Original ArticlePlasma renin levels and renin-blood pressure relationship in normal-weight and overweight children with obstructive sleep apnea and matched controls

- Renin levels are not different between obstructive sleep apnea (OSA) and control in normal-weight and overweight children.
- Negative renin-blood pressure (BP) associations are absent in both OSA and overweight children.
- Dysfunction of the renin-angiotensin system may be a potential mechanism of increased BP in OSA and overweight children.

BackgroundObstructive sleep apnea (OSA) has been increasingly linked to elevated blood pressure (BP) and hypertension. Repeated night-time hypoxia in OSA is associated with activation of two critical mechanisms of BP control: the autonomic nervous system and the renin-angiotensin system (RAS). The effects of OSA on the RAS are not well understood, especially in children. We hypothesized that children with OSA have elevated renin levels and abnormal relationships between BP and renin.MethodsPolysomnography was conducted in 173 children to diagnose OSA (apnea-hypopnea index [AHI] >1 event/h) and control (AHI ≤1 event/h) groups. Age- and gender-specific z-scores for body mass index (BMI) were calculated to divide subjects into obese (BMI ≥95%), overweight (BMI ≥85% and <95%) and normal-weight (BMI <85%) groups. Morning BP was measured with an automatic sphygmomanometer and venous blood samples were collected for measurements of plasma renin, after overnight polysomnography.ResultsPlasma renin levels were not significantly different in all four groups after adjustment of age, gender, and race. Significantly negative associations between renin and BP were present only in the normal-weight control group and were absent in the other three groups.ConclusionPlasma renin levels were not significantly increased in children with OSA compared to controls for both normal-weight and overweight subjects. The absence of normal, negative renin-BP relationships in both overweight and OSA children suggests a dysfunction of the RAS, which could be a mechanism for increased BP and the development of hypertension.