Disease relevance of VUR

• Primary vesicoureteric reflux (VUR) affects 1%-2% of whites, and reflux nephropathy (RN) causes up to 15% of end-stage renal failure in children and adults [1].
• Recently, VUR was observed as part of a syndrome, involving optic nerve colobomas and renal anomalies, caused by mutations of the PAX2 gene [2].
• Although renal-coloboma syndrome involves both ocular and renal anomalies, some patients are affected with vesico-ureteral reflux (VUR), high frequency hearing loss, central nervous system (CNS) anomalies, and/or genital anomalies, consistent with the expression of PAX2 in these tissues during development [3].
• Forty-eight children with unilateral primary VUR diagnosed after the first pyelonephritis were enrolled [4].
• We found no association between ACE I/D polymorphism and presence of hypertension, proteinuria, grade of VUR, or unilateral/bilateral VUR [5].

Psychiatry related information on VUR

• The patients were children with VUR or normal genitourinary anatomy who presented with UTI or dysfunctional voiding and children screened for genitourinary problems such as hematuria, sibling reflux or bedwetting [6].
• Although vesicoureteric reflux (VUR) is observed more commonly in infants than children with UTI, it is rare in uninfected patients at any age and should never be considered a normal finding during human development [7].
• MATERIALS AND METHODS: We reviewed the records of 32 consecutive children with complicated enuresis who were referred for neurosurgical evaluation, including those with a history of refractory voiding dysfunction or incontinence associated with persistent vesicoureteral reflux, encopresis, or associated leg or back pain [8].
• This includes improved evaluation of renal vasculature and parenchyma, assessment of vesicoureteral reflux in children, assessment of tubal patency in women, and evaluation of prostate diseases and erectile dysfunction in men [9].
• Here we report on a boy with mild mental retardation, lobar HPE, epilepsy, mild pyramidal syndrome of the legs, ventricular septal defect, vesicoureteral reflux, preaxial polydactyly, and facial dysmorphisms [10].

High impact information on VUR

• Mutation of the gene in a family with optic nerve colobomas, renal anomolies and vesicoureteral reflux [11].
• Mutation of the PAX2 gene in a family with optic nerve colobomas, renal anomalies and vesicoureteral reflux [12].
• Among 36 girls with recurrent pyelonephritis who did not have vesicoureteral reflux, we found that attaching bacteria were common and the P1 blood-group phenotype was present in 97 per cent, as compared with 75 per cent of 84 age-matched children without urinary-tract infection (P less than 0.01) [13].
• To define factors related to renal prognosis in children with vesicoureteral reflux and renal insufficiency, we reviewed 908 children with vesicoureteral reflux [14].
• Vesicoureteral reflux in children with uremia. Prognostic indicators for treatment and survival [14].

Chemical compound and disease context of VUR

• OBJECTIVES: Dextranomer/hyaluronic acid (Dx/HA) copolymer has favorable properties for endoscopic treatment of vesico-ureteral reflux (VUR) [15].
• Thirty-three point two percent of the patients with acute pyelonephritis, confirmed by 99mTc dimercaptosuccinic acid (DMSA) renal scan, had VUR [16].
• We report a case of vesicoureteral reflux (VUR) 3 years after intravesical instillation of bacillus Calmette-Guérin (BCG, Tokyo 172 strain) against carcinoma in situ of the bladder [17].
• At diagnosis hydronephrosis and vesicoureteral reflux were present in 40 and 33% of the patients, respectively, while serum creatinine was elevated in 35% and end stage renal disease had developed in 10% [18].
• PURPOSE: We evaluated the long-term efficacy of subureteral glutaraldehyde cross-linked collagen injection (GAX 35) for endoscopic treatment of vesicoureteral reflux in patients with neurogenic bladder dysfunction due to meningomyelocele [19].

Biological context of VUR

• The TGF-beta1 gene polymorphism was determined, and we found significant over-representation of the TT genotype in primary VUR patients with CRI compared with normal renal function (P= 0.0035) [20].
• Significantly higher K allele frequency was present in primary VUR with CRI children, as it was in the renal survival curve study [20].
• Hence, VUR maps to a locus on chromosome 1 [1].
• The VUR phenotype is associated with shortness of the submucosal segment of the ureter due to congenital lateral ectopia of the ureteric orifice [21].
• Single strand conformational polymorphism (SSCP) analysis of 23 affected subjects in eight families with primary familial VUR showed no alterations in exons 2-5 of the PAX2 gene [2].

