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      Aetiological Factors in Paediatric Urolithiasis

      Nephron Clinical Practice

      S. Karger AG

      Urolithiasis, aetiology, Calculi, paediatric, Metabolic evaluation

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          Abstract

          The aetiology of stones in children differs from that in adults. Young children, especially boys, are prone to infective stones, although this type of calculi is decreasing in frequency over time in prosperous countries. Two monogenic causes, cystinuria and hyperoxaluria, each account for 5–15% of paediatric stones. Increased factors for stone formation in children include prematurity, neurological problems, ketogenic diet and reconstructed or augmented bladders. Hypercalciuria is commonly found in paediatric stone formers, is usually idiopathic and is only rarely associated with hypercalcaemia. All children with stones should undergo a metabolic evaluation.

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          Most cited references 19

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          Absence of Oxalobacter formigenes in cystic fibrosis patients: a risk factor for hyperoxaluria.

          Patients with cystic fibrosis have an increased risk of hyperoxaluria, and of subsequent nephrocalcinosis and calcium-oxalate urolithiasis. Oxalate homoeostasis is controlled, in part, by the intestinal bacterium, Oxalobacter formigenes. The loss of this bacterium from the gut flora is associated with an increased risk of hyperoxaluria and calcium-oxalate urolithiasis. We investigated whether the absence of O. formigenes and the presence of hyperoxaluria are correlated in cystic fibrosis (CF) patients. Stool specimens from 43 patients with CF aged 3-9 years and from 21 similarly aged healthy volunteers were examined for O. formigenes by culture and DNA analysis. At the same time, 24 h urine samples were collected and analysed for oxalate and other factors that promote or inhibit stone formation. 15 (71%) of 21 healthy volunteers but only seven (16%) of 43 CF patients were colonised with O. formigenes. Detection of O. formigenes in six of these seven patients required DNA-based identification, suggesting low numbers of colony-forming units, and the CF patient with normal numbers of O. formigenes was the only one of the 43 patients who had not been treated with antibiotics. All seven CF patients colonised with O. formigenes had normal urinary oxalate levels, but 19 (53%) of 36 patients not colonised with O. formigenes were hyperoxaluric, with the most severe hyperoxaluria occurring in young patients. Absence of O. formigenes from the intestinal tract of CF patients appears to lead to increased absorption of oxalate, thereby increasing the risk of hyperoxaluria and its complications (eg, nephrocalcinosis, urolithiasis). Prolonged widespread use of antibiotics, and alterations of the gastrointestinal tract that occur in CF, may induce a permanent decolonisation in CF patients.
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            Clinical outcome of pediatric stone disease.

            The natural history of stone disease in children is not well defined. We evaluated the clinical outcome in children with urinary calculi. An 8-year retrospective review of 129 pediatric patients with primary urinary lithiasis was performed. Age, renal versus ureteral stone location, stone size, spontaneous passage, recurrence and metabolic evaluation were considered. Patients were divided into groups 1-0 to 5, 2-6 to 10 and 3-11 to 18 years old. Of the 25 group 1 patients 17 (68%) had renal and 8 (32%) had ureteral stones. Of the 36 group 2 patients 13 (36%) had renal and 23 (64%) had ureteral stones. Of the 68 group 3 patients 12 (18%) had renal and 56 (82%) had ureteral stones. These differences in stone location according to age were not due to chance (p <0.0001). In groups 1 to 3 renal calculi an average of 6.7, 9.2 and 6.8 mm. spontaneously passed in 24%, 8% and 50% of cases, while ureteral calculi an average of 4.5, 3.5 and 3.2 mm. passed in 63%, 61% and 64%, respectively. The spontaneous passage rate of ureteral stones was consistent in the 3 age groups and for stone size up to 5 mm. Only 1 stone greater than 5 mm. passed spontaneously at any age. The incidence of identifiable metabolic abnormalities believed responsible for stone disease was 50% in groups 1 and 2, and 38% in group 3. In all age groups there was symptomatic and/or radiographic stone recurrence in a third of the patients with an identifiable metabolic abnormality, such as hypercalciuria, hypocitruria, renal tubular acidosis and so forth. In children 10 years or younger this incidence increased to 50%. Less than 10% of those with no identifiable metabolic disorder have had recurrent stones to date. Younger patients are more likely to present with renal calculi and less likely to pass these stones, probably due to the relatively larger stone burden and location. The passage rate for ureteral calculi is surprisingly consistent in all age groups with stones greater than 5 mm. rarely passing spontaneously. Half of the children 10 years or younger who present with urinary calculi have an identifiable metabolic disorder. Thus, all children with stones should undergo metabolic evaluation. In addition, these children are nearly 5-fold more likely to have recurrent stones than those with no identifiable metabolic disorder. Thus, they should be followed aggressively.
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              Cystinuria subtype and the risk of nephrolithiasis.

               I Saadi,  P Goodyer,  G Elkas (1998)
              Cystinuria patients may be classified into several subgroups based on the urinary phenotype of heterozygotes. However, the relative risk for nephrolithiasis and the prevalence of SLC3A1 mutations in these subgroups are unknown. Urinary cystine excretion, age at onset of nephrolithiasis and nature of SLC3A1 mutations were assessed prospectively in 23 cystinuria patients identified primarily through the Quebec Newborn Screening Program. Probands were classified as to cystinuria subtype on the basis of parental urinary cystine excretion. For classical Type I/I cystinuria, both parents excrete cystine in the normal range and probands carry two mutations of the SLC3A1 gene in nearly every case. Between ages 1 to 7 years, mean cystine excretion was high (4566 +/- 480 microns cystine/g creatinine) and exceeded the theoretic threshold for solubility on 70% of visits. Four of eight Type I/I patients began forming stones in the first decade. Type I/III patients (N = 12) excreted less cystine (1544 +/- 163 mumol cystine/g creatinine), exceeded the threshold of urinary cystine solubility less frequently (22% of visits) and had no nephrolithiasis in the first decade; one formed a stone at age 16 years. Only one SLC3A1 mutation was identified in this group. Two Type II/N cystinuria children were identified. In these families, the same level of relatively high excretion (> 600 mumol cystine/g creatinine) was noted in two or three generations, but no SLC3A1 mutations were identified. Classical recessive Type I/I cystinuria is genetically and phenotypically distinct from the other subtypes (Type I/III and Type II/N) identified in our population.
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                Author and article information

                Journal
                NEC
                Nephron Clin Pract
                10.1159/issn.1660-2110
                Nephron Clinical Practice
                S. Karger AG
                978-3-8055-7852-3
                978-3-318-06156-7
                1660-2110
                2004
                October 2004
                17 November 2004
                : 98
                : 2
                : c45-c48
                Affiliations
                NephroUrology Unit, Great Ormond Street Hospital for Children, London, UK
                Article
                80251 Nephron Clin Pract 2004;98:c45–c48
                10.1159/000080251
                15499205
                © 2004 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 1, References: 25, Pages: 1
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                Self URI (application/pdf): https://www.karger.com/Article/Pdf/80251
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