Background: While the RAS is altered in youth born preterm and may play a role in development of HTN, this has not been investigated in youth with primary HTN. We hypothesized that lower gestational age (GA) and lower birth weight (BW) would be associated with higher Ang II, lower Ang-(1-7), and higher Ang II/Ang-(1-7) in plasma and urine. Methods: This is a secondary analysis of baseline data from a pilot prospective cohort study of 30 youth aged 5-17 years with newly diagnosed primary HTN per national guidelines. Exclusion criteria were heart or chronic kidney disease and diabetes mellitus. Exposures were GA, BW, and BW z-score on the continuous scale and as binary variables, preterm birth (GA <37 weeks) and low BW (<2500 g). RAS outcomes were Ang II and Ang-(1-7) measured in plasma and urine per well-validated RIAs; urinary values standardized to urine creatinine (Cr). Plasma renin activity and aldosterone were measured per well-validated methods. We estimated associations with unadjusted generalized linear models. Results: Median GA was 39 weeks [IQR 36, 40] with 28% (8/30) born preterm. Mean BW was 3.12 kg ( SD 0.65) with low BW in 17% (5/30). Preterm birth was associated with lower urine Ang-(1-7)/Cr and higher aldosterone/renin ratio and urine Ang II/Ang-(1-7) (Figure). Low BW was associated with higher plasma Ang-(1-7) and urine Ang II/Cr. Conclusion: Early-life risk factors were associated with intrarenal RAS alterations favoring Ang II activation and Ang-(1-7) suppression in youth with primary HTN. Our findings provide novel insight into the mechanistic role that the RAS may play in HTN development in youth born preterm or with low BW that differs from youth born at term who have HTN.