Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-8-7
pubmed:abstractText
Physiologic and biochemical studies have suggested that the inherited disorders cystinuria, Liddle's syndrome, and perhaps Bartter syndrome all result from defects in renal tubular transport processes. With the recent isolation of several candidate transporter genes, these clinically based hypotheses have begun to be confirmed at a molecular level. In addition, the cloning of the water-channel family of proteins has facilitated the characterization of a second gene defect in congenital nephrogenic diabetes insipidus. This review integrates the pathophysiology of these inherited renal tubular disorders with recent molecular genetic discoveries, and provides a starting point for unraveling their pathogenesis at the molecular level.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1062-4821
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
121-9
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Molecular insights into the pathogenesis of inherited renal tubular disorders.
pubmed:affiliation
Department of Medicine, University of Alabama at Birmingham, USA.
pubmed:publicationType
Journal Article, Review