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Disorders of renal magnesium handling explain renal magnesium transport


Wagner, C A (2007). Disorders of renal magnesium handling explain renal magnesium transport. Journal of Nephrology, 20(5):507-510.

Abstract

Magnesium is essential for bone stability, neuronal excitability, muscular relaxation and many other metabolic functions. Despite its fundamental biological importance, mechanisms controlling systemic magnesium homeostasis are only partially understood. The kidney plays a central role in maintaining magnesium balance as evident from several rare inherited disorders of renal magnesium transport. Recent studies shed new light on molecular mechanisms of renal magnesium handling and its control. Mutations in the claudin 16 (paracellin) paracellular protein in the thick ascending limb (TAL) of Henle's loop and in the transient receptor potential cation channel, subfamily 6, member 6 (TRPM6) magnesium channel expressed in distal tubules found in patients with renal magnesium wasting and hypomagnesemia underscore the importance of these transport proteins. A study by Hou et al (J Biol Chem 2007; 282: 17114-22) demonstrates a pathomechanism for claudin 16 mutations that gives interesting insights into the function of the TAL. Moreover, Groenestege and colleagues report (J Clin Invest 2007; 117: 2260-7) the identification of the epidermal growth factor (EGF) as a hormonal regulator of TRPM6 activity, and thereby explain how mutations in EGF can cause familial hypomagnesemia. Interestingly, cetuximab, a drug used in treatment of certain cancers, acts an inhibitor of the EGF receptor and causes hypomagnesemia which may be due to the inhibition of EGF signaling.

Magnesium is essential for bone stability, neuronal excitability, muscular relaxation and many other metabolic functions. Despite its fundamental biological importance, mechanisms controlling systemic magnesium homeostasis are only partially understood. The kidney plays a central role in maintaining magnesium balance as evident from several rare inherited disorders of renal magnesium transport. Recent studies shed new light on molecular mechanisms of renal magnesium handling and its control. Mutations in the claudin 16 (paracellin) paracellular protein in the thick ascending limb (TAL) of Henle's loop and in the transient receptor potential cation channel, subfamily 6, member 6 (TRPM6) magnesium channel expressed in distal tubules found in patients with renal magnesium wasting and hypomagnesemia underscore the importance of these transport proteins. A study by Hou et al (J Biol Chem 2007; 282: 17114-22) demonstrates a pathomechanism for claudin 16 mutations that gives interesting insights into the function of the TAL. Moreover, Groenestege and colleagues report (J Clin Invest 2007; 117: 2260-7) the identification of the epidermal growth factor (EGF) as a hormonal regulator of TRPM6 activity, and thereby explain how mutations in EGF can cause familial hypomagnesemia. Interestingly, cetuximab, a drug used in treatment of certain cancers, acts an inhibitor of the EGF receptor and causes hypomagnesemia which may be due to the inhibition of EGF signaling.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:October 2007
Deposited On:23 Mar 2009 15:33
Last Modified:05 Apr 2016 13:02
Publisher:Wichtig Editore
ISSN:1121-8428
Official URL:http://www.jnephrol.com/public/JN/Article/Articleabstract.aspx?UidArticle=5EC6B0EB-C5DB-496B-A75C-18BD1C276881&t=JN
Related URLs:http://www.jnephrol.com/public/JN/default.aspx (Publisher)
PubMed ID:17918133
Permanent URL: http://doi.org/10.5167/uzh-14222

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