Lipoprotein (a) is a residual risk of atherosclerotic renal artery stenosis in hypertensive patients: a hospital-based cross-sectional study
Background: Low-density lipoprotein cholesterol (LDL-c) has been proven to be a risk factor for atherosclerotic cardiovascular disease (CVD), while lipoprotein (a) (Lp(a)) is a residual risk factor for CVD, even though LDL-c is well controlled by statin use. Importantly, the role of Lp(a) in atherosclerotic renal artery stenosis (ARAS) is still unknown.
Methods: For this hospital-based cross-sectional study, patients who simultaneously underwent coronary and renal angiography were examined. ARAS was defined as a 50% reduction in the cross-sectional (two-dimensional plane) area of the renal artery. Data were collected and compared between ARAS and non-ARAS groups, including clinical history and metabolite profiles. Univariate analysis, three tertile LDL-c-based stratified analysis, and multivariate-adjusted logistic analysis were conducted, revealing a correlation between Lp(a) and ARAS.
Results: A total of 170 hypertensive patients were included in this study, 85 with ARAS and 85 with non-RAS. Baseline information indicated comparability between the two groups. In the univariate and multivariate analysis, common risk factors for atherosclerosis were not significantly different. Stratified analysis of LDL-c revealed a significant increase in the incidence of ARAS in patients who had high Lp(a) concentrations at low LDL-c levels (odds ratio (OR): 4.77, 95% confidence interval (CI): 1.04-21.79, P = 0.044). Further logistic analysis with adjusted covariates also confirmed the result, indicating that high Lp(a) levels were independently associated with ARAS (adjusted OR (aOR): 6.14, 95%CI: 1.03-36.47, P = 0.046). This relationship increased with increasing Lp(a) concentration based on a curve fitting graph. These results were not present in the low and intermediate LDL-c-level groups.
Conclusion: In hypertensive patients who present low LDL-c, high Lp(a) was significantly associated with atherosclerotic renal artery stenosis and thus is a residual risk factor.
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Lipoprotein (a) is a residual risk of atherosclerotic renal artery stenosis in hypertensive patients: a hospital-based cross-sectional study
Posted 12 May, 2020
On 23 Jul, 2020
On 28 Apr, 2020
On 27 Apr, 2020
On 26 Apr, 2020
On 26 Apr, 2020
Received 20 Apr, 2020
On 20 Apr, 2020
Received 16 Apr, 2020
Invitations sent on 16 Apr, 2020
On 16 Apr, 2020
On 16 Apr, 2020
On 16 Apr, 2020
Received 16 Apr, 2020
On 16 Apr, 2020
On 15 Apr, 2020
On 15 Apr, 2020
On 16 Mar, 2020
On 15 Mar, 2020
Received 15 Mar, 2020
Received 15 Mar, 2020
Received 12 Mar, 2020
On 12 Mar, 2020
Received 08 Mar, 2020
Received 03 Mar, 2020
Received 03 Mar, 2020
Received 02 Mar, 2020
On 02 Mar, 2020
Received 02 Mar, 2020
On 01 Mar, 2020
On 01 Mar, 2020
On 26 Feb, 2020
Invitations sent on 22 Feb, 2020
On 22 Feb, 2020
On 22 Feb, 2020
On 07 Feb, 2020
On 06 Feb, 2020
On 06 Feb, 2020
On 02 Feb, 2020
Background: Low-density lipoprotein cholesterol (LDL-c) has been proven to be a risk factor for atherosclerotic cardiovascular disease (CVD), while lipoprotein (a) (Lp(a)) is a residual risk factor for CVD, even though LDL-c is well controlled by statin use. Importantly, the role of Lp(a) in atherosclerotic renal artery stenosis (ARAS) is still unknown.
Methods: For this hospital-based cross-sectional study, patients who simultaneously underwent coronary and renal angiography were examined. ARAS was defined as a 50% reduction in the cross-sectional (two-dimensional plane) area of the renal artery. Data were collected and compared between ARAS and non-ARAS groups, including clinical history and metabolite profiles. Univariate analysis, three tertile LDL-c-based stratified analysis, and multivariate-adjusted logistic analysis were conducted, revealing a correlation between Lp(a) and ARAS.
Results: A total of 170 hypertensive patients were included in this study, 85 with ARAS and 85 with non-RAS. Baseline information indicated comparability between the two groups. In the univariate and multivariate analysis, common risk factors for atherosclerosis were not significantly different. Stratified analysis of LDL-c revealed a significant increase in the incidence of ARAS in patients who had high Lp(a) concentrations at low LDL-c levels (odds ratio (OR): 4.77, 95% confidence interval (CI): 1.04-21.79, P = 0.044). Further logistic analysis with adjusted covariates also confirmed the result, indicating that high Lp(a) levels were independently associated with ARAS (adjusted OR (aOR): 6.14, 95%CI: 1.03-36.47, P = 0.046). This relationship increased with increasing Lp(a) concentration based on a curve fitting graph. These results were not present in the low and intermediate LDL-c-level groups.
Conclusion: In hypertensive patients who present low LDL-c, high Lp(a) was significantly associated with atherosclerotic renal artery stenosis and thus is a residual risk factor.
Figure 1
Figure 2
Figure 3