Thiazide diuretics arrest the progression of nephrocalcinosis in children with X-linked hypophosphatemia.

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

OBJECTIVE: X-linked hypophosphatemia (XLH) is characterized clinically by rickets, hypophosphatemia, and hyperphosphaturia. Conventional treatment of XLH with oral phosphate and vitamin D is associated with increased urinary calcium excretion and nephrocalcinosis. Thiazide diuretics decrease urinary calcium excretion. The objective of this study was to determine the effect of thiazide diuretics on the clinical and radiologic course of nephrocalcinosis in children with XLH. METHODS: The effect of hydrochlorothiazide (HCTZ) on clinical and radiologic progression of nephrocalcinosis was evaluated in 11 children with XLH. All patients had been treated previously with vitamin D and oral phosphate and had radiologic evidence of nephrocalcinosis. The average age of the patients at the start of HCTZ was 6.6 +/- 1.0 years. The effect of oral HCTZ at 0.8 +/- 0.1 mg/kg body weight per day given for 3.3 +/- 0.6 years on the progression of nephrocalcinosis and urinary calcium excretion was evaluated. RESULTS: There was no change in serum phosphorous, calcium, potassium, and chloride after HCTZ therapy. HCTZ therapy increased serum bicarbonate and decreased urinary calcium excretion. The grade of nephrocalcinosis increased from 0.4 +/- 0.2 to 1.5 +/- 0.3 in the 2.3 +/- 0.3 years before initiation of HCTZ therapy, whereas the degree of nephrocalcinosis was stable after 3.3 +/- 0.6 years of HCTZ therapy (1.5 +/- 0.3 vs 3.0 +/- 0.3). CONCLUSION: HCTZ decreased urinary calcium excretion but did not result in the resolution of nephrocalcinosis. However, when compared with the control period, HCTZ prevented the progression of nephrocalcinosis in children with XLH.

Original languageEnglish (US)
JournalPediatrics
Volume108
Issue number1
StatePublished - Jul 2001

Fingerprint

Familial Hypophosphatemic Rickets
Nephrocalcinosis
Sodium Chloride Symporter Inhibitors
Hydrochlorothiazide
Calcium
Vitamin D
Phosphates
Familial Hypophosphatemia
Hypophosphatemia
Therapeutics
Calcium Chloride
Rickets
Potassium Chloride
Bicarbonates
Serum
Body Weight

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

@article{03444d78fa364b2eb504c0edced7c4f2,
title = "Thiazide diuretics arrest the progression of nephrocalcinosis in children with X-linked hypophosphatemia.",
abstract = "OBJECTIVE: X-linked hypophosphatemia (XLH) is characterized clinically by rickets, hypophosphatemia, and hyperphosphaturia. Conventional treatment of XLH with oral phosphate and vitamin D is associated with increased urinary calcium excretion and nephrocalcinosis. Thiazide diuretics decrease urinary calcium excretion. The objective of this study was to determine the effect of thiazide diuretics on the clinical and radiologic course of nephrocalcinosis in children with XLH. METHODS: The effect of hydrochlorothiazide (HCTZ) on clinical and radiologic progression of nephrocalcinosis was evaluated in 11 children with XLH. All patients had been treated previously with vitamin D and oral phosphate and had radiologic evidence of nephrocalcinosis. The average age of the patients at the start of HCTZ was 6.6 +/- 1.0 years. The effect of oral HCTZ at 0.8 +/- 0.1 mg/kg body weight per day given for 3.3 +/- 0.6 years on the progression of nephrocalcinosis and urinary calcium excretion was evaluated. RESULTS: There was no change in serum phosphorous, calcium, potassium, and chloride after HCTZ therapy. HCTZ therapy increased serum bicarbonate and decreased urinary calcium excretion. The grade of nephrocalcinosis increased from 0.4 +/- 0.2 to 1.5 +/- 0.3 in the 2.3 +/- 0.3 years before initiation of HCTZ therapy, whereas the degree of nephrocalcinosis was stable after 3.3 +/- 0.6 years of HCTZ therapy (1.5 +/- 0.3 vs 3.0 +/- 0.3). CONCLUSION: HCTZ decreased urinary calcium excretion but did not result in the resolution of nephrocalcinosis. However, when compared with the control period, HCTZ prevented the progression of nephrocalcinosis in children with XLH.",
author = "Seikaly, {M. G.} and M. Baum",
year = "2001",
month = "7",
language = "English (US)",
volume = "108",
journal = "Pediatrics",
issn = "0031-4005",
publisher = "American Academy of Pediatrics",
number = "1",

}

TY - JOUR

T1 - Thiazide diuretics arrest the progression of nephrocalcinosis in children with X-linked hypophosphatemia.

