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New roles for renal potassium channels


Wagner, C A (2010). New roles for renal potassium channels. Journal of Nephrology, 23(1):5-8.

Abstract

The role of the kidney in controlling and maintaining plasma potassium levels in the normal range requires the presence and activity of renal potassium channels, and their importance has been highlighted in patients with Bartter syndrome harboring mutations in the ROMK (Kir1.1, KCJN1) channel and hyperkalemia. However, the kidney expresses far more potassium channels than ROMK. Their functions are slowly emerging from studies in animal models and human rare inherited disorders that allow a better understanding of the plethora of functions that potassium channels fulfill in the kidney. Three recent studies shed light on the function of 2 members of the family of voltage-gated potassium channels. The group of René Bindels demonstrates that patients with isolated hypomagnesemia and inappropriately normal magnesuria carry mutations in the Kv1.1 (KCNA) potassium channel (Glaudemans B, et al. J Clin Invest. 2009;119:936-942). Two other studies elucidate a rather complex syndrome involving seizures, ataxia, deafness and renal salt loss, and show that mutations in the Kir4.1 (KCNJ10) potassium channel are responsible (Scholl UI, et al. Proc Natl Acad Sci U S A. 2009;106:5842-5847; Bockenhauer D, et al. N Engl J Med. 2009;360:1960-1970). This human disease is recapitulated by a mouse model deficient for the Kir4.1 channel presenting with similar symptoms. These studies together show that potassium channels in the kidney serve purposes far beyond controlling systemic potassium homeostasis, and are involved in various essential functions of the kidney. Moreover, defects of 2 different potassium channels expressed on opposing membrane domains of the same cells cause distinct symptoms.

The role of the kidney in controlling and maintaining plasma potassium levels in the normal range requires the presence and activity of renal potassium channels, and their importance has been highlighted in patients with Bartter syndrome harboring mutations in the ROMK (Kir1.1, KCJN1) channel and hyperkalemia. However, the kidney expresses far more potassium channels than ROMK. Their functions are slowly emerging from studies in animal models and human rare inherited disorders that allow a better understanding of the plethora of functions that potassium channels fulfill in the kidney. Three recent studies shed light on the function of 2 members of the family of voltage-gated potassium channels. The group of René Bindels demonstrates that patients with isolated hypomagnesemia and inappropriately normal magnesuria carry mutations in the Kv1.1 (KCNA) potassium channel (Glaudemans B, et al. J Clin Invest. 2009;119:936-942). Two other studies elucidate a rather complex syndrome involving seizures, ataxia, deafness and renal salt loss, and show that mutations in the Kir4.1 (KCNJ10) potassium channel are responsible (Scholl UI, et al. Proc Natl Acad Sci U S A. 2009;106:5842-5847; Bockenhauer D, et al. N Engl J Med. 2009;360:1960-1970). This human disease is recapitulated by a mouse model deficient for the Kir4.1 channel presenting with similar symptoms. These studies together show that potassium channels in the kidney serve purposes far beyond controlling systemic potassium homeostasis, and are involved in various essential functions of the kidney. Moreover, defects of 2 different potassium channels expressed on opposing membrane domains of the same cells cause distinct symptoms.

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Additional indexing

Item Type:Journal Article, not refereed, further contribution
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
Date:January 2010
Deposited On:19 Mar 2010 05:55
Last Modified:05 Apr 2016 13:59
Publisher:Wichtig Editore
ISSN:1121-8428
Free access at:Official URL. An embargo period may apply.
Official URL:http://www.jnephrol.com/public/JN/Article/Article.aspx?UidArticle=0DAD5010-25B2-45EC-A4FB-1B149461240F
PubMed ID:20091480
Permanent URL: http://doi.org/10.5167/uzh-31910

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