ArticlePediatric nephrology (Berlin, Germany)2008
A genome search for primary vesicoureteral reflux shows further evidence for genetic heterogeneity.
Article in Pediatric nephrology (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Whole exome sequencing identifies KIF26B, LIFR and LAMC1 mutations in familial vesicoureteral reflux.PloS one · 2022Article
- A genome-wide scan to locate regions associated with familial vesicoureteral reflux.Experimental and therapeutic medicine · 2022Article
- DNA copy number variations in children with vesicoureteral reflux and urinary tract infections.PloS one · 2019Article
- Genome-wide linkage and association study implicates the 10q26 region as a major genetic contributor to primary nonsyndromic vesicoureteric reflux.Scientific reports · 2017Article
- Genetic etiology of renal agenesis: fine mapping of Renag1 and identification of Kit as the candidate functional gene.PloS one · 2015Article
- Vesicoureteric reflux and reflux nephropathy: from mouse models to childhood disease.Pediatric nephrology (Berlin, Germany) · 2014Review
- A new genome scan for primary nonsyndromic vesicoureteric reflux emphasizes high genetic heterogeneity and shows linkage and association with various genes already implicated in urinary tract development.Molecular genetics & genomic medicine · 2014Article
- A single-center cohort of Canadian children with VUR reveals renal phenotypes important for genetic studies.Pediatric nephrology (Berlin, Germany) · 2013Article
- Chromosome 18q-syndrome and 1p terminal duplication in a patient with bilateral vesico-ureteral reflux: case report and literature revision.Italian journal of pediatrics · 2013Review
- Genes in the ureteric budding pathway: association study on vesico-ureteral reflux patients.PloS one · 2012Article
- Vesico-ureteric reflux: using mouse models to understand a common congenital urinary tract defect.Pediatric nephrology (Berlin, Germany) · 2011Article
- Genetics of vesicoureteral reflux.Nature reviews. Urology · 2011Review
- Genetics of innate immunity and UTI susceptibility.Nature reviews. Urology · 2011Review
- A genome scan in affected sib-pairs with familial vesicoureteral reflux identifies a locus on chromosome 5.European journal of human genetics : EJHG · 2010Article
- Whole-genome linkage and association scan in primary, nonsyndromic vesicoureteric reflux.Journal of the American Society of Nephrology : JASN · 2010Article
- Mutations in the ROBO2 and SLIT2 genes are rare causes of familial vesico-ureteral reflux.Pediatric nephrology (Berlin, Germany) · 2009Article
- A recessive gene for primary vesicoureteral reflux maps to chromosome 12p11-q13.Journal of the American Society of Nephrology : JASN · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vesicoureteral reflux (VUR) is the most common disease of the urinary tract in children. In order to identify gene(s) involved in this complex disorder, we performed a genome-wide search in a selected sample of 31 patients with primary VUR from eight families originating from southern Italy. Sixteen additional families with 41 patients were included in a second stage. Nonparametric, affected-only linkage analysis identified four genomic areas on chromosomes 1, 3, and 4 (p < 0.05); the best result corresponded to the D3S3681-D3S1569 interval on chromosome 3 (nonparametric linkage score, NPL = 2.75, p = 0.008). This region was then saturated with 26 additional markers, tested in the complete group of 72 patients from 24 families (NPL = 2.01, p = 0.01). We identified a genomic area on 3q22.2-23, where 26 patients from six multiplex families shared overlapping haplotypes. However, we did not find evidence for a common ancestral haplotype. The region on chromosome 1 was delimited to 1p36.2-34.3 (D1S228-D1S255, max. NPL = 1.70, p = 0.03), after additional fine typing. Furthermore, on chromosome 22q11.22-12.3, patients from a single family showed excess allele sharing (NPL = 3.35, p = 0.015). Only the chromosome 3q region has been previously reported in the single genome-wide screening available for primary VUR. Our results suggest the presence of several novel loci for primary VUR, giving further evidence for the genetic heterogeneity of this disorder.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.