Sex-Specific Association of Primary Aldosteronism With Visceral Adiposity

Yu Hatano; Nagisa Sawayama; Hiroshi Miyashita; Tomoyuki Kurashina; Kenta Okada; Manabu Takahashi; Masatoshi Matsumoto; Satoshi Hoshide; Takahiro Sasaki; Shuichi Nagashima; Ken Ebihara; Harushi Mori; Kazuomi Kario; Shun Ishibashi

Disclosures

J Endo Soc. 2022;6(8)

Abstract and Introduction

Abstract

Context: The association between primary aldosteronism and obesity, especially its sex difference, remains unknown.

Objective: To assess the association for each subtype of primary aldosteronism with obesity parameters including visceral adipose tissue and differences between sexes.

Methods: In this case-control study, 4 normotensive controls were selected for each case with primary aldosteronism. Multivariable conditional logistic regression models were used to estimate the association between each type of primary aldosteronism and obesity indicators. We used a random forest to identify which visceral or subcutaneous tissue areas had a closer association with disease status.

Results: The study subjects included 42 aldosterone-producing adenoma cases (22 women) and 68 idiopathic hyperaldosteronism cases (42 women). In multivariable conditional logistic regressions, aldosterone-producing adenoma was significantly associated with body mass index only in men (odds ratio [OR] [95% CI)], 4.62 [1.98–10.80] per 2.89 kg/m²) but not in women (OR [95% CI], 1.09 [0.69–1.72] per 3.93 kg/m²) compared with the matched controls, whereas idiopathic hyperaldosteronism was associated with body mass index in both men (OR [95% CI], 3.96 [2.03–7.73] per 3.75 kg/m²) and women (OR [95% CI], 2.65 [1.77–3.96] per 3.85 kg/m²) compared with the matched controls. In random forests, visceral adipose tissue areas were the better predictor of both aldosterone-producing adenoma and idiopathic hyperaldosteronism than subcutaneous adipose tissue.

Conclusions: Aldosterone-producing adenoma cases were obese among men, but not among women. Idiopathic hyperaldosteronism cases were obese among both men and women. Visceral adipose tissue may contribute to the pathophysiology of primary aldosteronism.

Introduction

Primary aldosteronism (PA) is the most frequent form of secondary hypertension, with a prevalence of 5% to 15% in all hypertensive patients.^[1,2] The 2 predominant causes of PA are aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA).^[3,4] Patients with PA have a higher prevalence of cardiovascular events and mortality than patients with essential hypertension.^[4–7] Primary aldosteronism is a major public health issue given the increase in its prevalence.^[8] There is therefore a pressing unmet need to identify the mechanisms of PA to drive preventative initiatives and improve health outcomes.

Although the increase in its prevalence is most likely a reflection of active screening and surveillance of at-risk patients, other environmental factors such as the substantial increase in the prevalence of obesity could be related to its development.^[9,10] A prior study suggested that the prevalence of obesity was significantly higher in patients with IHA than in patients with essential hypertension.^[11] However, other studies found no significant association between PA and obesity.^[12–14] These studies used subjects with essential hypertension, which is also significantly associated with obesity, as controls. This could mask the association between PA and obesity.^[15] Therefore, it is necessary to compare PA cases with normotensive controls who have standard obesity parameters to determine whether PA is associated with obesity.

Ohno et al suggested that patients with IHA were more obese than those with APA.^[11] In addition, a difference between sexes has been reported; body mass index (BMI) was significantly higher in IHA patients compared with APA among women, but not among men.^[16] However, it remains uncertain whether the association between each subtype of PA and obesity differ by sex compared with non-PA cases. Elucidating the sex-specific association may clarify the underlying mechanisms of PA.

Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) are different in their patterns of molecular properties and their roles in the regulation of whole-body metabolism.^[17–20] Abdominal VAT is considered to be the more pathogenic fat depot because of stronger associations with most cardiometabolic risk factors compared with SAT.^[21,22] A prior study reported a positive association of plasma aldosterone (PAC) with visceral fat area among IHA cases.^[23] However, this is limited only among PA cases; it did not include any control groups. To the best of our knowledge, there have been no previous studies comparing the distribution of adipose tissue between PA cases and control groups. We hypothesized that VAT area had a closer association with each subtype of PA than SAT area because patients with PA have a high prevalence of cardiovascular events.^[4–7] However, conventional generalized linear model may not be appropriate because of multicollinearity between BMI, VAT, and SAT areas. Thus, we used a random forest, a machine learning algorithm, which can minimize the effect of multicollinearity.^[24]

Using a dataset of PA patients and health checkup participants whose adipose tissue areas were measured by computed tomography (CT), we assessed (1) whether obesity parameters, including VAT area, were associated with each type of PA; (2) whether the associations differed by sex; and (3) which of the VAT and SAT areas had a closer association with each type of PA.

