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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2014  |  Volume : 25  |  Issue : 5  |  Page : 1093-1094
Remarks about the study on idiopathic urolithiasis in Tunisian children

Department of Pediatrics, Al-Kindy College of Medicine, Baghdad University, Baghdad, Iraq

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Date of Web Publication2-Sep-2014

How to cite this article:
Al-Mendalawi MD. Remarks about the study on idiopathic urolithiasis in Tunisian children. Saudi J Kidney Dis Transpl 2014;25:1093-4

How to cite this URL:
Al-Mendalawi MD. Remarks about the study on idiopathic urolithiasis in Tunisian children. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2021 Dec 3];25:1093-4. Available from: https://www.sjkdt.org/text.asp?2014/25/5/1093/139954
To the Editor,

With reference to the interesting study by Alaya et al, [1] I have two comments.

First, apart from hypercalciuria (Hcal) (28.3%), Alaya et al [1] did not address the exact fre­quency distribution of other altered urinary constituents in their studied cohort although they mentioned in the methodology that urinary constituents of oxalate, uric acid and citrate were considered.

Second, Alaya et al [1] stated that Hcal (28.3%) was the dominant risk factor in their studied cohort with urolithiasis (UL). I presume that that finding must be taken cautiously. It is well known that citrate is a weak acid synthesized inside Krebs' cycle. It is a powerful inhibitor of the crystallization of calcium salts. The acid pH (systemic, tubular and intracellular) is the main determinant of citrate excretion in the urine. The protective role of citrate is linked to several mechanisms; citrate reduces urinary supersaturation of calcium salts by forming soluble complexes with calcium ions and by inhibiting crystal growth and aggregation. Furthermore, citrate increases the activity of some macromolecules in the urine like Tamm-Horsfall protein that inhibits calcium oxalate aggregation. [2] Hypocitraturia (Hcit) is a com­mon laboratory finding in patients with UL. Over the recent years, increasing preponde­rance of Hcit has been reported worldwide, questioning the shift in the dominant urinary constituent's derangement from Hcal to Hcit in children with UL. [3],[4],[5],[6],[7],[8] Nutritional, environmental and genetic factors cannot be excluded behind that shift. I presume that such a shift has also occurred in Tunisian stone-forming children. It is partially supported by the observation in Alaya et al's study [1] that 24-h urinary citrate assays were only performed in 20 (14.9%) subjects of 134, and revealed Hcit in 15 cases (75%). Failure to precisely demonstrate that shift by Alaya et al [1] might be related to the following three points:

  1. Variation in the size of the studied cohort undergoing urinary metabolic assay where urinary citrate was estimated in only 20 children of 134 children while urinary cal­cium was estimated in all the children studied (n = 134).
  2. Obesity can increase the risk of stone for­mation and its recurrence rate where Hcit is a common presenting metabolic abnor­mality among these obese patients (54%). [9] Because the prevalence of obesity among Tunisian children is substantial (11.6%), [10] I presume that the confounding effect of obesity on urinary constituents' excretion needs to be considered by Alaya et al. [1] They did not address clearly whether their studied cohort included obese children.
  3. Variation in the sensitivity and specificity of the method of urinary citrate estimation, whether it is the enzymatic method using citrate lyase or liquid chromatography tandem mass spectrometry, as Alaya et al [1] did not mention their method of urinary citrate assay.

Finally, I presume that documenting the shift in the altered excretion of urinary constituents toward predominance of Hcit through large-scale studies is of utmost importance to help explain the pathogenesis of stone formation on one hand and to implement a causative pro­phylaxis in Tunisian children with UL on the other hand.

Conflict of Interest: None.

Author's Reply

Reply from the authors is awaited.

   References Top

1.Alaya A, Sakly R, Nouri A, Najjar MF, Belgith M, Jouini R. Idiopathic urolithiasis in Tunisian children: A report of 134 cases. Saudi J Kidney Dis Transpl 2013;24:1055-61.  Back to cited text no. 1
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2.Caudarella R, Vescini F. Urinary citrate and renal stone disease: The preventive role of alkali citrate treatment. Arch Ital Urol Androl 2009;81:182-7.  Back to cited text no. 2
3.Rizvi SA, Sultan S, Zafar MN, et al. Evaluation of children with urolithiasis. Indian J Urol 2007;23:420-7.  Back to cited text no. 3
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4.Karabacak OR, Ipek B, Ozturk U, Demirel F, Saltas H, Altug U. Metabolic evaluation in stone disease metabolic differences between the pediatric and adult patients with stone disease. Urology 2010;76:238-41.  Back to cited text no. 4
5.Sepahi MA, Heidari A, Shajari A. Clinical manifestations and etiology of renal stones in children less than 14 years age. Saudi J Kidney Dis Transpl 2010;21:181-4.  Back to cited text no. 5
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6.Gürgöze MK, Sarý MY. Results of medical treat­ment and metabolic risk factors in children with urolithiasis. Pediatr Nephrol 2011;26:933-7.  Back to cited text no. 6
7.Sas DJ. An update on the changing epide­miology and metabolic risk factors in pediatric kidney stone disease. Clin J Am Soc Nephrol 2011;6:2062-8.  Back to cited text no. 7
8.Kovacevic L, Wolfe-Christensen C, Edwards L, Sadaps M, Lakshmanan Y. From hypercal-ciuria to hypocitraturia: A shifting trend in pediatric urolithiasis? J Urol 2012;188(4 Suppl): 1623-7.  Back to cited text no. 8
9.Ekeruo WO, Tan YH, Young MD, et al. Meta­bolic risk factors and the impact of medical therapy on the management of nephrolithiasis in obese patients. J Urol 2004;172:159-63.  Back to cited text no. 9
10.Abdelkafi Koubaa A, Younes K, Gabsi Z, et al. Risk factors of children overweight and obesity. Tunis Med 2012;90:387-93.  Back to cited text no. 10

Correspondence Address:
Prof. Mahmood Dhahir Al-Mendalawi
Department of Pediatrics, Al-Kindy College of Medicine, Baghdad University, Baghdad
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DOI: 10.4103/1319-2442.139954

PMID: 25193920

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