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Background: A great majority of children with idiopathic nephrotic syndrome will relapse after successful treatment of the initial episode. The possibility that different steroid dosing regimens at onset, adjusted for risk factors, can reduce the rate of relapse represents an interesting option to investigate. Objectives: To evaluate the effect of the initial steroid regimen, adjusted for time to remission (TTR), on the frequency of relapses and steroid dependence, and to verify the influence of prognostic factors on disease course. Methods: A multicentre, prospective, cohort study. Children with nephrotic syndrome, with TTR ≤ 10 days (Group A), were given a 20-week prednisone regimen (2,828 mg/m2) and those with a TTR >10 days, a 22-week regimen (3,668 mg/m2) (Group B). Previously published retrospective data from the same centers were also evaluated. Main outcomes were: relapse rate, number of frequent relapsers + steroid dependent children and total prednisone dose after induction. Results: 143 children were enrolled. Rate of relapsed subjects (77 vs. 79%) and frequent relapsers + steroid dependent subjects (40 vs. 53%) did not differ between Groups A and B, or between the retrospective and prospective cohorts. The cumulative prednisone dose taken after the induction treatment was similar in both groups and in the retrospective and prospective cohorts. TTR was not associated with relapse risk. Age at onset and total serum protein were significantly lower in relapsing patients. At ROC analysis, the best cut-off was 5.3 years for age at onset and 4.2 g/dL for total serum protein. According to these cut-offs, older children with higher total serum protein had a higher relapse free survival rate (58%) than younger children with lower total serum protein (17%). Conclusions: TTR was not found to be a prognostic factor of relapse; because of this, different steroid regimens, adjusted for TTR, did not modify the relapse rate in any relevant measure. Conversely, younger age and low total serum protein were independent predictors of relapse risk, however this outcome was not modified by higher prednisone regimens. Clinical Trial Registration:https://www.ClinicalTrials.gov/, identifier: NCT01386957 (www.nefrokid.it).

PubMedID: 29481636 Background: We investigated the effects of nutritional vitamin D supplementation on markers of bone and mineral metabolism, i.e. serum levels of fibroblast growth factor 23(FGF23), Klotho, bone alkaline phosphatase (BAP) and sclerostin, in two cohorts with chronic kidney disease (CKD). Methods: In all, 80 vitamin D-deficient children were selected: 40 with mild to moderate CKD from the ERGO study, a randomized trial of ergocalciferol supplementation [estimated glomerular filtration rate (eGFR) 55 mL/min/1.73 m 2 ], and 40 with advanced CKD from the observational Cardiovascular Comorbidity in Children with Chronic Kidney Disease (4C) study (eGFR 24 mL/min/1.73 m 2 ). In each study, vitamin D supplementation was started in 20 children and 20 matched children not receiving vitamin D served as controls. Measures were taken at baseline and after a median period of 8 months. Age- and gender-related standard deviation scores (SDSs) were calculated. Results: Before vitamin D supplementation, children in the ERGO study had normal FGF23 (median 0.31 SDS) and BAP (-0.10 SDS) but decreased Klotho and sclerostin (-0.77 and - 1.04 SDS, respectively), whereas 4C patients had increased FGF23 (3.87 SDS), BAP (0.78 SDS) and sclerostin (0.76 SDS) but normal Klotho (-0.27 SDS) levels. Vitamin D supplementation further increased FGF23 in 4C but not in ERGO patients. Serum Klotho and sclerostin normalized with vitamin D supplementation in ERGO but remained unchanged in 4C patients. BAP levels were unchanged in all patients. In the total cohort, significant effects of vitamin D supplementation were noted for Klotho at eGFR 40-70mL/min/1.73m 2 . Conclusions: Vitamin D supplementation normalized Klotho and sclerostin in children with mild to moderate CKD but further increased FGF23 in advanced CKD. © The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. American Society of Pediatric Nephrology: ESPN 2014.3 This work was supported by the European Society for Pediatric Nephrology (reference number ESPN 2014.3), KfH Foundation for Preventive Medicine and ERA-EDTA (to D.H.).

Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of renal failure. For several decades, ADPKD was regarded as an adult-onset disease. In the past decade, it has become more widely appreciated that the disease course begins in childhood. However, evidence-based guidelines on how to manage and approach children diagnosed with or at risk of ADPKD are lacking. Also, scoring systems to stratify patients into risk categories have been established only for adults. Overall, there are insufficient data on the clinical course during childhood. We therefore initiated the global ADPedKD project to establish a large international pediatric ADPKD cohort for deep characterization. Methods: Global ADPedKD is an international multicenter observational study focusing on childhood-diagnosed ADPKD. This collaborative project is based on interoperable Web-based databases, comprising 7 regional and independent but uniformly organized chapters, namely Africa, Asia, Australia, Europe, North America, South America, and the United Kingdom. In the database, a detailed basic data questionnaire, including genetics, is used in combination with data entry from follow-up visits, to provide both retrospective and prospective longitudinal data on clinical, radiologic, and laboratory findings, as well as therapeutic interventions. Discussion: The global ADPedKD initiative aims to characterize in detail the most extensive international pediatric ADPKD cohort reported to date, providing evidence for the development of unified diagnostic, follow-up, and treatment recommendations regarding modifiable disease factors. Moreover, this registry will serve as a platform for the development of clinical and/or biochemical markers predicting the risk of early and progressive disease. C1 [De Rechter, Stephanie; Mekahli, Djalila] Univ Hosp Leuven, Dept Pediat Nephrol, Herestr 49, B-3000 Leuven, Belgium. [De Rechter, Stephanie; Mekahli, Djalila] Katholieke Univ Leuven, Dept Dev & Regenerat, PKD Res Grp, Leuven, Belgium. [Bockenhauer, Detlef] UCL Ctr Nephrol, London, England. [Bockenhauer, Detlef] Great Ormond St Hosp NHS Fdn Trust, London, England. [Guay-Woodford, Lisa M.] Childrens Natl Hlth Syst, Ctr Translat Sci, Washington, DC USA. [Liu, Isaac] Natl Univ Hlth Syst, Khoo Teck Puat Natl Univ, Childrens Med Inst, Singapore, Singapore. [Mallett, Andrew J.] Royal Brisbane & Womens Hosp, Kidney Hlth Serv, Brisbane, Qld, Australia. [Mallett, Andrew J.] Royal Brisbane & Womens Hosp, Conjoint Renal Res Lab, Brisbane, Qld, Australia. [Mallett, Andrew J.] Univ Queensland, Fac Med, Brisbane, Qld, Australia. [Mallett, Andrew J.] Univ Queensland, Inst Mol Biosci, Brisbane, Qld, Australia. [Mallett, Andrew J.] KidGen Collaborat & Australian Genom Hlth Allianc, Melbourne, Vic, Australia. [Soliman, Neveen A.] Cairo Univ, Ctr Pediat Nephrol & Transplantat, Kasr Al Ainy Sch Med, Dept Pediat, Cairo, Egypt. [Sylvestre, Lucimary C.] Hosp Pequeno Principe, Curitiba, Parana, Brazil. [Schaefer, Franz] Heidelberg Univ, Ctr Pediat & Adolescent Med, Div Pediat Nephrol, Med Ctr, Heidelberg, Germany. [Liebau, Max C.] Univ Hosp Cologne, Dept Pediat, Cologne, Germany. [Liebau, Max C.] Univ Hosp Cologne, Ctr Mol Med, Cologne, Germany. [Adamczyk, P.; Bjanid, O.; Brylka, A.; Morawiec-Knysak, A.; Szczepanska, M.] Dept Pediat, Zabrze, Poland. [Akinci, N.] Sariyer SISLI Hamidiye Etfal Res & Educ Hosp, Istanbul, Turkey. [Alpay, H.; Cicek, N.; Gokce, I] Marmara