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Table 1. Baseline characteristics of the patients with primary aldosteronism and matched controls
	APA (n = 42)	Control matched with APA (n = 168)	P value	IHA (n = 68)	Control matched with IHA (n = 272)	P value
Women, n (%)	22 (52.4)	88 (52.4)	1.000	42 (61.8)	168 (61.8)	1.000
Age, mean ± SD, y	50.9 ± 11.2	51.1 ± 10.8	0.934	51.8 ± 8.9	52.0 ± 8.8	0.897
Current smokers, n (%)	6 (14.3)	24 (14.3)	1.000	18 (26.5)	58 (21.3)	0.454
Alcohol drinking, n (%)	10 (23.8)	40 (23.8)	1.000	17 (25.0)	68 (25.0)	1.000
Body mass index, mean ± SD, kg/m²	24.4 ± 4.3 ^a	22.8 ± 3.5	0.010	26.8 ± 4.2 ^a	22.7 ± 3.3	<0.001
Systolic blood pressure, mean ± SD, mm Hg	144.1 ± 15.2	117.1 ± 11.3	<0.001	142.0 ± 14.8	117.0 ± 12.1	<0.001
Diastolic blood pressure, mean ± SD, mm Hg	87.7 ± 8.8	72.6 ± 8.9	<0.001	88.1 ± 11.4	72.3 ± 8.9	<0.001
Fasting glucose, mean ± SD, mg/dL	106.1 ± 26.3 (n = 31)	98.5 ± 15.2	0.027	103.9 ± 19.1 (n = 57)	97.8 ± 16.3	0.013
Hemoglobin A1c, %, mean ± SD	5.6 ± 1.1 (n = 37)	5.6 ± 0.5	0.630	5.8 ± 0.7 (n = 62)	5.6 ± 0.5	0.002
Diabetes mellitus, n (%)	9 (29.0) (n = 31)	11 (6.5)	<0.001	11 (20.0) (n = 55)	13 (4.8)	<0.001
Triglyceride, median (IQR), mg/dL	109.0 (71.0–141.0) (n = 35)	84.5 (62.8–119.3)	0.017	125.0 (100.0–166.0) (n = 57)	84.5 (63.05–126.0)	<0.001
HDL cholesterol, mean ± SD, mg/dL	54.9 ± 15.3 (n = 34)	68.1 ± 18.5	<0.001	49.8 ± 13.7 (n = 57)	69.7 ± 18.7	<0.001
LDL cholesterol, mean ± SD, mg/dL	110.6 ± 30.5 (n = 33)	127.6 ± 31.8	0.005	117.2 ± 27.7 (n = 56)	126.8 ± 29.7	0.027
eGFR, mean ± SD, mL/min/1.73 m²	82.6 ± 13.2	82.4 ± 10.8	0.930	82.9 ± 10.1	82.2 ± 9.0	0.573
Serum sodium, mean ± SD, mEq/L	144.0 ± 2.0 ^a	141.4 ± 1.8	<0.001	142.2 ± 1.5 ^a	141.8 ± 1.8	0.096
Serum potassium, mean ± SD, mEq/L	3.3 ± 0.6 ^a	4.1 ± 0.3	<0.001	4.0 ± 0.4 ^a	4.1 ± 0.3	<0.001
Serum uric acid, mean ± SD, mg/dL	5.1 ± 1.5	5.2 ± 1.4	0.566	5.4 ± 1.3	5.1 ± 1.4	0.156
Serum albumin, mean ± SD, mg/dL	4.3 ± 0.3	4.5 ± 0.2	<0.001	4.5 ± 0.4	4.5 ± 0.3	0.558
Plasma aldosterone, median (IQR), pg/mL	305.5 (167.5–480.8) ^a	–	–	120.0 (95.6–158.0) ^a	–	–
Plasma renin activity, median (IQR), ng/mL/h	0.2 (0.1–0.3) ^a	–	–	0.2 (0.3–0.5) ^a	–	–
ARR, median (IQR)	1435 (774–2411) ^a	–	–	368 (241–600) ^a	–	–
Serum cortisol in the morning, median (IQR), μg/dL	11.6 (7.1–14.6) (n = 39)	–	–	9.0 (7.1–11.7) (n = 61)	–	–
Antihyperglycemic medication, n (%)	5 (11.9)	4 (2.4)	0.021	8 (11.8)	9 (3.3)	0.011
Lipid lowering medication, n (%)	8 (19.0)	13 (7.7)	0.058	17 (25.0)	23 (8.5)	<0.001
Statin, n (%)	7 (16.7)	8 (4.8)	0.019	13 (19.1)	17 (6.2)	0.002
Potassium supplement, n (%)	25 (59.5) ^a	0 (0.0)	<0.001	5 (7.4) ^a	0 (0.0)	<0.001
Number of hypertensive medications, median (IQR)	1.0 (1.0–2.0)	–	–	1.0 (1.0–1.0)	–	–
Years to be hypertensive, median (IQR)	8.5 (3.0–16.0) ^a	–	–	1.0 (1.0–4.0) ^a	–	–
Medical history of CHD, n (%)	0 (0.0)	2 (1.2)	1.000	1 (1.5)	2 (0.7)	1.000
Medical history of stroke, n (%)	3 (7.1)	0 (0.0)	0.006	1 (1.5)	0 (0.0)	0.453
VAT areas, mean ± SD, cm²	111.9 ± 69.4	86.1 ± 55.7	0.012	1404.5 ± 70.9	89.0 ± 56.9	<0.001
SAT areas, mean ± SD, cm²	138.7 ± 68.5 ^a	125.2 ± 60.2	0.207	187.9 ± 75.8 ^a	125.2 ± 64.3	<0.001
VAT/SAT areas ratio, median (IQR)	0.73 (0.44–1.15)	0.62 (0.40–0.95)	0.097	0.68 (0.50–1.06)	0.62 (0.43–0.94)	0.052
Adrenal mass, n (%)	41 (97.6) ^a	–	–	24 (35.3) ^a	–	–

