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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1993-3-18
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pubmed:abstractText |
A fundamental mechanism for hypercalciuria in genetic hypercalciuric rats appears due to a primary increase in intestinal calcium absorption. However previous studies could not exclude additional mechanisms to account for the hypercalciuria. To determine if enhanced bone mineral dissolution either as a primary abnormality or secondary to a defect in renal tubule calcium reabsorption is responsible for a component of the augmented calcium excretion we studied rats continually inbred for hypercalciuria. Nineteenth generation adult female idiopathic hypercalciuric (IH) and non-inbred control (Ctl) rats were fed 13 g/day of a normal calcium diet (0.6% calcium, NCD) for 10 days. Urine calcium excretion over the last seven days was greater in IH (34 +/- 2 mg/7 day) than in Ctl (2.9 +/- 0.3, P < 0.01) rats. Some rats in each group were continued on the same diet while others were fed a low calcium diet (0.02% calcium, LCD) for an additional 10 days; balance measurements were made over the final seven days. With LCD, urine calcium excretion was approximately 8-fold higher in IH compared to Ctl (13 +/- 2 mg/7 day vs. 1.6 +/- 0.1, IH vs. Ctl, respectively, P < 0.01). In IH rats percent calcium absorption was greater (59 +/- 3% vs. 45 +/- 3, IH vs. Ctl, P < 0.01), however calcium retention was negative (-1.9 +/- 2.0 mg/7 day vs. 6.5 +/- 0.5, IH vs. Ctl, P < 0.01) compared to Ctl rats. The fall in urine calcium excretion when IH rats are fed LCD indicates that enhanced intestinal calcium absorption is a primary mechanism of the hypercalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcitriol,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium, Dietary,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphorus,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0085-2538
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
189-96
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8433558-Animals,
pubmed-meshheading:8433558-Calcitriol,
pubmed-meshheading:8433558-Calcium,
pubmed-meshheading:8433558-Calcium, Dietary,
pubmed-meshheading:8433558-Female,
pubmed-meshheading:8433558-Intestinal Absorption,
pubmed-meshheading:8433558-Male,
pubmed-meshheading:8433558-Phosphorus,
pubmed-meshheading:8433558-Potassium,
pubmed-meshheading:8433558-Rats,
pubmed-meshheading:8433558-Rats, Sprague-Dawley,
pubmed-meshheading:8433558-Sodium
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pubmed:year |
1993
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pubmed:articleTitle |
Response of genetic hypercalciuric rats to a low calcium diet.
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pubmed:affiliation |
Nephrology Unit, University of Rochester, New York.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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