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The aim of this report was to estimate the risk of hypertension in children with primary vesicoureteral reflux (VUR). Between 1970 and 2004, 735 patients were diagnosed with VUR at a single tertiary renal unit. Of 735 patients, 664 (90%) were systematically followed and had multiple measurements of blood pressure. Hypertension was defined as values persistently above 95th for age, sex, and height in three consecutive visits. Risk of hypertension was analyzed by the Kaplan-Meier method. Of 664 patients followed, 20 (3%) developed hypertension. The estimated probability of hypertension was 2% (95%CI, 0.5%–3%), 6% (95%CI, 2%–10%), 15% (95%CI, 11%–20%) at 10, 15, and 21 years of age, respectively. The prevalence of hypertension has increased with age: it was 1.7% for patients with 1 yr–9.9 yr, 1.8% for adolescents with 10 yr–14.9 yr, 4.7% for patients with 15–19.9 yr, and 35% for patients >20 years at the end of the follow-up (P < 0.001). It was estimated by survival analysis that 50% of patients with unilateral and bilateral renal damage would have sustained hypertension at about 30 and 22 years of age, respectively. Hypertension increased with age and was strongly associated with renal damage at entry in an unselected population of primary VUR. [ABSTRACT FROM AUTHOR]

The two papers in this section evaluate different diseases in children, but the two subjects are of considerable importance: nocturnal enuresis and VUR. OBJECTIVE To identify independent factors predicting the resolution of primary vesico-ureteric reflux (VUR) in a cohort of medically managed children. PATIENTS AND METHODS Between 1977 and 2003, 506 children were diagnosed with VUR and were conservatively managed and prospectively followed. All of the children were maintained on antibiotic prophylaxis. Follow-up imaging consisted of voiding cysto-urethrography (VCUG) or a direct isotope cystogram at intervals of 2–3 years. The predictive factors used are based on the patient data at the time of entry in the protocol. The dependent variable was VUR resolution. The criterion for resolution was based on a single negative VCUG or direct isotope cystogram. A survival analysis identified variables significantly associated with VUR resolution. Cox's regression model was applied to identify variables independently associated with the dependent variable. RESULTS After adjustment, four variables remained as independent predictors of VUR resolution: nonwhite race, relative risk (95% confidence interval) of 1.5 (1.1–1.9; P = 0.009); mild grade of VUR, 3.3 (2.1–5.3; P < 0.001); absence of renal damage, 3.3 (2.4–4.5; P < 0.001); and absence of dysfunctional voiding, 2.0 (1.4–3.1; P < 0.001). For mild VUR, three variables were significantly associated: male gender, 1.7 (1.1–2.6; P = 0.012); absence of renal damage, 3.4 (1.8–6.4; P < 0.001); and unilateral VUR, 1.6 (1.1–2.3; P = 0.004). For moderate/severe VUR, three variables were significantly associated: nonwhite race, 1.7 (1.1–2.6; P = 0.01); absence of renal damage, 3.0 (2.0–4.4; P < 0.001); and absence of dysfunctional voiding, 2.8 (1.4–5.5; P = 0.004). CONCLUSION Few factors are amenable to intervention to modify the natural history of VUR. According to our findings, there are only two possible interventions: avoiding renal scars and managing voiding dysfunction. [ABSTRACT FROM AUTHOR]