Data are expressed as means ± SD, median (IQR), or counts (percentages). For the difference of characteristics, skewed variables were tested using 2-sample Wilcoxon rank-sum (Mann-Whitney) test; normal variables were tested using 2-sample t test; categorical variables were tested using χ² test. Statistical significance was defined by a 2-sided P value < 0.017 according to Bonferroni correction from multiple comparison test. Significant values are displayed in bold.
Abbreviations: ARR, plasma aldosterone to active renin ratio; CHD, coronary heart disease; eGFR, estimated glomerular filtration; HDL, high-density lipoprotein; IQR, interquartile range; LDL, low-density lipoprotein; SAT, subcutaneous adipose tissue; VAT, visceral adipose tissue.
^aSignificant associations were found between APA vs IHA.

Table 2. The association between the parameters of obesity and disease status
		Odds ratio (95% CI)	P value	AUC (95% CI)	The difference of AUC	P value
APA vs matched control
Model 1	BMI (kg/m²)	1.61 (1.13–2.30)	0.009	–	–	–
Model 2	VAT area (cm²)	1.88 (1.24–2.87)	0.003	0.69 (0.61–0.77)	0.10 (0.03, 0.20)	0.011
Model 3	SAT area (cm²)	1.23 (0.90–1.69)	0.192	0.59 (0.49–0.68)	Reference	–
Model 4	VAT area (cm²)	2.11 (1.23–3.62)	0.006	–	–	–
	SAT area (cm²)	0.87 (0.57–1.31)	0.495
Model 5	BMI (kg/m²)	1.67 (1.15–2.42)	0.007	–	–	–
	Residual VAT area (cm²)	1.18 (0.84–1.68)	0.344
	Residual SAT area (cm²)	0.71 (0.50–1.02)	0.067
IHA vs matched control
Model 1	BMI (kg/m²)	3.09 (2.18–4.38)	<0.001	–	–	–
Model 2	VAT area (cm²)	3.15 (2.14–4.63)	<0.001	0.78 (0.71–0.83)	-0.01 (-0.06, 0.04)	0.783
Model 3	SAT area (cm²)	2.33 (1.71–3.18)	<0.001	0.78 (0.72–0.83)	Reference	–
Model 4	VAT area (cm²)	2.37 (1.46–3.86)	<0.001	–	–	–
	SAT area (cm²)	1.42 (0.95, 2.12)	0.086
Model 5	BMI (kg/m²)	3.09 (2.17–4.39)	<0.001	–	–	–
	Residual VAT area (cm²)	1.19 (0.87–1.63)	0.286
	Residual SAT area (cm²)	0.94 (0.71–1.24)	0.645
IHA vs APA
Model 1	BMI (kg/m²)	2.46 (1.48–4.41)	0.001	–	–	–
Model 2	VAT area (cm²)	2.48 (1.46–4.55)	0.002	0.72 (0.62–0.81)	-0.01 (-0.10, 0.08)	0.886
Model 3	SAT area (cm²)	2.40 (1.47–4.24)	0.001	0.73 (0.63–0.82)	Reference	–
Model 4	VAT area (cm²)	1.69 (0.90–3.39)	0.116	–	–	–
	SAT area (cm²)	1.83 (1.02–3.49)	0.051
Model 5	BMI (kg/m²)	2.47 (1.48–4.45)	0.001	–	–	–
	Residual VAT area (cm²)	1.40 (0.88–2.27)	0.159
	Residual SAT area (cm²)	1.38 (0.88–2.26)	0.178

