Abstract
To explore the clinical features of coexisting primary aldosteronism (PA) and renal artery stenosis (RAS), we retrospectively analyzed records from 71 patients with PA with RAS and a control group of 121 patients with PA without RAS. Aldosterone-to-renin concentration ratio tests and computerized tomography (CT) scanning of the adrenal and renal arteries were routinely conducted to screen for PA and RAS. Color Doppler flow and/or magnetic resonance imaging were used as substitute testing of patients for whom CT was contraindicated. Standard percutaneous renal arteriography (PTRA) was considered for patients with RAS exceeding 70% based on non-invasive tests and for those without PTRA contraindications. The patients with PA with RAS were further divided into severe (RAS>70%) and moderate (50% < RAS <70%) RAS groups. The prevalence of RAS among PA patients was 6.9% (71/1,033), including 3.2% (33/1,033) with severe RAS. Compared with the PA without RAS group, the severe RAS group showed higher levels of systolic blood pressure (SBP) (171.82 ± 18.24 vs. 154.11 ± 18.96 mmHg; P < 0.001) and diastolic BP(DBP) (110.76 ± 15.90 vs. 91.73 ± 12.85 mmHg; P < 0.001) and prevalence of resistant hypertension (RH) (90.9 vs. 66.9%; P = 0.008), whereas the moderate RAS group merely showed higher DBP (98.63 ± 14.90 vs. 91.73 ± 12.85 mmHg; P = 0.006). The direct renin concentrations (DRCs) (5.37 ± 3.94 vs. 3.71 ± 2.10 μU/mL; P < 0.001) and false-negative rate (33.8 vs. 3.3%; P < 0.01) of PA screening tests were significantly higher in the PA with RAS group than in the control group, but only in severe RAS group, in subgroup analysis. Among patients who underwent successful treatment for severe RAS, mean DRC decreased from 11.22 ± 9.10 to 3.24 ± 2.69 μIU/mL (P < 0.001). Overall, the prevalence of RH decreased from 81.7 to 2.8% (P < 0.001) when both PA and RAS were treated with standard methods. PA with concurrent severe RAS is a condition that induces RH. PA can be easily missed in patients with coexisting RAS. RAS patients with RH after successful revascularization for RAS should be evaluated for coexisting PA.
Highlights
Primary aldosteronism (PA) is the most common cause of secondary hypertension (HTN) and accounts for 10–20% of all-cause secondary HTN cases [1, 2]
1033 patients were diagnosed with primary aldosteronism (PA) from January, 2008 to December, 2019, and 71 of these were diagnosed with renal artery stenosis (RAS), including 33 with severe RAS and 38 with moderate RAS
These 71 patients were enrolled in the PA with RAS group, and 121 patients with PA only were included in the PA without RAS group (Figure 1)
Summary
Primary aldosteronism (PA) is the most common cause of secondary hypertension (HTN) and accounts for 10–20% of all-cause secondary HTN cases [1, 2]. Endothelial dysfunction, vascular remodeling [4, 5], sympathetic nervous system (SNS) activation [6], and baroreflex dysfunction [7] induced by aldosterone excess may be additional mechanisms by which HTN develops in patients with PA. Goldblatt et al [12] demonstrated that the regulation of the BP was far more complex than merely the regulation of blood volume by the kidney. His demonstration that unilateral RAS causes HTN without significant volume expansion spurred the search for other mechanisms of BP homeostasis including the renin-angiotensin-aldosterone system (RAAS) [13]. RAS induces excessive activation of the RAAS because the low blood flow and pressure to affected kidney stimulate the release of renin, which further increase the synthesis of Ang-II and aldosterone [14, 15]. In spite the effects of aldosterone, increased Ang II in RAS recruits additional pressor mechanisms, including sympathetic adrenergic pathways, vasoconstriction and vascular remodeling, inflammatory and fibrogenic mechanisms [16, 17]
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