Effect of Accessory Renal Arteries on Essential Hypertension and Related Mechanisms

This case-control study aimed to determine whether there were differences between patients with essential hypertension with accessory renal arteries (ARAs) and those without ARAs.

ARAs could contribute a higher BP of patients with essential hypertension and might promote the development of essential hypertension. The mechanism might be related to overactivation of the renin-angiotensin-aldosterone system and sympathetic nervous system.

The enrolled patients with essential hypertension were divided into the ARA group (n=200) and control group without ARAs (n=238). After propensity matching, 394 patients (197 in each of the 2 groups), were included. The 24-hour BP (4.33/2.43 mm Hg) and daytime BP (4.48/2.61 mm Hg) of patients in the ARA group were significantly higher than those of the control group (P<0.05). The flow-mediated dilation was lower in the ARA group (5.98±2.70 versus 5.18±2.66; P<0.05). In correlation analysis, the horizontal plasma aldosterone concentration had the highest correlation with 24-hour, daytime, and nighttime systolic BP (r=0.263, 0.247, and 0.243, respectively; P<0.05) and diastolic BP (r=0.325, 0.298, and 0.317, respectively; P<0.05). As for multivariate regression analysis, plasma aldosterone concentration was a significant risk factor for elevated 24-hour, daytime, and nighttime systolic BP (β=0.249 [95% CI, 0.150-0.349], 0.228 [95% CI, 0.128-0.329], and 0.282 [95% CI, 0.187-0.377], respectively; P<0.05) and elevated diastolic BP (β=0.289 [95% CI, 0.192-0.385], 0.256 [95% CI, 0.158-0.353], and 0.335 [95% CI, 0.243-0.427], respectively; P<0.05). Direct renin concentration was also a risk factor for 24-hour and daytime BPs, whereas heart rate was a risk factor correlated with 24-hour, daytime, and nighttime diastolic BP (all P<0.05). For the mixed-effects model for repeated measures, the results were similar to results of the multivariate regression analysis (all P<0.05). Conclusions: ARAs could contribute a higher BP of patients with essential hypertension and might promote the development of essential hypertension. The mechanism might be related to overactivation of the renin-angiotensin-aldosterone system and sympathetic nervous system.