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<title>Clinical Journal of the American Society of Nephrology Nephrolithiasis</title>
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<description>Clinical Journal of the American Society of Nephrology RSS feed -- recent Nephrolithiasis articles</description>
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<title>Clinical Journal of the American Society of Nephrology</title>
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<title><![CDATA[RANKL Is a Mediator of Bone Resorption in Idiopathic Hypercalciuria]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1446?rss=1</link>
<description><![CDATA[
<P>Background and objectives: This study aimed to determine the expression of osteoprotegerin, receptor activator of nuclear factor B ligand, interleukin-1, transforming growth factor-&beta;, and basic fibroblast growth factor in stone-forming patients with idiopathic hypercalciuria.</P>
<P>Design, setting, participants, &amp; measurements: Immunohistochemical analysis was performed in undecalcified bone samples previously obtained from 36 transiliac bone biopsies of patients who had idiopathic hypercalciuria and whose histomorphometry had shown lower bone volume, increased bone resorption, and prolonged mineralization lag time.</P>
<P>Results: Bone expression of receptor activator of nuclear factor B ligand and osteoprotegerin was significantly higher in patients with idiopathic hypercalciuria <I>versus</I> control subjects. Transforming growth factor-&beta; immunostaining was lower in patients with idiopathic hypercalciuria than in control subjects and correlated directly with mineralization surface. Interleukin-1 and basic fibroblast growth factor staining did not differ between groups. Receptor activator of nuclear factor B ligand bone expression was significantly higher in patients who had idiopathic hypercalciuria and exhibited higher <I>versus</I> normal bone resorption.</P>
<P>Conclusion: A higher expression of receptor activator of nuclear factor B ligand in bone tissue suggests that increased bone resorption in patients with idiopathic hypercalciuria is mediated by receptor activator of nuclear factor B ligand. Osteoprotegerin bone expression might have been secondarily increased in an attempt to counteract the actions of receptor activator of nuclear factor B ligand. The low bone expression of transforming growth factor-&beta; could contribute to the delayed mineralization found in such patients.</P>
]]></description>
<dc:creator><![CDATA[Gomes, S. A., dos Reis, L. M., Noronha, I. L., Jorgetti, V., Heilberg, I. P.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00240108</dc:identifier>
<dc:title><![CDATA[RANKL Is a Mediator of Bone Resorption in Idiopathic Hypercalciuria]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1452</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1446</prism:startingPage>
<prism:section>Nephrolithiasis</prism:section>
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<title><![CDATA[Determinants of 24-hour Urinary Oxalate Excretion]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1453?rss=1</link>
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<P>Background and objectives: Higher levels of urinary oxalate substantially increase the risk of calcium oxalate kidney stones. However, the determinants of urinary oxalate excretion are unclear. The objective was to examine the impact of dietary factors, age, body size, diabetes, and urinary factors on 24-h urinary oxalate.</P>
<P>Design, setting, participants, and measurements: We conducted a cross-sectional study of 3348 stone forming and non&ndash;stone-forming participants in the Health Professionals Follow-up Study (men), the Nurses&rsquo; Health Study (older women), and the Nurses&rsquo; Health Study II (younger women).</P>
<P>Results: Median urinary oxalate was 39 mg/d in men, 27 mg/d in older women, and 26 mg/d in younger women. Participants in the highest quartile of dietary oxalate excreted 1.7 mg/d more urinary oxalate than participants in the lowest quartile (<I>P</I> trend 0.001). The relation between dietary and urinary oxalate was similar in individuals with and without nephrolithiasis. Participants consuming 1000 mg/d or more of vitamin C excreted 6.8 mg/d more urinary oxalate than participants consuming &lt;90 mg/d (<I>P</I> trend &lt; 0.001). Body mass index, total fructose intake, and 24-h urinary potassium, magnesium, and phosphorus levels also were positively associated with urinary oxalate. Calcium intake and age were inversely associated with urinary oxalate. After adjustment for body size, participants with diabetes excreted 2.0 mg/d more urinary oxalate than those without diabetes (<I>P</I> &lt; 0.01).</P>
<P>Conclusions: The impact of dietary oxalate on urinary oxalate appears to be small. Further investigation of factors influencing urinary oxalate may lead to new approaches to prevent calcium kidney stones.</P>
]]></description>
<dc:creator><![CDATA[Taylor, E. N., Curhan, G. C.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01410308</dc:identifier>
<dc:title><![CDATA[Determinants of 24-hour Urinary Oxalate Excretion]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1460</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1453</prism:startingPage>
<prism:section>Nephrolithiasis</prism:section>
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