Az idiopathiás hypercalciuria gyermekkorban.

Translated title of the contribution: Idiopathic hypercalciuria in childhood

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

This review describes the supposed mechanisms leading to idiopathic hypercalciuria (IHU) in childhood, further the diagnostic criteria and the proposed treatment modalities are discussed. IHU is not only one of the main causes of renal stone disease in children but it's also at the origin of the postglomerular haematuria and the frequency-dysuria syndrome. Its role in the development of osteoporosis in adults is also documented. The diagnosis of raised calcium excretion is based on age specific values during early infancy. In older children and adults a urinary calcium/creatinine ratio exceeding 0.6 mmol/mmol is regarded as elevated. Dietary calcium restriction can no longer be recommended for the treatment of IHU because it results in secondary hyperoxaluria and on the long-term causes decreased bone mineral density. Patients should be kept on dietary sodium restriction and high fluid intake. In cases IHU associated with recurrent episodes of macroscopic haematuria or recurrent stone disease a therapeutic trial with hydrochlorothiazide in the dose of 0.5-1 mg/kg/day with potassium-citrate supplementation and possibly magnesium citrate should be started. In some special forms of hypercalciuria such as the X-linked recessive nephrolithiasis syndrome or Bartter syndrome the localization and in some cases even the molecular mechanism of the events leading to increased calcium excretion are elucidated. In IHU enhanced Ca(++)-ATPase, and Na-Li countertransport activity and decreased Na+/K+ ATPase activity were described in the erythrocyte membrane model. It is expected that with the molecular genetic development the clinical classification of the hypercalciuric syndromes will become a rational genome-based one.

Original languageHungarian
Pages (from-to)2957-2962
Number of pages6
JournalOrvosi Hetilap
Volume139
Issue number49
Publication statusPublished - Dec 6 1998

Fingerprint

Hypercalciuria
Hematuria
Calcium
Potassium Citrate
Bartter Syndrome
Hyperoxaluria
Dietary Sodium
Dysuria
Dietary Calcium
Nephrolithiasis
Hydrochlorothiazide
Erythrocyte Membrane
Bone Density
Osteoporosis
Molecular Biology
Creatinine
Therapeutics
Childhood idiopathic hypercalciuria
Genome
Kidney

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Az idiopathiás hypercalciuria gyermekkorban. / Reusz, G.

In: Orvosi Hetilap, Vol. 139, No. 49, 06.12.1998, p. 2957-2962.

Research output: Contribution to journalArticle

Reusz, G 1998, 'Az idiopathiás hypercalciuria gyermekkorban.', Orvosi Hetilap, vol. 139, no. 49, pp. 2957-2962.
Reusz, G. / Az idiopathiás hypercalciuria gyermekkorban. In: Orvosi Hetilap. 1998 ; Vol. 139, No. 49. pp. 2957-2962.
@article{73c13357f43e493b9f2c0314ad86a5a7,
title = "Az idiopathi{\'a}s hypercalciuria gyermekkorban.",
abstract = "This review describes the supposed mechanisms leading to idiopathic hypercalciuria (IHU) in childhood, further the diagnostic criteria and the proposed treatment modalities are discussed. IHU is not only one of the main causes of renal stone disease in children but it's also at the origin of the postglomerular haematuria and the frequency-dysuria syndrome. Its role in the development of osteoporosis in adults is also documented. The diagnosis of raised calcium excretion is based on age specific values during early infancy. In older children and adults a urinary calcium/creatinine ratio exceeding 0.6 mmol/mmol is regarded as elevated. Dietary calcium restriction can no longer be recommended for the treatment of IHU because it results in secondary hyperoxaluria and on the long-term causes decreased bone mineral density. Patients should be kept on dietary sodium restriction and high fluid intake. In cases IHU associated with recurrent episodes of macroscopic haematuria or recurrent stone disease a therapeutic trial with hydrochlorothiazide in the dose of 0.5-1 mg/kg/day with potassium-citrate supplementation and possibly magnesium citrate should be started. In some special forms of hypercalciuria such as the X-linked recessive nephrolithiasis syndrome or Bartter syndrome the localization and in some cases even the molecular mechanism of the events leading to increased calcium excretion are elucidated. In IHU enhanced Ca(++)-ATPase, and Na-Li countertransport activity and decreased Na+/K+ ATPase activity were described in the erythrocyte membrane model. It is expected that with the molecular genetic development the clinical classification of the hypercalciuric syndromes will become a rational genome-based one.",
author = "G. Reusz",
year = "1998",
month = "12",
day = "6",
language = "Hungarian",
volume = "139",
pages = "2957--2962",
journal = "Orvosi Hetilap",
issn = "0030-6002",
publisher = "Akademiai Kiado",
number = "49",

