Literature DB >> 6277190

Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects.

F L Coe, M J Favus, T Crockett, A L Strauss, J H Parks, A Porat, C L Gantt, L M Sherwood.   

Abstract

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally. SErum 1,25(OH)2D3 levels were the same in patients and normal subjects, even though PTH levels of the patients were below those of he normal subjects. Urine magnesium excretion and phosphorus excretion were both increased in the patients who excreted calcium in excess of intake. Our findings suggest that renal and absorptive hypercalciuria may not be distinct entities but rather the two extremes of a continuum of behavior. A uniform elevation of intestinal calcium absorption and a variable defect of renal calcium reabsorption could explain our results far better than the hypothesis of distinct absorptive and renal forms of hypercalciuria.

Entities:  

Mesh:

Substances:

Year:  1982        PMID: 6277190     DOI: 10.1016/0002-9343(82)90567-8

Source DB:  PubMed          Journal:  Am J Med        ISSN: 0002-9343            Impact factor:   4.965


  48 in total

1.  What is the value of distinguishing pathophysiological subgroups and what is the appropriate duration of specific therapy in children with significant hypercalciuria?

Authors:  F B Stapleton
Journal:  Pediatr Nephrol       Date:  1990-01       Impact factor: 3.714

Review 2.  Environmental factors in the pathophysiology of recurrent idiopathic calcium urolithiasis (RCU), with emphasis on nutrition.

Authors:  P O Schwille; U Herrmann
Journal:  Urol Res       Date:  1992

3.  Nephrolithiasis and nephrocalcinosis in rats with small bowel resection.

Authors:  R Corey O'Connor; Elaine M Worcester; Andrew P Evan; Shane Meehan; Dimitri Kuznetsov; Brett Laven; Andre' J Sommer; Sharon B Bledsoe; Joan H Parks; Fredric L Coe; Marc Grynpas; Glenn S Gerber
Journal:  Urol Res       Date:  2005-05

Review 4.  Nephrolithiasis.

Authors:  Elaine M Worcester; Fredric L Coe
Journal:  Prim Care       Date:  2008-06       Impact factor: 2.907

5.  Involvement of low-calcium diet in the reduced bone mineral content of idiopathic renal stone formers.

Authors:  M Fuss; T Pepersack; J Van Geel; J Corvilain; J C Vandewalle; P Bergmann; J Simon
Journal:  Calcif Tissue Int       Date:  1990-01       Impact factor: 4.333

Review 6.  Bone disease in pediatric idiopathic hypercalciuria.

Authors:  Maria Goretti Moreira Guimarães Penido; Marcelo de Sousa Tavares
Journal:  World J Nephrol       Date:  2012-04-06

7.  Expression of fibroblast growth factor 23, vitamin D receptor, and sclerostin in bone tissue from hypercalciuric stone formers.

Authors:  Viviane Barcellos Menon; Rosa Maria Affonso Moysés; Samirah Abreu Gomes; Aluizio Barbosa de Carvalho; Vanda Jorgetti; Ita Pfeferman Heilberg
Journal:  Clin J Am Soc Nephrol       Date:  2014-04-24       Impact factor: 8.237

Review 8.  Bone mineral content in calcium renal stone formers.

Authors:  A Trinchieri
Journal:  Urol Res       Date:  2005-08-03

9.  The relation between bone and stone formation.

Authors:  Nancy S Krieger; David A Bushinsky
Journal:  Calcif Tissue Int       Date:  2012-12-18       Impact factor: 4.333

10.  Heritability of urinary traits that contribute to nephrolithiasis.

Authors:  John C Lieske; Stephen T Turner; Samuel N Edeh; Jennifer A Smith; Sharon L R Kardia
Journal:  Clin J Am Soc Nephrol       Date:  2014-02-27       Impact factor: 8.237

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.