All models are adjusted for sex, age, current smoker, and drinking habit. Adjusted odds ratio (95% CIs) associated with a 1-SD increase of each obesity parameter are shown. For APA patients and the matched controls, the 1-SD increment of each obesity parameter is as follows: BMI, 3.65 kg/m²; VAT area, 59.40 cm²; SAT area, 62.03 cm²; residual VAT area, 34.89 cm²; and residual SAT area, 35.81 cm². For IHA patients and the matched controls, the 1-SD increment of each obesity parameter is as follows: BMI, 3.88 kg/m²; VAT area, 63.85 cm²; SAT area, 71.21 cm²; residual VAT area, 34.98 cm²; and residual SAT area, 38.52 cm². For APA and IHA patients, the 1-SD increment of each obesity parameter is as follows: BMI, 4.27 kg/m²; VAT area, 71.78 cm²; SAT area, 76.60 cm²; residual VAT area, 42.07 cm²; and residual SAT area, 44.39 cm². Residuals of VAT and SAT areas were derived from Willett and Stampfer's residual approach and were uncorrelated with BMI. Statistical significance was defined by a 2-sided P value < 0.017 according to Bonferroni correction from multiple comparison test. Significant values are displayed in bold.
Abbreviations: APA, aldosterone-producing adenoma; AUC, the area under the receiver operating characteristic curves; BMI, body mass index; CI, confidence interval; IHA, idiopathic hyperaldosteronism; SAT, subcutaneous adipose tissue; VAT, visceral adipose tissue.

