Phosphate homeostasis in Bartter syndrome: a case–control study

• Published in: Pediatric nephrology (Berlin, West) Vol. 29; no. 11; pp. 2133 - 2138
• Main Authors: Bettinelli, Alberto, Viganò, Cristina, Provero, Maria Cristina, Barretta, Francesco, Albisetti, Alessandra, Tedeschi, Silvana, Scicchitano, Barbara, Bianchetti, Mario G.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.11.2014; Springer; Springer Nature B.V
• Subjects: Adolescent; Bartter Syndrome - genetics; Bartter Syndrome - metabolism; Bartter Syndrome - physiopathology; Blood pressure; Calcium - blood; Calcium - metabolism; Care and treatment; Case-Control Studies; Child; Child, Preschool; Chloride; Chloride Channels - genetics; Creatinine; Diagnosis; Female; Glomerular Filtration Rate; Health care; Homeostasis; Hormones; Hormones - metabolism; Humans; Hyperaldosteronism; Hypokalemia; Male; Medicine; Medicine & Public Health; Metabolism; Mutation; Nephrology; Original Article; Orthopedics; Osteocalcin - blood; Parathyroid hormone; Parathyroid Hormone - blood; Patient outcomes; Patients; Pediatrics; Phosphatase; Phosphates - metabolism; Potassium; Solute Carrier Family 12, Member 1 - genetics; Urology; United States; Italy; Switzerland; Bartter syndrome; Hypophosphatemia; Calcium; Parathyroid hormone; Maximal tubular reabsorption of phosphate
• ISSN: 0931-041X; 1432-198X; 1432-198X
• DOI: 10.1007/s00467-014-2846-z

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.