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Phosphate homeostasis in Bartter syndrome: a case-control study

Bettinelli, Alberto ; Viganò, Cristina ; Provero, Maria ; Barretta, Francesco ; Albisetti, Alessandra ; Tedeschi, Silvana ; Scicchitano, Barbara ; Bianchetti, Mario

In: Pediatric Nephrology, 2014, vol. 29, no. 11, p. 2133-2138

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    Title
    • Phosphate homeostasis in Bartter syndrome: a case-control study
    Author
    • Bettinelli, Alberto. Division of Pediatrics, San Leopoldo Mandic Hospital, Merate, Lecco, Italy
    • Viganò, Cristina. Division of Orthopedics, San Leopoldo Mandic Hospital, Merate, Lecco, Italy
    • Provero, Maria. Division of Pediatrics, San Leopoldo Mandic Hospital, Merate, Lecco, Italy
    • Barretta, Francesco. Department of Clinical Sciences and Community Health, University of Milan and Epidemiology Unit, Milan, Italy
    • Albisetti, Alessandra. Department of Clinical Orthopedics and Rehabilitation, University of Milan, Milan, Italy
    • Tedeschi, Silvana. Laboratory of Medical Genetics, Foundation IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
    • Scicchitano, Barbara. Division of Pediatrics, San Leopoldo Mandic Hospital, Merate, Lecco, Italy
    • Bianchetti, Mario. Integrated Department of Pediatrics, Ente Ospedaliero Cantonale Ticinese, University of Berne, Berne, Switzerland
    Document Type
    • Postprint
    OAI-PMH Identifier
    • oai:doc.rero.ch:325216
    Summary
    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.