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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-14240

Wagner, C A (2007). Metabolic acidosis: new insights from mouse models. Current Opinion in Nephrology and Hypertension, 16(5):471-476.

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Abstract

PURPOSE OF REVIEW: Metabolic acidosis is a severe disturbance of extracellular pH homeostasis that can be caused both by inborn or acquired defects in renal acid excretion or metabolic acid production. Chronic metabolic acidosis causes osteomalacia with nephrocalcinosis and urolithiasis. In the setting of end-stage renal disease, metabolic acidosis is often associated with increased peripheral insulin resistance, and represents an additional independent morbidity risk factor. This review summarizes recent insight, gained primarily from mouse models, into the mechanisms whereby the kidney regulates and adapts acid excretion. RECENT FINDINGS: Human genetics and various mouse models have shed new light on mechanisms that contribute to the kidney's ability to excrete acid and adapt appropriately to metabolism. Progress in four specific areas will be highlighted: mechanisms contributing to the synthesis and excretion of ammonia; insights into adaptive processes during acidosis; mechanisms by which the kidney may sense acidosis; and the pathophysiology of acquired and inborn errors of renal acid handling. SUMMARY: Genetic mouse models and various messenger RNA and proteome profiling and screening technologies demonstrate the importance of various acid-base transporting proteins and a metabolic and regulatory network that contributes to the kidney's ability to maintain the systemic acid-base balance.

Item Type:Journal Article, 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
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:September 2007
Deposited On:20 Mar 2009 12:20
Last Modified:27 Nov 2013 19:16
Publisher:Lippincott Wiliams & Wilkins
ISSN:1062-4821
Publisher DOI:10.1097/MNH.0b013e3282a4a69c
PubMed ID:17693764
Citations:Web of Science®. Times Cited: 12
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Scopus®. Citation Count: 17

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