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NDT Advance Access published online on February 25, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm952
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Renal magnification by EGF*

David H. Ellison

Division of Nephrology & Hypertension, Department of Medicine & Department of Physiology & Pharmacology & Heart Research Center, Oregon Health & Science University, and VA Medical Center Portland, OR 97239, USA

Correspondence and offprint requests to: David H. Ellison, Division of Nephrology and Hypertension, Oregon Health and Science University, 3314 SW US Veterans Hospital Road, Portland, OR 97239, USA. Fax: +1-503-494-5330; E-mail: ellisond@ohsu.edu

Keywords: epidermal growth factor; genetic disease; hypomagnesemia; magnesium

The first 10% of the full text of this article appears below.

A paper recently published by Groenestege and colleagues [8] used positional cloning to determine the cause of a rare inherited magnesium-wasting syndrome, autosomal recessive renal hypomagnesemia. The results showed that certain mutations in the epidermal growth factor (EGF) gene cause this disease. This suggests, perhaps surprisingly, that EGF and its receptor comprise a previously unrecognized signaling pathway in the human kidney that participates importantly in magnesium homeostasis. The EGF gene is highly expressed along the distal convoluted tubule (DCT), an important site for regulating urinary magnesium excretion. The product of the gene is a large membrane-bound molecule, expressed at both the apical and basolateral surfaces. A portion of the extracellular domain . . . [Full Text of this Article]



   Magnesium homeostasis in health and disease
 


   Magnesium reabsorption by the kidney
 


   Implications for clinical practice
 

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