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Literature DB >> 17464515

Pathophysiology of hypercalciuria in children.

Abstract

Urinary excretion of calcium is the result of a complex interplay between three organs-namely, the gastrointestinal tract, bone, and kidney-which is finely orchestrated by multiple hormones. Hypercalciuria is believed to be a polygenic trait and is influenced significantly by diet. This paper briefly reviews calcium handling by the renal tubule in normal and in hereditary disorders as it relates to the pathophysiology of hypercalciuria. The effects of dietary sodium, potassium, protein, calcium, and phosphate on calcium excretion, and the association of hypercalciuria with bone homeostasis is discussed, leading to recommendations on means to address excessive urinary calcium excretion.

Entities: Chemical Disease Gene Mutation Species

Mesh：

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Year: 2007 PMID： 17464515 PMCID： PMC6904412 DOI： 10.1007/s00467-007-0482-6

Source DB: PubMed Journal: Pediatr Nephrol ISSN： 0931-041X Impact factor: 3.714

139 in total

1. Hyperresponsiveness of vitamin D receptor gene expression to 1,25-dihydroxyvitamin D3. A new characteristic of genetic hypercalciuric stone-forming rats.

Authors: J Yao; P Kathpalia; D A Bushinsky; M J Favus
Journal: J Clin Invest Date: 1998-05-15 Impact factor: 14.808

2. "Idiopathic" hypercalciuria and hereditary hypophosphatemic rickets. Two phenotypical expressions of a common genetic defect.

Authors: M Tieder; D Modai; U Shaked; R Samuel; R Arie; A Halabe; J Maor; J Weissgarten; Z Averbukh; N Cohen
Journal: N Engl J Med Date: 1987-01-15 Impact factor: 91.245

Review 3. Threading through the mizmaze of Bartter syndrome.

Authors: Willem Proesmans
Journal: Pediatr Nephrol Date: 2006-05-16 Impact factor: 3.714

4. Increased serum 1,25-(OH)2-vitamin D concentrations fail to affect serum or urine phosphate in humans.

Authors: J Lemann; W J Maierhofer; N D Adams; R W Gray
Journal: Adv Exp Med Biol Date: 1982 Impact factor: 2.622

5. Increased sensitivity to 1,25(OH)2D3 in bone from genetic hypercalciuric rats.

Authors: N S Krieger; V M Stathopoulos; D A Bushinsky
Journal: Am J Physiol Date: 1996-07

6. Clinical presentation and natural course of idiopathic hypercalciuria in children.

Authors: C Polito; A La Manna; F Cioce; J Villani; B Nappi; R Di Toro
Journal: Pediatr Nephrol Date: 2000-12 Impact factor: 3.714

7. Bone alterations in children with idiopathic hypercalciuria at the time of diagnosis.

Authors: Maria-Goretti Moreira Guimarães Penido; Eleonora Moreira Lima; Viviane Santuari Parizotto Marino; Ana-Luiza Fialho Tupinambá; Anderson França; Marcelo Ferraz Oliveira Souto
Journal: Pediatr Nephrol Date: 2002-12-19 Impact factor: 3.714

8. Reduced bone mass in children with idiopathic hypercalciuria and in their asymptomatic mothers.

Authors: Michael Freundlich; Evelyn Alonzo; Ezequiel Bellorin-Font; Jose R Weisinger
Journal: Nephrol Dial Transplant Date: 2002-08 Impact factor: 5.992

Review 9. Calcium transport in the nephron.

Authors: W N Suki
Journal: Am J Physiol Date: 1979-07

9. Urinary excretion of calcium, magnesium, phosphate, citrate, oxalate, and uric acid by healthy schoolchildren using a 12-h collection protocol.

Authors: Concepción Sáez-Torres; Dolores Rodrigo; Félix Grases; Ana M García-Raja; Cristina Gómez; Javier Lumbreras; Guiem Frontera
Journal: Pediatr Nephrol Date: 2014-02-12 Impact factor: 3.714

Review 10. Medical treatment of pediatric urolithiasis.

Authors: Uri S Alon
Journal: Pediatr Nephrol Date: 2008-02-14 Impact factor: 3.714

Pathophysiology of hypercalciuria in children.

1. Hyperresponsiveness of vitamin D receptor gene expression to 1,25-dihydroxyvitamin D3. A new characteristic of genetic hypercalciuric stone-forming rats.

2. "Idiopathic" hypercalciuria and hereditary hypophosphatemic rickets. Two phenotypical expressions of a common genetic defect.

Review 3. Threading through the mizmaze of Bartter syndrome.

4. Increased serum 1,25-(OH)2-vitamin D concentrations fail to affect serum or urine phosphate in humans.

5. Increased sensitivity to 1,25(OH)2D3 in bone from genetic hypercalciuric rats.

6. Clinical presentation and natural course of idiopathic hypercalciuria in children.

7. Bone alterations in children with idiopathic hypercalciuria at the time of diagnosis.

8. Reduced bone mass in children with idiopathic hypercalciuria and in their asymptomatic mothers.

Review 9. Calcium transport in the nephron.

10. Disorders of the calcium-sensing receptor.

Review 1. Pediatric nephrolithiasis: a systematic approach from diagnosis to treatment.

2. Accentuated hyperparathyroidism in type II Bartter syndrome.

3. Pediatric primary urolithiasis: Symptoms, medical management and prevention strategies.

Review 4. Use of calcimimetics in children with normal kidney function.

Review 5. History, epidemiology and regional diversities of urolithiasis.

6. Spontaneous urinary calcium oxalate crystallization in hypercalciuric children.

Review 7. Current medical treatment in pediatric urolithiasis.

8. Risk factors for urinary stones in healthy schoolchildren with and without a family history of nephrolithiasis.

9. Urinary excretion of calcium, magnesium, phosphate, citrate, oxalate, and uric acid by healthy schoolchildren using a 12-h collection protocol.

Review 10. Medical treatment of pediatric urolithiasis.