title: Phosphate homeostasis in Bartter syndrome: a case-control study.
abstract: BACKGROUND
  Bartter patients may be hypercalciuric. Additional abnormalities in the metabolism of calcium, phosphate, and calciotropic hormones have occasionally been reported.
  
  
  METHODS
  The metabolism of calcium, phosphate, and calciotropic hormones was investigated in 15 patients with Bartter syndrome and 15 healthy subjects.
  
  
  RESULTS
  Compared to the controls, Bartter patients had significantly reduced plasma phosphate {mean [interquartile range]:1.29 [1.16-1.46] vs. 1.61 [1.54-1.67] mmol/L} and maximal tubular phosphate reabsorption (1.16 [1.00-1.35] vs. 1.41 [1.37-1.47] mmol/L) and significantly increased parathyroid hormone (PTH) level (6.1 [4.5-7.7] vs. 2.8 [2.2-4.4] pmol/L). However, patients and controls did not differ in blood calcium, 25-hydroxyvitamin D, alkaline phosphatase, and osteocalcin levels. In patients, an inverse correlation (P < 0.05) was noted between total plasma calcium or glomerular filtration rate and PTH concentration. A positive correlation was also noted between PTH and osteocalcin concentrations (P < 0.005), as well as between chloriduria or natriuria and phosphaturia (P < 0.001). No correlation was noted between calciuria and PTH concentration or between urinary or circulating phosphate and PTH.
  
  
  CONCLUSIONS
  The results of this study demonstrate a tendency towards renal phosphate wasting and elevated circulating PTH levels in Bartter patients.
authors.affiliation: Division of Pediatrics, San Leopoldo Mandic Hospital, Merate, Lecco, Italy.
authors.forename: Alberto
authors.initials: A
authors.lastname: Bettinelli
authors.forename: Cristina
authors.initials: C
authors.lastname: Viganò
authors.forename: Maria Cristina
authors.initials: MC
authors.lastname: Provero
authors.forename: Francesco
authors.initials: F
authors.lastname: Barretta
authors.forename: Alessandra
authors.initials: A
authors.lastname: Albisetti
authors.forename: Silvana
authors.initials: S
authors.lastname: Tedeschi
authors.forename: Barbara
authors.initials: B
authors.lastname: Scicchitano
authors.forename: Mario G
authors.initials: MG
authors.lastname: Bianchetti
mesh_terms: D000293:Adolescent; D001477:Bartter Syndrome / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D002118:Calcium / Q000097:blood / Q000378:metabolism; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D018118:Chloride Channels / Q000235:genetics; D005260:Female; D005919:Glomerular Filtration Rate; D006706:Homeostasis; D006728:Hormones / Q000378:metabolism; D006801:Humans; D008297:Male; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000378:metabolism*; D064466:Solute Carrier Family 12, Member 1 / Q000235:genetics
chemical_list: C412733:CLCNKB protein, human; D018118:Chloride Channels; D006728:Hormones; D010281:Parathyroid Hormone; D010710:Phosphates; C578714:SLC12A1 protein, human; D064466:Solute Carrier Family 12, Member 1; D015675:Osteocalcin; D002118:Calcium