Anatomical context of VUR

• VUR is found in 30-50% of infants and young children with a urinary tract infection [21].
• Catheterized urine cultures were obtained annually, but bacteriuria ( > 10,000 colony-forming units of a single organism per milliliter) was treated only if the patients had symptoms or if vesicoureteral reflux (VUR) was present [22].
• In 10 patients reflux appeared in the postoperative period where there had been none in the preoperative study; 8 of the 10 had a postoperative stricture of the distal urethra, and VUR subsided in 4 after adequate dilatation [23].
• METHODS: Samples of urothelium were collected from 13 children with primary VUR, four children with secondary VUR and from seven children with non-refluxing disorders of the urinary tract [24].
• Meatal stenosis and müllerian duct remnants are known to occur in this condition, but vesicoureteral reflux (VUR) was an unexpected finding in many boys who were asymptomatic and had no evidence of urinary tract infection [23].

Associations of VUR with chemical compounds

• Renal ultrasonography and cystography were done on the newborn babies soon after delivery, and a dimercaptosuccinic acid (DMSA) radioisotope scan at 3 months was done on those with VUR [25].
• 91 children (143 ureters) with primary vesicoureteric reflux (VUR) treated endoscopically by subureteric injection of 'Polytef' (polytetrafluoroethylene) paste were followed up for 2 to 5 1/2 years [26].
• This study also suggests that VUR is almost certain to have occurred in a child who has bilateral abnormal 99mTc-DMSA images following UTI and is also commonly present in those with definite unilateral defects [27].
• All patients underwent renal cortical scintigraphy (with technetium-99m dimercaptosuccinic acid or Tc-99m gluconate) and voiding cystourethrography (VCUG) to identify the presence of cortical defects and VUR, respectively [28].
• MATERIALS AND METHODS: A total of 32 males and 81 females with a median age of 1 year (range 3 months to 10 years) underwent endoscopic correction of primary VUR with dextranomer/hyaluronic acid copolymer [29].

Regulatory relationships of VUR

• Furthermore, 10 of 23 (44%) patients with VUR and seven of 19 (42%) controls carried the AT2 receptor gene variation [30].
• RESULTS: The mean serum ICAM-1 level in the control group was 202 +/- 79 ng/mL (mean +/- 1 SD) compared with 347 +/- 96 ng/mL in children with VUR (P < 0.001) [31].
• RESULTS: The mean serum ELAM-1 levels were 54.23 +/- 20.11 ng/ml in controls and 77.79 +/- 34.50 ng/ml in children with vesicoureteral reflux (p < 0.05) [32].

Other interactions of VUR

• However, the frequency distribution of KLK1 promoter among VUR patients with or without CRI (A, 50.0% and 67.5%; B, 17.9% and 8.3%; H, 14.3% and 18.3%; K, 17.9% and 5.8%, respectively) was statistically different (P = 0.008) [20].
• No significant linkage was found to 6p, where a renal and ureteric malformation locus has been reported, or to PAX2, mutations of which cause VUR in renal-coloboma syndrome [1].
• There seems no doubt that VUR is linked to HLA whilst the case for PUJO is equivocal [33].
• CONCLUSION: A prediction rule based on age, gender, family history, CRP and US results is useful in assessing the probability of VUR in the individual child with a first UTI and may help the physician to make decisions about performing additional imaging techniques [34].
• The data showed that ACE gene polymorphisms were associated with progressive renal deterioration in Taiwanese children with VUR and might act synergistically with the -6 G allele of the AGT gene [35].

Analytical, diagnostic and therapeutic context of VUR

• These included 69 patients with VUR, 110 with RN (determined by absence/presence of renal scarring on dimercaptosuccinc acid scan), 27 with chronic renal failure due to RN, and 40 patients (control group) with urinary tract infection and normal findings on renal ultrasonography and voiding cystoureterogram [5].
• In this study, independent predictors obtained from patient history, physical examination and laboratory results for vesico-ureteric reflux (VUR) in children of 0-5 y with a first urinary tract infection (UTI) were assessed and the added value of renal ultrasound (US) investigated [34].
• A systematic literature review and meta-analysis was performed to determine how effectively the finding of primary vesicoureteric reflux (VUR) on micturating cystography (MCU) in children hospitalized with UTI predicted renal parenchymal disease on (99m)Technetium-dimercaptosuccinic acid ((99m)Tc-DMSA) scintigraphy [36].
• MATERIALS AND METHODS: Three hundred two children younger than 11 years with urinary tract infection and grade III or IV VUR were randomly assigned to surgical (n = 149) or medical (n = 153) treatment and were followed up at serial intravenous urography for up to 5 years; 223, for up to 10 years (surgical, n = 110; medical, n = 113) [37].
• MATERIALS AND METHODS: Two groups of children were examined prospectively: 124 with severe urinary tract infection, defined as patient hospitalization or a maximum temperature greater than 39.5 degrees C, and 135 with previously diagnosed VUR [38].

References