Linked Life Data

10592935

Source:http://linkedlifedata.com/resource/pubmed/id/10592935

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1999-12-21
pubmed:abstractText
Recent progress in molecular genetics have improved our understanding of the pathophysiology of several inherited diseases characterized by a renal hypokalemia. Some of these diseases result from inactivating mutations on the main cotransports involved in the reabsorption of sodium, namely the Gitelman and Bartter syndromes, that clinically mimics diuretic abuse with mild hypovolemia and low or normal blood pressure. Conversely some affections eventually lead to an increase in sodium reabsorption with hypervolemia and arterial hypertension: Liddle syndrome, apparent mineralocorticoid excess and dexamethasone suppressible hyperaldosteronism.
pubmed:language
fre
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0250-4960
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
329-33
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
[Tubular hypokalemia of genetic origin].
pubmed:affiliation
Service de néphrologie, Hôpitaux universitaires de Strasbourg.
pubmed:publicationType
Journal Article, English Abstract, Review