AU - Seikaly, M. G.

AU - Baum, M.

PY - 2001/7

Y1 - 2001/7

N2 - OBJECTIVE: X-linked hypophosphatemia (XLH) is characterized clinically by rickets, hypophosphatemia, and hyperphosphaturia. Conventional treatment of XLH with oral phosphate and vitamin D is associated with increased urinary calcium excretion and nephrocalcinosis. Thiazide diuretics decrease urinary calcium excretion. The objective of this study was to determine the effect of thiazide diuretics on the clinical and radiologic course of nephrocalcinosis in children with XLH. METHODS: The effect of hydrochlorothiazide (HCTZ) on clinical and radiologic progression of nephrocalcinosis was evaluated in 11 children with XLH. All patients had been treated previously with vitamin D and oral phosphate and had radiologic evidence of nephrocalcinosis. The average age of the patients at the start of HCTZ was 6.6 +/- 1.0 years. The effect of oral HCTZ at 0.8 +/- 0.1 mg/kg body weight per day given for 3.3 +/- 0.6 years on the progression of nephrocalcinosis and urinary calcium excretion was evaluated. RESULTS: There was no change in serum phosphorous, calcium, potassium, and chloride after HCTZ therapy. HCTZ therapy increased serum bicarbonate and decreased urinary calcium excretion. The grade of nephrocalcinosis increased from 0.4 +/- 0.2 to 1.5 +/- 0.3 in the 2.3 +/- 0.3 years before initiation of HCTZ therapy, whereas the degree of nephrocalcinosis was stable after 3.3 +/- 0.6 years of HCTZ therapy (1.5 +/- 0.3 vs 3.0 +/- 0.3). CONCLUSION: HCTZ decreased urinary calcium excretion but did not result in the resolution of nephrocalcinosis. However, when compared with the control period, HCTZ prevented the progression of nephrocalcinosis in children with XLH.

AB - OBJECTIVE: X-linked hypophosphatemia (XLH) is characterized clinically by rickets, hypophosphatemia, and hyperphosphaturia. Conventional treatment of XLH with oral phosphate and vitamin D is associated with increased urinary calcium excretion and nephrocalcinosis. Thiazide diuretics decrease urinary calcium excretion. The objective of this study was to determine the effect of thiazide diuretics on the clinical and radiologic course of nephrocalcinosis in children with XLH. METHODS: The effect of hydrochlorothiazide (HCTZ) on clinical and radiologic progression of nephrocalcinosis was evaluated in 11 children with XLH. All patients had been treated previously with vitamin D and oral phosphate and had radiologic evidence of nephrocalcinosis. The average age of the patients at the start of HCTZ was 6.6 +/- 1.0 years. The effect of oral HCTZ at 0.8 +/- 0.1 mg/kg body weight per day given for 3.3 +/- 0.6 years on the progression of nephrocalcinosis and urinary calcium excretion was evaluated. RESULTS: There was no change in serum phosphorous, calcium, potassium, and chloride after HCTZ therapy. HCTZ therapy increased serum bicarbonate and decreased urinary calcium excretion. The grade of nephrocalcinosis increased from 0.4 +/- 0.2 to 1.5 +/- 0.3 in the 2.3 +/- 0.3 years before initiation of HCTZ therapy, whereas the degree of nephrocalcinosis was stable after 3.3 +/- 0.6 years of HCTZ therapy (1.5 +/- 0.3 vs 3.0 +/- 0.3). CONCLUSION: HCTZ decreased urinary calcium excretion but did not result in the resolution of nephrocalcinosis. However, when compared with the control period, HCTZ prevented the progression of nephrocalcinosis in children with XLH.

UR - http://www.scopus.com/inward/record.url?scp=0035407041&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035407041&partnerID=8YFLogxK

M3 - Article

C2 - 11433085

AN - SCOPUS:0035407041

VL - 108

JO - Pediatrics

JF - Pediatrics

SN - 0031-4005

IS - 1

ER -