24mo pre-GH Baseline Hydrochlorothiazide Hydrochlorothiazide + phosphate + K-citrate +calcitriol+rhGH 22.0-28.0 24 mo post-GH Hydrochlorothiazide + phosphate +K-citrate +calcitriol +rhGH 122 (before GH therapy) 300.5 - 496 (with GH therapy) > 2 GH peaks at night (nl > 20 mU/L) GH peaks with provocative stimuli (nl nd > 20 mU/L) IGF-1 (9 y: nl 123-275 ng/ml) (11 y: 139-395 ng/ml) (12 y: 143-693 ng/ml) Calcium (s) (nl 2.1-2.5 mmol/L) Phosphate (s) (nl 0.8-1.5 mmol/L) iPTH (nl 0.95-5.7 pmol/l) ALP (5-10 yr: 110-341 U/L) (Puberty: < 500) TRP (nl 85-98%) Creatinine clearance (nl 89-165 ml/min/1.73 m2) b2-microglobulin (nl < 0.03-0.37 mg/24 h) Protein excretion (nl < 0.150 g/24 h) Calcium excretion (nl < 4 mg/kg/24 h) nd 2.4 1.0 n.d 224.70 65-77 92.8 81.6 1.86 10.1 ALP: alkaline phosphatase; iPTH intact parathyroid hormone; nd: not determined; nl: normal level Samardzic et al. Journal of Medical Case Reports 2011, 5:400 http://www.jmedicalcasereports.com/content/5/1/400 Page 3 of 6 Table 1 Laboratory investigation before and after three years of combined conventional and GH replacement therapy nd nd 2.4 0.74 6.1 926.0 75 99.8 nd 3.21 10.9 12. 3 11 143.5 -1.4 78 1.18 +1.14 -1.58 nd nd 2.4 0.96 n.d 638 57 107 nd 2.1 8.9 36mo post-GH Hydrochlorothiazide + phosphate +K-citrate +calcitriol+rhGH nd 33 (2 mo without GH therapy) 90-125 (2 mo without GH therapy) 2.3 1-1.25 2.68 160-174 50-60 112.7 nd 2.0-3.0 6.7-7.2 global kidney functions. Sheffer-Babila et al. [13] studied the case of two brothers, 10 and 13 and a half years old, suffering from Dent’s disease and GH deficiency, with- out symptoms of rickets. At the time of setting the diag- nosis their growth retardation was -2.2 and -1.2 SD respectively. One brother had a diminished estimated glomerular filtration rate (GFR) (creatinine clearance: 68-83 ml/min/1.73 m2); the other had normal estimated Table 2 Anthropometric characteristics of rhGH-treated child with Dent’s disease Baseline 24 mo 36 mo post-GH post-GH Age (y) Bone age (y) Height (cm) Height (SDS) Sitting height (cm) Sitting height/Leg length BMI (SDS) Parental adjusted height (SDS) -3.08 BMI: body mass index; SDS: standard deviation score 24mo pre-GH 7.3 4 4/12 6 110.5 -2.89 59 1.16 +1,26 9. 3 120.0 -2.93 64 1.14 +1.02 -3.11 11. 3 9 138 -1.83 74 1.19 +1.16 -2.02 GFR (creatinine clearance: 101-143 ml/min/1.73 m2). These patients were treated with enalapril, hydrochlor- othiazide, calcitriol, phosphate supplements, vitamin E, vitamin C, potassium citrate and growth hormone. Two years after initiating GH therapy their growth velocity was 8 and 10 cm/yr respectively. In cases of short sta- ture of various origins but without GH deficiency, such as Turner syndrome or short children born small for gestational age (SGA), the treatment used is rhGH. Not all patients with Dent’s disease have GH deficiency, but reasons for treatment in our case were the presence of short stature and chronic renal disease [8]. In the first two years after starting our patient on GH and other therapies, the boy grew 9 cm/yr, and in the third year he grew 5.5 cm. His IGF-1 levels were below normal range before treatment and increased to normal levels after treatment. The acceleration in growth velocity could be attributed to the increased concentration of circulating IGF-1, the increase in efficiency of food utili- zation with rhGH, and the conventional therapy for hypophosphatemic rickets. Pharmacologic treatment of X-linked hypophosphatemia rickets leads to an improve- ment in the rickets, but effects on longitudinal growth