Effect of Accessory Renal Arteries on Essential Hypertension and Related Mechanisms

Abstract

Background 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. Methods and Results 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.