Univ, Sch Med, Div Pediat Nephrol, Istanbul, Turkey. [Ardelean, C.; Chirita, A.; Gafencu, M.; Stroescu, R.] Timisoara Children Hosp, Timisoara, Romania. [Ayasreh, N.; Furlano, M.; Torra, R.] Fundacio Puigvert, Barcelona, Spain. [Aydin, Z.; Bayrakci, U. S.] Ankara Univ Hlth Sci, Child Hlth & Dis, Ankara, Turkey. [Bael, A.; Docx, M.; Segers, N.] Koningin Paola Kinderziekenhuis Antwerpen, Antwerp, Belgium. [Baudouin, V; Cambier, A.; Couderc, A.; Dossier, C.; Kwon, V] Hop Robert Debre, AP HP, Paris, France. [Bensman, A.; Biebuyck, A.; Boyer, O.; Charbit, M.; Heidet, L.; Krid, S.; Krug, P.; Salomon, R.] Pediat Nephrol Necker Hosp, Paris, France. [Bialkevich, H.; Kazyra, I] 2nd City Childrens Clin Hosp, Natl Ctr Pediat Nephrol & RRT, Minsk, BELARUS. [Caliskan, S.; Ozcan, S.; Saygili, S. K.] Istanbul Cerrahpasa Fac Med, Istanbul, Turkey. [Camelio, A.; Nobili, F.; Vieux, R.] CHU Besancon, Besancon, France. [Carbone, V; Diomeda, F.; Torres, D.] Pediat Nephrol Unit Bari, Bari, Italy. [Chiodini, B.] HUDERF, Brussels, Belgium. [Collard, L.] CHR La Citadelle, Liege, Belgium. [Conceicao, M.; Teixeira, A.] Ctr Hosp Porto, Ctr Materno Infantil Norte, Porto, Portugal. [Constantinescu, I; Lungu, A. C.; Marin, A.; Negru, I; Stroescu, R.] Fundeni Clin Inst, Bucharest, Romania. [Crapella, B.; Giani, M.; Mastrangelo, A.; Montini, G.] Fdn IRCCS Ca Granda, Pediat Nephrol Dialysis & Transplant Unit, Milan, Italy. [Cvetkovic, M.; Gojkovic, I] Univ Childrens Hosp, Belgrade, Serbia. [Dima, B.] Clin Europe Hop St Elisabeth, Brussels, Belgium. [Dolan, N.] Our Ladys Childrens Hosp, Dublin, Ireland. [Drozdz, D.; Miklaszewska, M.; Zachwieja, K.] Jagiellonian Univ, Med Coll Cracow, Pediat Nephrol & Hypertens, Krakow, Poland. [Drube, J.; Pape, L.] Hannover Med Sch, Hannover, Germany. [Dunand, O.; Leroy, V] Pediat Nephrol Unit St Denis, St Denis, Reunion, France. [Dusan, P.; Spasojevic, B.; Stabouli, S.] Aristotle Univ Thessaloniki, Dept Pediat, Thessaloniki, Greece. [Eid, L. A.] Dubai Hosp, Pediat Nephrol Dept, Dubai, U Arab Emirates. [Emma, F.; Massella, L.] Bambino Gesu Pediat Hosp, Rome, Italy. [Espino Hernandez, M.] Hosp Infantil 12 Octubre Madrid, Madrid, Spain. [Fila, M.; Hemery, F.; Morin, D.] CHU Arnaud Villeneuve, Montpellier, France. [Ghuysen, Ms] CHU Liege, Liege, Belgium. [Giordano, M.] Pediat Nephrol Unit, Bari, Italy. [Girisgen, I; Yuksel, S.] Pamukkale Univ, Med Fac, Dept Pediat Nephrol, Denizli, Turkey. [Godefroid, N.; Ranguelov, N.] Clin Univ St Luc, Brussels, Belgium. [Godron-Dubrasquet, A.; Harambat, J.; Ilanas, B.] Bordeaux Univ Childrens Hosp, Bordeaux, France. [Gonzalez, E.] Childrens Univ Hosp, Geneva, Switzerland. [Groothoff, J. W.] Emma Childrens Hosp, Amsterdam, Netherlands. [Guarino, S.; La Manna, A.; Marzuillo, P.] Univ Campania Luigi Vanvitelli, Caserta, Italy. [Guffens, A.] CHC Clin Esperence, Montegnee, Belgium. [Hansen, P.] CHU Tivoli, La Louviere, Belgium. [Haumann, S.] Univ Klinikum Koln, Cologne, Germany. [He, G.] Foshan Women & Children Hosp, Foshan, Peoples R China. [Helmy, R.] Cairo Univ, Kasr Al Ainy Sch Med, Cairo, Egypt. [Hooman, N.; Otoukesh, H.] Iran Univ Med Sci, Aliasghar Clin Res Dev Unit, Tehran, Iran. [Janssens, P.] Univ Hosp Brussels, Brussels, Belgium. [Karamaria, S.; Prytula, A.; Raes, A.; Snauwaert, E.; Vande Walle, J.] UZ Gent, Ghent, Belgium. [Koenig, J.] Univ Hosp Muenster, Munster, Germany. [Litwin, M.; Obrycki, L.] Childrens Mem Hlth Inst, Warsaw, Poland. [Lombet, J.] CHR