Meta-analysis of the Risk Factors for Urinary Tract Infection in Children.

CONTEXT: The incidence of urinary tract infection (UTI) varies with age, but there is limited evidence on the role of other risk factors. OBJECTIVE: The aim of this meta-analysis was to investigate the risk factors for UTIs in children. DATA SOURCES: PubMed from 1966 to May 2019. STUDY SELECTION: All studies assessing at least 1 possible risk factor for occurrence or recurrence of UTI with a clear definition of symptomatic UTI in children were eligible. We excluded studies with UTIs related to hospital treatment or severe congenital renal abnormalities. DATA EXTRACTION: After the quality assessment we extracted data on the given risk factor in children with and without UTI. The data were extracted separately for the occurrence and recurrence of UTIs. RESULTS: We included 24 studies in the meta-analysis. Circumcision decreased the occurrence of UTIs with an odds ratio (OR) of 0.1 [95% confidence interval (CI): 0.06-0.17) and breast-feeding with an OR of 0.4 (CI: 0.19-0.86), both with low heterogeneity. Being overweight or obese increased the risk of UTI (OR: 2.23; CI: 1.37-3.63). Both poor fluid intake (OR: 6.39; CI: 3.07-13.39) and infrequent voiding (OR: 3.54; CI: 1.68-7.46) were associated with recurrent UTIs. LIMITATIONS: The design, populations and definitions varied between the studies. CONCLUSIONS: Being overweight or obese and having poor fluid intake are modifiable risk factors that increase the risk for UTIs in children. Breast-feeding and circumcision are associated with a decreased occurrence of UTIs.

Intestinal microbiome as a risk factor for urinary tract infections in children.

As urinary tract infection (UTI) pathogens originate from the gut, we hypothesized that the gut environment reflected by intestinal microbiome influences the risk of UTI. Our prospective case-control study compared the intestinal microbiomes of 37 children with a febrile UTI with those of 69 healthy children. We sequenced the regions of the bacterial 16S rRNA gene and used the LefSe algorithm to calculate the size of the linear discriminant analysis (LDA) effect. We measured fecal lactoferrin and iron concentrations and quantitative PCR for Escherichia coli. At the phylum level, there were no significant differences. At the genus level, Enterobacter was more abundant in UTI patients with an LDA score > 3 (log 10), while Peptostreptococcaceae were more abundant in healthy subjects with an LDA score > 3 (log 10). In total, 20 OTUs with significantly different abundances were observed. Previous use of antimicrobials did not associate with intestinal microbiome. The relative abundance of E. coli was 1.9% in UTI patients and 0.5% in controls (95% CI of the difference-0.8 to 3.6%). The mean concentration of E.coli in quantitative PCR was 0.14 ng/µl in the patients and 0.08 ng/µl in the controls (95% CI of the difference-0.04 to 0.16). Fecal iron and lactoferrin concentrations were similar between the groups. At the family and genus level, we noted several differences in the intestinal microbiome between children with UTI and healthy children, which may imply that the gut environment is linked with the risk of UTI in children.

Divergent effects of losartan and metoprolol on cardiac remodeling, c-kit+ cells, proliferation and apoptosis in the left ventricle after myocardial infarction.

There is strong evidence for the use of angiotensin converting enzyme inhibitors and beta-blockers to reduce morbidity and mortality in patients with myocardial infarction (MI), whereas the effect of angiotensin receptor blockers is less clear. We evaluated the effects of an angiotensin receptor blocker losartan and a beta-blocker metoprolol on left ventricular (LV) remodeling, c-kit+ cells, proliferation, fibrosis, apoptosis, and angiogenesis using a model of coronary ligation in rats. Metoprolol treatment for 2 weeks improved LV systolic function. In contrast, losartan triggered deleterious structural remodeling and functional deterioration of LV systolic function, ejection fraction being 41% and fractional shortening 47% lower in losartan group than in controls 2 weeks after MI. The number of c-kit+ cells as well as expression of Ki-67 was increased by metoprolol. Losartan-induced thinning of the anterior wall and ventricular dilation were associated with increased apoptosis and fibrosis, while losartan had no effect on the expression of c-kit or Ki-67. Metoprolol or losartan had no effect on microvessel density. These results demonstrate that beta-blocker treatment attenuated adverse remodeling via c-kit+ cells and proliferation, whereas angiotensin receptor blocker-induced worsening of LV systolic function was associated with increased apoptosis and fibrosis in the peri-infarct region.