Table 3. The association between the parameters of obesity and disease status by sex
			Odds ratio (95% CI)	P value	AUC (95% CI)	The difference of AUC	P value
APA vs matched control
Men	Model 1	BMI (kg/m²)	4.62 (1.98–10.80)	<0.001	–	–	–
	Model 2	VAT area (cm²)	2.49 (1.38–4.49)	0.003	0.77 (0.66–0.87)	0.01 (-0.11, 0.12)	0.895
	Model 3	SAT area (cm²)	2.68 (1.38–5.22)	0.004	0.76 (0.64–0.87)	Reference	–
	Model 4	VAT area (cm²)	1.82 (0.93–3.54)	0.080	–	–	–
		SAT area (cm²)	1.96 (0.99–3.88)	0.054
	Model 5	BMI (kg/m²)	4.79 (2.02–11.36)	<0.001	–	–	–
		Residual VAT area (cm²)	1.21 (0.69–2.11)	0.499
		Residual SAT area (cm²)	0.89 (0.51–1.57)	0.691
Women	Model 1	BMI (kg/m²)	1.09 (0.69–1.72)	0.721	–	–	–
	Model 2	VAT area (cm²)	1.19 (0.76–1.86)	0.233	0.59 (0.46–0.72)	0.02 (-0.17, 0.21)	0.825
	Model 3	SAT area (cm²)	0.78 (0.46–1.33)	0.370	0.57 (0.44–0.70)	Reference	–
	Model 4	VAT area (cm²)	1.95 (0.96–4.00)	0.066	–	–	–
		SAT area (cm²)	0.49 (0.23–1.04)	0.065
	Model 5	BMI (kg/m²)	1.11 (0.67–1.84)	0.693	–	–	–
		Residual VAT area (cm²)	1.30 (0.78–2.18)	0.310
		Residual SAT area (cm²)	0.52 (0.28–0.94)	0.030
IHA vs matched control
Men	Model 1	BMI (kg/m²)	3.96 (2.03–7.73)	< 0.001	–	–	–
	Model 2	VAT area (cm²)	2.39 (1.44–3.96)	< 0.001	0.75 (0.64, 0.84)	-0.10 (-0.19, -0.01)	0.037
	Model 3	SAT area (cm²)	3.36 (1.72–6.54)	< 0.001	0.85 (0.76, 0.92)	Reference	–
	Model 4	VAT area (cm²)	1.25 (0.63–2.49)	0.521	–	–	–
		SAT area (cm²)	2.83 (1.29–6.47)	0.014
	Model 5	BMI (kg/m²)	4.22 (2.13–8.35)	< 0.001	–	–	–
		Residual VAT area (cm²)	0.67 (0.37–1.22)	0.192
		Residual SAT area (cm²)	1.26 (0.75–2.09)	0.383
Women	Model 1	BMI (kg/m²)	2.65 (1.77–3.96)	< 0.001	–	–	–
	Model 2	VAT area (cm²)	3.13 (1.99–4.90)	< 0.001	0.80 (0.73–0.87)	0.05 (0.01, 0.10)	0.024
	Model 3	SAT area (cm²)	2.03 (1.42–2.90)	< 0.001	0.75 (0.68–0.82)	Reference	–
	Model 4	VAT area (cm²)	3.57 (1.90–6.70)	< 0.001	–	–	–
		SAT area (cm²)	0.84 (0.48–1.48)	0.549
	Model 5	BMI (kg/m²)	2.70 (1.75–4.17)	< 0.001	–	–	–
		Residual VAT area (cm²)	1.90 (1.24–2.92)	0.003
		Residual SAT area (cm²)	0.76 (0.52–1.12)	0.172
IHA vs APA
Men	Model 1	BMI (kg/m²)	1.65 (0.86–3.56)	0.158	–	–	–
	Model 2	VAT area (cm²)	1.51 (0.81–3.08)	0.220	0.59 (0.42, 0.78)	0.02 (-0.12, 0.19)	0.755
	Model 3	SAT area (cm²)	1.34 (0.68–2.95)	0.419	0.57 (0.40, 0.73)	Reference	–
	Model 4	VAT area (cm²)	1.47 (0.68–3.43)	0.344	–	–	–
		SAT area (cm²)	1.06 (0.45–2.63)	0.898
	Model 5	BMI (kg/m²)	1.61 (0.84–3.49)	0.178	–	–	–
		Residual VAT area (cm²)	1.07 (0.55–2.11)	0.834
		Residual SAT area (cm²)	0.84 (0.42–1.67)	0.602
Women	Model 1	BMI (kg/m²)	2.93 (1.47–6.88)	0.006	–	–	–
	Model 2	VAT area (cm²)	3.53 (1.70–8.75)	0.002	0.80 (0.68, 0.91)	-0.03 (-0.15, 0.01)	0.599
	Model 3	SAT area (cm²)	4.23 (1.93–11.80)	0.001	0.83 (0.73, 0.93)	Reference	–
	Model 4	VAT area (cm²)	2.00 (0.85–5.43)	0.139	–	–	–
		SAT area (cm²)	2.91 (1.15–8.74)	0.035
	Model 5	BMI (kg/m²)	3.46 (1.63–8.86)	0.004	–	–	–
		Residual VAT area (cm²)	2.01 (0.97–4.65)	0.073
		Residual SAT area (cm²)	2.39 (1.16–5.63)	0.027

