Samardzic et al. Journal of Medical Case Reports 2011, 5:400 http://www.jmedicalcasereports.com/content/5/1/400 The growth of our patient was improved and propor- tional to his pubertal state. Since the therapy was started before the patient reached puberty it is not possible to estimate how the GH therapy will continue to affect our patient’s final height. However after two years of ther- apy, growth started to slow down. Although a correlation was found between renal func- tion and growth impairment, significant short stature was seen at all levels of renal function. The etiology of growth delay in children with chronic kidney disease is multifactorial, including rickets, GH resistance, reduced GH secretion rate or greater loss of GH, functional IGF deficiency and increased IGFBP -1,-2,-4 and -6 [16]. The aim of therapy in Dent’s disease and hypopho- sphatemic rickets is to normalize serum alkaline phos- phatase and achieve longitudinal growth. Conventional treatment with oral phosphate and calcitriol can heal rickets, but it does not always raise serum phosphate concentrations significantly, nor does it always normal- ize linear growth [12]. Both endogenous and exogenous GH result in an increase in GFR. It is likely that the increased GFR is mediated by IGF-1 [17]. It is of concern that long-term rhGH treatment could produce hyperfiltration with resultant glomerulosclerosis and an accelerated decline in renal function [18]. In our patient’s case, GFR, mea- sured as creatinine clearance at the beginning and at the end of monitoring, remained normal, but it increased from 92.8 to 112.7 ml/min/1.73 m2. We were also con- cerned that rhGH might induce hypercalciuria during calcitriol treatment, however calcium excretion did not change significantly. Conclusion Effects of GH therapy in children with Dent’s disease and short stature are positive, but it is difficult to reach conclusions because of the small sample size in the lit- erature, the short duration of the therapy and the lack of a control group. Thus, further studies are needed to determinate the pathophysiological mechanism of rhGH action in Dent’s disease. Consent Written informed consent was obtained from the patient’s mother for publication of this case report and any accompanying images. A copy of the written con- sent is available for review by the Editor-in-Chief of this journal. Abbreviations GH: gGrowth hormone; GRF: glomerular filtration rate; IGF-1: insulin-like growth factor 1; IGFBP-3: insulin-like growth factor binding protein-3; SD: standard deviation; TRP: tubular reabsorption of phosphate; rhGH: recombinant human growth hormone. Page 5 of 6 Acknowledgements This study was assessed and approved by the institutional review board and the letter of approval is available for examination. Author details 1Institute for Sick Children, Department of Endocrinology and Nephrology, Ljubljanska bb, 20 000 Podgorica, Montenegro. 2Department of Clinical Chemistry and Clinical Pharmacology, University of Bonn, Bonn, Germany. 3Institute for Mother and Child Health Care of Serbia, Department of Nephrology, Radoja Dakica 10, 11 000 Belgrade, Serbia. Authors’ contributions MS analyzed and interpreted the patient data regarding the endocrinological follow- up and was a major contributor in writing the manuscript. SP and RB performed nephrology management and consulted in the case. ML performed the molecular genetic analysis. All authors read and approved the final manuscript. Competing interests The authors declare that they have no competing interests. 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