Citadelle, Liege, Belgium. [Longo, G.; Murer, L.] Hosp Univ Padova, Pediat Nephrol Dialysis & Transplant Unit, Padua, Italy. [Mallawaarachchi, A.] Garvan Inst, Darlinghurst, NSW, Australia. [Mallawaarachchi, A.] Royal Prince Alfred Hosp, Camperdown, NSW, Australia. [Mallawaarachchi, A.; McCarthy, H.; Quinlan, C.] KidGen, Sydney, NSW, Australia. [McCarthy, H.] Childrens Hosp Westmead, Westmead, NSW, Australia. [McCarthy, H.] Sydney Childrens Hosp, Sydney, NSW, Australia. [Papizh, S.; Prikhodina, L.] Pirogov Russian Nat Res Med Uni, Res & Clin Inst Pediat, Moscow, Russia. [Parvex, P.; Wilhelm-Bals, A.] Childrens Univ Hosp Geneva, Geneva, Switzerland. [Pawlak-Bratkowska, M.; Szczepanik, E.; Tkaczyk, M.] Polish Mothers Mem Hosp, Res Inst, Lodz, Poland. [Quinlan, C.] RCH Melbourne, Melbourne, Vic, Australia. [Ranchin, B.] Hop Femme Mere Enfant, Bron, France. [Ronit, C.] Ctr Hosp Luxembourg, Clin Pediat, Luxembourg, Luxembourg. [Schaefer, S.; Wuehl, E.] Ctr Pediat & Adolescent, Div Pediat Nephrol, Heidelberg, Germany. [Schreuder, M.] Radboudumc Amalia Childrens Hosp, Nijmegen, Netherlands. [Schurmans, T.; Tram, N.] CHU Charleroi, Charleroi, Belgium. [Seeman, T.] Charles Univ Prague, Prague, Czech Republic. [Seeman, T.] Motol Univ Hosp, Prague, Czech Republic. [Sinha, M.] Evelina London Childrens Hosp, London, England. [Taranta-Janusz, K.] Dept Pediat & Nephrol, Bialystok, Poland. [Thumfart, J.] Berlin Charite Univ Med, Berlin, Germany. [Utsch, B.] Herford Hosp, Dept Paediat, Herford, Germany. [Yildirim, Z. Y.] Istanbul Univ, Fac Med, Pediat Nephrol Dept, Istanbul, Turkey.

Membranoproliferative GN (MPGN) was recently reclassified as alternative pathway complement–mediated C3 glomerulopathy (C3G) and immune complex–mediated membranoproliferative GN (IC-MPGN). However, genetic and acquired alternative pathway abnormalities are also observed in IC-MPGN. Here, we explored the presence of distinct disease entities characterized by specific pathophysiologic mechanisms. We performed unsupervised hierarchical clustering, a data-driven statistical approach, on histologic, genetic, and clinical data and data regarding serum/plasma complement parameters from 173 patients with C3G/IC-MPGN. This approach divided patients into four clusters, indicating the existence of four different pathogenetic patterns. Specifically, this analysis separated patients with fluid-phase complement activation (clusters 1–3) who had low serum C3 levels and a high prevalence of genetic and acquired alternative pathway abnormalities from patients with solid-phase complement activation (cluster 4) who had normal or mildly altered serum C3, late disease onset, and poor renal survival. In patients with fluid-phase complement activation, those in clusters 1 and 2 had massive activation of the alternative pathway, including activation of the terminal pathway, and the highest prevalence of subendothelial deposits, but those in cluster 2 had additional activation of the classic pathway and the highest prevalence of nephrotic syndrome at disease onset. Patients in cluster 3 had prevalent activation of C3 convertase and highly electron-dense intramembranous deposits. In addition, we provide a simple algorithm to assign patients with C3G/IC-MPGN to specific clusters. These distinct clusters may facilitate clarification of disease etiology, improve risk assessment for ESRD, and pave the way for personalized treatment.

