapy , ErbB Receptors/genetics , ErbB Receptors/metabolism , Female , Humans , Kidney/metabolism , Male , Pedigree , Protein Processing, Post-Translational/drug effects , Renal Tubular Transport, Inborn Errors/chemically induced , TRPM Cation Channels/biosynthesis , TRPM Cation Channels/genetics , Tetany/chemically induced , Tetany/genetics , Tetany/metabolism
5.
J Am Soc Nephrol ; 17(4): 1035-43, 2006 Apr.
Article in English | MEDLINE | ID: mdl-16524949

ABSTRACT

The kidney is the principal organ responsible for the regulation of the body Mg(2+) balance. Identification of the gene defect in hypomagnesemia with secondary hypocalcemia recently elucidated transient receptor potential melastatin 6 (TRPM6) as the gatekeeper in transepithelial Mg(2+) transport, whereas its homolog, TRPM7, is implicated in cellular Mg(2+) homeostasis. The aim of this study was to determine the tissue distribution in mouse and regulation of TRPM6 and TRPM7 by dietary Mg(2+) and hormones. This study demonstrates that TRPM6 is expressed predominantly in kidney, lung, cecum, and colon, whereas TRPM7 is distributed ubiquitously. Dietary Mg(2+) restriction in mice resulted in hypomagnesemia and renal Mg(2+) and Ca(2+) conservation, whereas a Mg(2+)-enriched diet led to increased urinary Mg(2+) and Ca(2+) excretion. Conversely, Mg(2+) restriction significantly upregulated renal TRPM6 mRNA levels, whereas a Mg(2+) enriched diet increased TRPM6 mRNA expression in colon. Dietary Mg(2+) did not alter TRPM7 mRNA expression in mouse kidney and colon. In addition, it was demonstrated that 17beta-estradiol but not 1,25-dihydroxyvitamin D(3) or parathyroid hormone regulates TRPM6 renal mRNA levels. Renal TRPM7 mRNA abundance remained unaltered under these conditions. The renal TRPM6 mRNA level in ovariectomized rats was significantly reduced, whereas 17beta-estradiol treatment normalized TRPM6 mRNA levels. In conclusion, kidney, lung, cecum, and colon likely constitute the main sites of active Mg(2+) (re)absorption in the mouse. In addition, Mg(2+) restriction and 17beta-estradiol upregulated renal TRPM6 mRNA levels, whereas a Mg(2+)-enriched diet stimulated TRPM6 mRNA expression in colon, supporting the gatekeeper function of TRPM6 in transepithelial Mg(2+) transport.


Subject(s)
Kidney/metabolism , Magnesium/metabolism , TRPM Cation Channels/metabolism , Animals , Base Sequence , Calcium/metabolism , DNA, Complementary/genetics , Epithelium/drug effects , Epithelium/metabolism , Estradiol/pharmacology , Female , Kidney/drug effects , Magnesium/administration & dosage , Mice , Mice, Inbred C57BL , Mice, Knockout , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rats , TRPM Cation Channels/genetics
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