LETTER TO THE EDITORS Does thiazide treatment improve bone mineral density in hypercalciuric children? Maria Goretti Moreira Guimarães Penido & Marcelo de Sousa Tavares Received: 7 February 2012 / Accepted: 1 March 2012 / Published online: 13 April 2012 # IPNA 2012 Dear Sir, We read with great interest the article entitled “Effect of thiazides on bone mineral density in children with idiopathic hypercalciuria” by Garcia Nieto et al. published in the February 2012 issue of Pediatric Nephrology [1]. In this article, the authors analyzed 22 children aged 11.7± 2.7 years diagnosed with idiopathic hypercalciuria (IH) and osteopenia who had received thiazides for 2.4 years and compared these children with 32 IH children with osteopenia of the same age who had not received thiazide treatment. Based on the results of this comparison, the authors concluded that thiazide treatment does not improve the bone density (BMD) z-score in children with IH. Initial recommendations for the treatment of pediatric patients with IH consist of lifestyle changes and adequate diet. Children rarely comply with the initial dietary recom- mendations or with prescribed physical exercise regimens. They commonly require potassium citrate supplementation or pharmacotherapy to reduce calciuria. However, antical- ciuric therapy in children is not based on strong clinical evidence, although in hypercalciuric osteopenic adults, thi- azide diuretics have been described to be effective in simul- taneously reversing hypercalciuria and improving reduced BMD [2]. We describe here our experience with pediatric IH treat- ment at our institution. Over the years we have followed 91 pediatric hypercalciuric patients (54 % boys) aged 10.5± 3.5 years for a median time of 6.0 (range 4.5–8.3) years. The initial approach consisted of dietary modifications for 4 months: high fluid intake, normal dietary calcium and protein according to the recommended daily allowance, sodium restriction (2.0–2.4 g/day) and potassium supple- mentation (3.0–3.5 g/day), with fruit and vegetables. In cases of no normalization of calcium excretion with these dietary measures, potassium citrate supplementation was initiated (0.5–1.0 mEq/kg/day), together with dietary measures for 2 months. Treatment with thiazides was initi- ated (0.5–1.0 mg/ kg/day) in association with potassium citrate if there was no improvement of calciuria levels after 2 months on alkali treatment and if the symptoms continued in the patient. Patients took potassium citrate alone or com- bined with thiazides for at least 1 year. Initial bone densi- tometry was performed when the patients started treatment with potassium citrate, and the final bone densitometry was conducted at the end of follow-up. Low bone density for chronologic age has been the terminology recommended for a BMD z-score of below -2.0. Twenty-seven patients took potassium citrate alone (Group 1, G1) and 64 received thiazides and potassium citrate (Group 2, G2). There were no differences in the BMI z-score, age and biochemical parameters between G1 and G2 before and after treatment. The BMD z-score of the lumbar spine (L1–L4) increased significantly after the treat- ment in G2 (from -0.9 to -0.7; p 0 0.04, Wilcoxon signed- rank test) and there was no improvement in G1 (from -0.5 to -0.4; p 0 0.16, Wilcoxon signed-rank test). Our results point to a beneficial effect of thiazides on BMD z-score in children with IH, in contrast to the findings of Garcia Nieto et al. We do believe that the best way to express bone mass is the BMD z-score, which is calculated in relation to a non- affected, age- and gender-matched control population and corrected for height. In addition, we suggest the use of the terminology low bone density for chronologic age for a BMD z-score below -2.0. M. G. Moreira Guimarães Penido (*) : M. de Sousa Tavares Pediatric Nephrology Unit, Clinics Hospital, School of Medicine, Federal University of Minas Gerais, Avenida Alfredo Balena, 190 Room 267, 30130-100 Santa Efigênia, Belo Horizonte, Brazil e-mail: mariagorettipenido@yahoo.com.br Pediatr Nephrol (2012) 27:1417–1418 DOI 10.1007/s00467-012-2159-z