PubMed ID: 29930161, Background Although pharmacotherapeutic proteinuria lowering was found to be nephroprotective in adults, the predictive value of early drug-induced proteinuria reduction for long-term renal survival in pediatric CKD is unknown. We analyzed data from the ESCAPE Trial for a potential association between initial antiproteinuric effect of standardized angiotensin-converting enzyme (ACE) inhibition and renal disease progression in children with CKD. Methods In total, 280 eligible children with CKD stages 2-4 (mean age 11.7 years old, median eGFR 46 ml/min per 1.73 m2, 71% congenital renal malformations) received a fixed dose of ramipril (6 mg/m2 per day) and were subsequently randomized to conventional or intensified BP control. We assessed initial proteinuria reduction from baseline to first measurement on ramipril (at 2.561.3 months). We used multivariable Cox modeling to estimate the association between initial proteinuria reduction and the risk of reaching a renal end point (50% eGFR decline or ESRD), which occurred in 80 patients during 5 years of observation. Results Ramipril therapy lowered proteinuria by a mean of 43.5% (95% confidence interval, 36.3% to 49.9%). Relative to proteinuria reduction,30%, 30%-60% and .60% reduction resulted in hazard ratios (95% confidence intervals) of 0.70 (0.40 to 1.22) and 0.42 (0.22 to 0.79), respectively. This association was independent of age, sex, CKD diagnosis, baseline eGFR, baseline proteinuria, initial BP, and concomitant BP reduction. Conclusions The early antiproteinuric effect of ACE inhibition is associated with long-term preservation of renal function in children with CKD. Proteinuria lowering should be considered an important target in the management of pediatric CKD. Copyright © 2018 by the American Society of Nephrology., Baxter Nederland Fifth Framework Programme: QLRT-2001-00908 Boehringer Ingelheim Stiftung Cancer Research Foundation European Commission American College of Endocrinology, The Effect of Strict Blood Pressure Control and ACE inhibition on the Progression of CRF in Pediatric Patients (ESCAPE) Trial was supported by grants from the Boehringer Ingelheim Stiftung, the European Commission (Fifth Framework Programme QLRT-2001-00908), the Kuratorium für Dialyse und Nierentransplantation e.V., Neu-Isenburg, and the Baxter Extramural Grant Program. Aventis Pharmaceuticals supplied ramipril and financed the Good Clinical Practice audit.

PubMed ID: 26069294, Angiotensin-converting enzyme inhibitors (ACEi) for renin-angiotensin-aldosterone system (RAAS) blockade are routinely used to slow CKD progression. However, Vitamin D may also promote renoprotection by suppressing renin transcription through cross-talk between RAAS and Vitamin D -fibroblast growth factor-23 (FGF-23)-Klotho pathways. To determine whether Vitamin D levels influence proteinuria and CKD progression in children, we performed a post hoc analysis of the Effect of Strict Blood Pressure Control and ACE Inhibition on Progression of CKD in Pediatric Patients (ESCAPE) cohort. In 167 children (median EGFR 51 ml/min per 1.73 m2), serum 25-hydroxyvitaminD(25(OH)D),FGF-23, andKlotho levelsweremeasuredatbaselineandafteramedian8months onACEi.Childrenwith lower 25(OH)D levels had higher urinary protein/creatinine ratios at baseline (P=0.03) and at follow-up (P=0.006). Levels of 25(OH)D and serum Vitamin D -binding protein were not associated, but 25(OH)D #50 nmol/L associated with higher diastolicBP(P=0.004).ACEi therapy alsoassociatedwith increasedKlotho levels (P

Background The optimal therapeutic regimen for managing childhood idiopathic nephrotic syndrome (INS) is still under debate. We have evaluated the choice of steroid regimen and of symptomatic treatment adopted by pediatricians and pediatric nephrologists in a large number of centers as the first step towards establishing a shared protocol Methods This was a multicenter, retrospective study. A total of 231 children (132 admitted to pediatric units) aged 6 months to

Aim. Despite its established utility in non-Hodgkin's lymphoma, not much is reported on FDG positron emission tomography (PET) with respect to radioimmunotherapy (RIT). In this paper we investigate its value in patients affected by follicular lymphoma (FL) before and after treatment with [Y-90]Ibritumomab Tiuxetan (Zevalin (R)). Methods. We evaluated 38 relapsed or refractory FL patients. All had a PET scan performed before and 3 months after radioimmunotherapy. Final assessment was done 9 months post-RIT, including clinical evaluation, other imaging techniques and/or biopsy, when necessary. Results. At the first PET scan 20 patients out of 38 had a limited disease (nodal involvement on one side of the diaphragm: 7 above and 13 below), 11 patients had nodal findings on both sides of the diaphragm and the remaining 7 patients had both nodal and extra-nodal findings. At three months post-KIT, 21 patients (55%) were in complete remission, 13 patients (34%) had a partial response (PR) and four patients (11%) had a progression disease (PD). The corresponding rates at final assessment were all consistent with the 3-month evaluation: 55% CR, 13% PR and 32% PD. FDG PET scan revealed maximal predictive values. When comparing the disease extent at relapse and the response to treatment, we could testify a higher rate of CR (75%) in patients with limited disease, while in patients with diffused nodal and/or extra-nodal findings, it was more frequent a PR or PD (66%). Conclusion. Our data are concordant with the expected results on MT, and FDG PET is confirmed to be useful in assessing treatment response. Potential correlation can also be picked out between the disease extent at relapse and the CR rate, with reasonable PET predictivity for the final outcome.

