Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2003-6-23
pubmed:abstractText
Hypercalciuria is the most common risk factor for kidney stones and has a recognized familial component. The genetic hypercalciuric stone-forming (GHS) rat is an animal model that closely resembles human idiopathic hypercalciuria, with excessive intestinal calcium absorption, increased bone resorption, and impaired renal calcium reabsorption; overexpression of the vitamin D receptor (VDR) in target tissues; and calcium nephrolithiasis. For identifying genetic loci that contribute to hypercalciuria in the GHS rat, an F2 generation of 156 rats bred from GHS female rats and normocalciuric WKY male rats was studied. The calcium excretion was six- to eightfold higher in the GHS female than in the WKY male progenitors. Selective genotyping of those F2 rats with the highest 30% and lowest 30% rates of calcium excretion was performed, scoring 98 markers with a mean interval of 23 cM across all 20 autosomes and the X chromosome. With the use of strict criteria for significance, significant linkage was found between hypercalciuria and a region of chromosome 1 at D1Rat169 (LOD, 2.91). Suggestive linkage to regions of chromosomes 4, 7, 10, and 14 was found. The proportion of phenotypic variance contributed by the region on chromosome 1, with appropriate adjustments, was estimated to be 7%. Candidate genes encoding the VDR and the calcium-sensing receptor were localized to regions on rat chromosomes 7 and 11, respectively, but the suggestive quantitative trait locus on chromosome 7 was not in the region of the VDR gene locus. Identification of genes that contribute to hypercalciuria in this animal model should prove valuable in understanding idiopathic hypercalciuria and kidney stone disease in humans.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1844-50
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:12819244-Animals, pubmed-meshheading:12819244-Calcium, pubmed-meshheading:12819244-Calcium Metabolism Disorders, pubmed-meshheading:12819244-Chromosome Mapping, pubmed-meshheading:12819244-Crosses, Genetic, pubmed-meshheading:12819244-Disease Models, Animal, pubmed-meshheading:12819244-Female, pubmed-meshheading:12819244-Genetic Linkage, pubmed-meshheading:12819244-Genetic Markers, pubmed-meshheading:12819244-Genotype, pubmed-meshheading:12819244-Kidney Calculi, pubmed-meshheading:12819244-Male, pubmed-meshheading:12819244-Models, Genetic, pubmed-meshheading:12819244-Phenotype, pubmed-meshheading:12819244-Quantitative Trait Loci, pubmed-meshheading:12819244-Rats, pubmed-meshheading:12819244-Rats, Inbred F344, pubmed-meshheading:12819244-Rats, Inbred WKY, pubmed-meshheading:12819244-Risk Factors
pubmed:year
2003
pubmed:articleTitle
Quantitative trait loci for hypercalciuria in a rat model of kidney stone disease.
pubmed:affiliation
Department of Medicine, State University of New York Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't