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10.1097/MOP.0000000000000450

http://scihub22266oqcxt.onion/10.1097/MOP.0000000000000450
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C5572672!5572672!27906866
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suck abstract from ncbi


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pmid27906866      Curr+Opin+Pediatr 2017 ; 29 (2): 187-98
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  • Inherited and Acquired Disorders of Magnesium Homeostasis #MMPMID27906866
  • Wolf MTF
  • Curr Opin Pediatr 2017[Apr]; 29 (2): 187-98 PMID27906866show ga
  • Purpose of review: Magnesium (Mg2+) imbalances are frequently overlooked. Hypermagnesemia usually occurs in preeclamptic women after Mg2+ therapy or in end-stage renal disease patients, while hypomagnesemia is more common with a prevalence of up to 15% in the general population. Increasing evidence points towards a role for mild to moderate, chronic hypomagnesemia in the pathogenesis of hypertension, type 2 diabetes mellitus, and metabolic syndrome. Recent findings: The kidneys are the major regulator of total body Mg2+ homeostasis. Over the last decade the identification of the responsible genes in rare genetic disorders has enhanced our understanding of how the kidney handles Mg2+. The different genetic disorders and medications contributing to abnormal Mg2+ homeostasis are reviewed. Summary: As dysfunctional Mg2+ homeostasis contributes to the development of many common human disorders, serum Mg2+ deserves closer monitoring. Hypomagnesemic patients may be asymptomatic or may have mild symptoms. In severe hypomagnesemia patients may present with neurological symptoms such as seizures, spasms or cramps. Renal symptoms include nephrocalcinosis and impaired renal function. Most conditions affect tubular Mg2+ reabsorption by disturbing the lumen-positive potential in the thick ascending limb or the negative membrane potential in the distal convoluted tubule.
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