Objective: 18F-FDG PET is of limited value for the assessment of lung neuroendocrine tumours (NET). Sixty-eight Ga-DOTA-NOC, has been reported to be useful for the assessment of gastro-entero-pancreatic NET expressing somatostatin receptors (SSR). To our knowledge, 68Ga-DOTA-NOC has never been studied in patients with lung NET. Aim of the study was to evaluate the role of 68Ga-DOTA-NOC PET for the evaluation of lung NET. Methods: Eleven patients (mean age: 62 years [44–80], M:F=6:5) with pathology proven lung NET were scheduled for 68Ga-DOTA-NOC PET. Indications to perform PET included staging (2), evaluation of equivocal conventional imaging findings (2) and follow-up after surgical excision of the primary tumour (7). PET results were compared with CT and with follow-up data. Results: PET showed at least one positive lesion in 7/11 cases and was negative in 4. Considering all lesions, the mean SUV max was 29.1 [range: 4.4–60.5]. 68Ga-DOTA-NOC PET was concordant with CT in 3/11. Of the remaining eight cases, PET identified a higher number of pathologic areas in 3/8 and excluded the malignant nature of suspicious CT findings in 4/11. In one case a suspicious liver lesion documented by CT and undetected on the PET scan was subsequently excised and immunohistochemistry showed the lack of SSR on tumour cells. Overall, PET provided additional information in 8/11 cases, changing the clinical management in 4/8 and contributing to better evaluate the extent of the disease in 4. Conclusions: Preliminary data show that 68Ga-DOTA-NOC is useful for evaluation of lung NET contributing to more accurate evaluation of disease.

OBJECTIVES. Febrile urinary tract infections are common in children and associated with the risk for renal scarring and long-term complications. Antimicrobial prophylaxis has been used to reduce the risk for recurrence. We performed a study to determine whether no prophylaxis is similar to antimicrobial prophylaxis for 12 months in reducing the recurrence of febrile urinary tract infections in children after a first febrile urinary tract infection.METHODS. The study was a controlled, randomized, open-label, 2-armed, noninferiority trial comparing no prophylaxis with prophylaxis (co-trimoxazole 15 mg/kg per day or co-amoxiclav 15 mg/kg per day) for 12 months. A total of 338 children who were aged 2 months to RESULTS. Intention-to-treat analysis showed no significant differences in the primary outcome between no prophylaxis and prophylaxis: 12 (9.45%) of 127 vs 15 (7.11%) of 211. In the subgroup of children with reflux, the recurrence of febrile urinary tract infections was 9 (19.6%) of 46 on no prophylaxis and 10 (12.1%) of 82 on prophylaxis. No significant difference was found in the secondary outcome: 2 (1.9%) of 108 on no prophylaxis versus 2 (1.1%) of 187 on prophylaxis. Bivariate analysis and Cox proportional hazard model showed that grade III reflux was a risk factor for recurrent febrile urinary tract infections. Whereas increasing age was protective, use of no prophylaxis was not a risk factor.CONCLUSIONS. For children with or without primary nonsevere reflux, prophylaxis does not reduce the rate of recurrent febrile urinary tract infections after the first episode.

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