Background-Hypertension is the leading risk factor for cardiovascular disease. Although accumulating evidence suggests tracking of blood pressure from childhood into adult life, there is little information regarding the relative contributions of genetic, prenatal, biological, behavioral, environmental, and social determinants to childhood blood pressure. Methods and Results-Blood pressure and an array of potential anthropometric, prenatal, environmental, and familial risk factors for high blood pressure, including parental smoking habits, were determined as part of a screening project in 4236 preschool children (age 5.7Ϯ0.4 years). Smoking was reported by 28.5% of fathers and 20.7% of mothers, and by both parents 11.9%. In addition to classic risk factors such as body mass index, prematurity, low birth weight, and parental hypertension, both systolic (ϩ1.0 [95% confidence interval, ϩ0.5 to ϩ1.5] mm Hg; Pϭ0.0001) and diastolic blood pressure (ϩ0.5 [ϩ0.03 to ϩ0.9] mm Hg; Pϭ0.03) were higher in children of smoking parents. Parental smoking independently affected systolic blood pressure (Pϭ0.001) even after correction for other risk factors, such as body mass index, parental hypertension, or birth weight, increasing the likelihood of having a systolic blood pressure in the top 15% of the population by 21% (2% to 44%; Pϭ0.02). Conclusions-In healthy preschool children, parental smoking is an independent risk factor for higher blood pressure, adding to other familial and environmental risk factors. Implementing smoke-free environments at home and in public places may provide a long-term cardiovascular benefit even to young children. (Circulation. 2011;123:292-298.)

Fifty children with idiopathic membranoproliferative glomerulonephritis (MPGN), aged 2-14 years at apparent onset, were monitored for the presence of C3 nephritic factor (C3 NeF) and signs of complement activation in serum. In addition, C3 allotyping was performed in 32 patients. Observation time ranged from 2 to 20 (median 11) years. C3 NeF activity was detected at least once in 60% of the patients (in 11 of 26 with type I, in 15 of 17 with type II, and in four of seven with type III). C3 NeF-positive patients had significantly reduced levels of CH50 and C3 and elevated levels of C3dg/C3d. During follow-up, C3 levels were persistently normal in 62% of the patients with MPGN type I and in 43% with type III but in only 18% with type II. C3 allotype frequencies differed from those found in healthy controls with a significant shift to the C3F/C3FS variants in C3 NeF-positive patients. C3b(Bb)P as a marker for alternative pathway activation was not increased in C3 NeF-positive patients. Despite the presence of C3 NeF activity, C3 levels remained normal in six patients throughout the observation period. C3 NeF became undetectable in six patients, whereas seven developed C3 NeF activity during follow-up. There was no significant difference in renal survival probability in patients with or without C3 NeF activity. Neither C3 variants nor continuous low C3 or low CH50 levels had any prognostic value for the clinical outcome. No factor H deficiency was detected.