}

TY - JOUR

T1 - Az idiopathiás hypercalciuria gyermekkorban.

AU - Reusz, G.

PY - 1998/12/6

Y1 - 1998/12/6

N2 - This review describes the supposed mechanisms leading to idiopathic hypercalciuria (IHU) in childhood, further the diagnostic criteria and the proposed treatment modalities are discussed. IHU is not only one of the main causes of renal stone disease in children but it's also at the origin of the postglomerular haematuria and the frequency-dysuria syndrome. Its role in the development of osteoporosis in adults is also documented. The diagnosis of raised calcium excretion is based on age specific values during early infancy. In older children and adults a urinary calcium/creatinine ratio exceeding 0.6 mmol/mmol is regarded as elevated. Dietary calcium restriction can no longer be recommended for the treatment of IHU because it results in secondary hyperoxaluria and on the long-term causes decreased bone mineral density. Patients should be kept on dietary sodium restriction and high fluid intake. In cases IHU associated with recurrent episodes of macroscopic haematuria or recurrent stone disease a therapeutic trial with hydrochlorothiazide in the dose of 0.5-1 mg/kg/day with potassium-citrate supplementation and possibly magnesium citrate should be started. In some special forms of hypercalciuria such as the X-linked recessive nephrolithiasis syndrome or Bartter syndrome the localization and in some cases even the molecular mechanism of the events leading to increased calcium excretion are elucidated. In IHU enhanced Ca(++)-ATPase, and Na-Li countertransport activity and decreased Na+/K+ ATPase activity were described in the erythrocyte membrane model. It is expected that with the molecular genetic development the clinical classification of the hypercalciuric syndromes will become a rational genome-based one.

AB - This review describes the supposed mechanisms leading to idiopathic hypercalciuria (IHU) in childhood, further the diagnostic criteria and the proposed treatment modalities are discussed. IHU is not only one of the main causes of renal stone disease in children but it's also at the origin of the postglomerular haematuria and the frequency-dysuria syndrome. Its role in the development of osteoporosis in adults is also documented. The diagnosis of raised calcium excretion is based on age specific values during early infancy. In older children and adults a urinary calcium/creatinine ratio exceeding 0.6 mmol/mmol is regarded as elevated. Dietary calcium restriction can no longer be recommended for the treatment of IHU because it results in secondary hyperoxaluria and on the long-term causes decreased bone mineral density. Patients should be kept on dietary sodium restriction and high fluid intake. In cases IHU associated with recurrent episodes of macroscopic haematuria or recurrent stone disease a therapeutic trial with hydrochlorothiazide in the dose of 0.5-1 mg/kg/day with potassium-citrate supplementation and possibly magnesium citrate should be started. In some special forms of hypercalciuria such as the X-linked recessive nephrolithiasis syndrome or Bartter syndrome the localization and in some cases even the molecular mechanism of the events leading to increased calcium excretion are elucidated. In IHU enhanced Ca(++)-ATPase, and Na-Li countertransport activity and decreased Na+/K+ ATPase activity were described in the erythrocyte membrane model. It is expected that with the molecular genetic development the clinical classification of the hypercalciuric syndromes will become a rational genome-based one.

UR - http://www.scopus.com/inward/record.url?scp=0032491643&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032491643&partnerID=8YFLogxK

M3 - Article

C2 - 9879200

AN - SCOPUS:0032491643

VL - 139

SP - 2957

EP - 2962

JO - Orvosi Hetilap

JF - Orvosi Hetilap

SN - 0030-6002

IS - 49

ER -