All models are adjusted for age, current smoker, and drinking habit. Adjusted odds ratio (95% CIs) associated with a 1-SD increase of each obesity parameter are shown. For men among APA patients and the matched controls, the 1-SD increment of each obesity parameter is as follows: BMI, 2.89 kg/m²; VAT area, 57.94 cm²; SAT area, 54.52 cm²; residual VAT area, 42.58 cm²; and residual SAT area, 32.83 cm². For women among APA patients and the matched controls, the 1-SD increment of each obesity parameter is as follows: BMI, 3.93 kg/m²; VAT area, 41.22 cm²; SAT area, 68.35 cm²; residual VAT area, 26.24 cm²; and residual SAT area, 38.46 cm². For men among IHA patients and the matched controls, the 1-SD increment of each obesity parameter is as follows: BMI, 3.75 kg/m²; VAT area, 70.87 cm²; SAT area, 66.81 cm²; residual VAT area, 43.66 cm²; and residual SAT area, 38.04 cm². For women among IHA patients and the matched controls, the 1-SD increment of each obesity parameter is as follows: BMI, 3.85 kg/m²; VAT area, 46.02 cm²; SAT area, 73.29 cm²; residual VAT area, 28.43 cm²; and residual SAT area, 38.91 cm². For men among APA and IHA patients, the 1-SD increment of each obesity parameter is as follows: BMI, 3.39 kg/m²; VAT area, 70.67 cm²; SAT area, 73.69 cm²; residual VAT area, 47.20 cm²; and residual SAT area, 43.73 cm². For women among APA and IHA patients, the 1-SD increment of each obesity parameter is as follows: BMI, 4.46 kg/m²; VAT area, 54.84 cm²; SAT area, 78.76 cm²; residual VAT area, 38.35 cm²; and residual SAT area, 45.21 cm². Residuals of VAT and SAT areas were derived from Willett and Stampfer's residual approach and were uncorrelated with BMI. Statistical significance was defined by a 2-sided P value < 0.017 according to Bonferroni correction from multiple comparison test. Significant values are displayed in bold.
APA, aldosterone-producing adenoma; AUC, the area under the receiver operating characteristic curves; BMI, body mass index; CI, confidence interval; IHA, idiopathic hyperaldosteronism; SAT, subcutaneous adipose tissue; VAT, visceral adipose tissue.

Authors and Disclosures

Yu Hatano^1,*, Nagisa Sawayama^2,*, Hiroshi Miyashita³, Tomoyuki Kurashina⁴, Kenta Okada², Manabu Takahashi², Masatoshi Matsumoto⁵, Satoshi Hoshide⁶, Takahiro Sasaki⁷, Shuichi Nagashima⁸, Ken Ebihara², Harushi Mori⁷, Kazuomi Kario⁶ and Shun Ishibashi²

¹Department of Family Medicine and Community Health, Duke University, Durham, NC, 27705, USA
²Division of Endocrinology and Metabolism, Department of Internal Medicine, Jichi Medical University, Shimotsuke-shi, Tochigi-ken 329–0498, Japan
³Jichi Medical University Health Care Center, Shimotsuke-shi, Tochigi-ken 329–0493, Japan
⁴School of Nursing, Jichi Medical University, Shimotsuke-shi, Tochigi-ken 329–0498, Japan
⁵Department of Community-Based Medical System, Graduate School of Biomedical and Health Sciences, Hiroshima University, Minami-ku, Hiroshima 734–8551, Japan
⁶Division of Cardiology, Department of Internal Medicine, Jichi Medial University, Shimotsuke-shi, Tochigi-ken 329–0498, Japan
⁷Department of Radiology, Jichi Medial University, Shimotsuke-shi, Tochigi-ken 329–0498, Japan
⁸Department of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Omiya-ku, Saitama-shi, Saitama-ken 330- 8503, Japan

Correspondence
Yu Hatano, MD, MPH, PhD, Department of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, 53 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606–8507, Japan. Email: yu.hatano@cira.kyoto-u.ac.jp; or Shun Ishibashi, MD, PhD, Department of Internal Medicine, Division of Endocrinology and Metabolism, Jichi Medical University, 3311–1 Yakushiji, Shimotsuke-shi, Tochigi-ken 329–0498, Japan. Email: ishibash@jichi.ac.jp.

*Contributed equally as first authors.

Author Contributions
Study concept and design: Y.H., K.O., T.K., M.M., S.H., S.N., K.E., and S.I. Acquisition of data: N.S., H.M., and MT. Analysis and interpretation of data: Y.H., K.O., T.K., M.T., T.S., H.M., K.K., and S.I. Drafting of the manuscript: Y.H., N.S., T.K., and S.I. Critical revision of the manuscript for important intellectual content: M.T., M.M., S.H., T.S., S.N., K.E., H.M., K.K., and S.I. Statistical analysis: Y.H. Study supervision: S.I. Y.H. and N.S. had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Disclosures
S.I. has received personal fees or grants from MSD, Amgen Astellas BioPharma, Eli Lilly Japan, Sanofi, Astellas Pharma, Nippon Boehringer Ingelheim, Mitsubishi Tanabe Pharma, Daiichi Sankyo, Takeda Pharmaceutical, Ono Pharmaceutical, Shionogi, Teijin Pharma, and Kowa Pharmaceutical. The other authors state that they have no conflicts of interest.

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Sex-Specific Association of Primary Aldosteronism With Visceral Adiposity

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