Mechanisms and causes of hypomagnesemia

Agus, Zalman S.

doi:10.1097/mnh.0000000000000238

Cited by 67 publications

(85 citation statements)

References 31 publications

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“…Interestingly, they all presented with a kidney stone before 14 years of age. Moreover, they all had normal PTH and normal or lower 25-hydroxyvitamin D levels, but two patients had increased 1,25 dihydroxyvitamin D. All four patients displayed increased urinary magnesium excretion (i.e., >2% FEMg (Agus, 1999)).…”

Section: Snp Rs78250838:c>t Is More Frequent In Children With Hypercamentioning

confidence: 91%

A variant in acis-regulatory element enhances claudin-14 expression and is associated with pediatric-onset hypercalciuria and kidney stones

et al. 2017

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The greatest risk factor for kidney stones is hypercalciuria, the etiology of which is largely unknown. A recent genome-wide association study (GWAS) linked hypercalciuria and kidney stones to a claudin-14 (CLDN14) risk haplotype. However, the underlying molecular mechanism was not delineated. Recently, renal CLDN14 expression was found to increase in response to increased plasma calcium, thereby inducing calciuria. We hypothesized therefore that some children with hypercalciuria and kidney stones harbor a CLDN14 variant that inappropriately increases gene expression. To test this hypothesis, we sequenced the CLDN14 risk haplotype in a cohort of children with idiopathic hypercalciuria and kidney stones. An intronic SNP was more frequent in affected children. Dual luciferase and cell-based assays demonstrated increased reporter or CLDN14 expression when this polymorphism was introduced. In silico studies predicted the SNP introduced a novel insulinoma-associated 1 (INSM1) transcription factor binding site. Consistent with this, repeating the dual luciferase assay in the presence of INSM1 further increased reporter expression. Our data suggest that children with the INSM1 binding site within the CLDN14 risk haplotype have a higher likelihood of hypercalciuria and kidney stones. Enhanced CLDN14 expression may play a role in the pathophysiology of their hypercalciuria.

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Section: Snp Rs78250838:c>t Is More Frequent In Children With Hypercamentioning

confidence: 91%

A variant in acis-regulatory element enhances claudin-14 expression and is associated with pediatric-onset hypercalciuria and kidney stones

et al. 2017

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“…[90] This also requires pharmacological assessment (which is not limited to single particle motion in Intensive Care Unit) have been diagnosed with hypomagnesemia. [101] Further, it should be noted that the inherent H 2 gas production (upon reaction of HCl with Zn) is a common feature of gut microflora activity and should not be of greater concern if within safe limits. [102] While one may argue that mode of action of a PPI is completely different than that of an antacid (to which this class of micromotors actually resembles more) the inherent novelty of such a design may actually be a clinically relevant idea which needs to be further investigated.…”

Section: Accepted Manuscript 4 Micromotors In Gi Tramentioning

confidence: 99%

Micromotors for drug delivery in vivo: The road ahead

Srivastava

Clergeaud

Andresen

et al. 2019

Advanced Drug Delivery Reviews

107

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Autonomously propelled/externally guided micromotors overcome current drug delivery challenges by providing (a) higher drug loading capacity, (b) localized delivery (less toxicity), (c) enhanced tissue penetration and (d) active maneuvering in vivo. These microscale drug delivery systems can exploit biological fluids, as well as exogenous stimuli, like light-NIR, ultrasound and magnetic fields (or a combination of these), towards propulsion/drug release. Ability of these wireless drug carriers towards localized targeting and controlled drug release, makes them a lucrative candidate for drug administration in complex microenvironments (like solid tumors or gastrointestinal tract). In this report, we discuss these microscale drug delivery systems for their therapeutic benefits under in vivo setting and provide a design-application rationale towards greater clinical significance. Also, a proof-of-concept depicting 'microbots-in-a-capsule' towards oral drug delivery has been discussed.

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“…Gastrointestinal causes for hypomagnesaemia include inadequate dietary magnesium intact, gastrointestinal loss through vomiting or diarrhoea, malabsorption, small bowel surgery and alcoholism [46,52]. Primary familial hypomagnesaemia caused by TRPM6 mutations can result in reduced gastrointestinal absorption and renal loss.…”

Section: Hypomagnesaemiamentioning

confidence: 99%

“…Excessive renal magnesium loss at the PCT is seen with the use of frusemide and in Bartter syndrome; although this is usually mild due to distal compensation. Hypercalcaemia leads to hypomagnesaemia due to competition for transport at the TALH and CaSR activation [52]. Familial hypomagnesaemia with hypercalciuria can occur in mutations of claudin-16 and 19 [53].…”

Section: Hypomagnesaemiamentioning

confidence: 99%

Calcium, Phosphate and Magnesium Disorders

Heron¹

2019

Fluid and Electrolyte Disorders

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Calcium, phosphate and magnesium are essential for human function and life. Each electrolyte is readily found in the human diet, and homeostasis is tightly regulated by the intestine, kidney and bone as well as other critical hormones, receptors and transporters. Disturbance to this balance can result in symptomatic disease and life-threatening manifestations. Calcium and phosphate are particularly co-dependent with disruption to the balance of one often influencing the other. It is important that clinicians have a thorough understanding of the mechanisms underplaying the homeostasis of each electrolyte as they have implications for prevention and management of disease. This chapter aims to outline the importance of calcium, phosphate and magnesium; the regulation of each electrolyte and the consequences of imbalance.

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Mechanisms and causes of hypomagnesemia

Abstract: The recognition of new mechanisms and causes of magnesium absorption and reabsorption should enhance the ability to monitor patients at risk for hypomagnesemia and improve our ability to mitigate the serious symptoms associated with this disorder.

Cited by 67 publications

References 31 publications

A variant in acis-regulatory element enhances claudin-14 expression and is associated with pediatric-onset hypercalciuria and kidney stones

A variant in acis-regulatory element enhances claudin-14 expression and is associated with pediatric-onset hypercalciuria and kidney stones

Micromotors for drug delivery in vivo: The road ahead

Calcium, Phosphate and Magnesium Disorders

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