Table 2.
Nonhypertensive participants | Hypertensive participants | |||
---|---|---|---|---|
Incident/total | HR (95% CI ) | Incident/total | HR/OR (95% CI) † | |
Continuous increment of aldosterone and renin in FOS | ||||
1‐SD increment of PRC | 193/1476 | 1.00 (0.90, 1.12) | 398/1433 | 0.97 (0.83, 1.13) |
1‐SD increment of SAC | 0.90 (0.76, 1.07) | 1.11 (1.02, 1.21) ‡ | ||
Continuous increment of aldosterone, by renin phenotype in FOS | ||||
1‐SD increment of SAC when PRC >15 mIU/L | 61/544 | 0.84 (0.61, 1.17) | 141/562 | 1.09 (0.98, 1.23) |
1‐SD increment of SAC when PRC ≤15 mIU/L | 132/932 | 0.97 (0.74, 1.26) | 257/871 | 1.19 (1.02, 1.39) ‡ |
Categories of aldosterone and renin phenotype in FOS* | ||||
SAC <10 ng/dL | 105/715 | Reference | 161/644 | Reference |
SAC ≥10 ng/dL and PRC >15 mIU/L | 32/357 | 0.86 (0.61, 1.23) | 93/357 | 1.19 (0.89, 1.60) |
SAC≥10 ng/dL and PRC ≤15 mIU/L | 56/404 | 1.16 (0.86, 1.56) | 144/432 | 1.40 (1.08, 1.82) ‡ |
Continuous increment of aldosterone and renin in CONPASS | ||||
1‐SD increment of PRC | … | … | 160/2612 | 1.01 (0.88, 1.18) |
1‐SD increment of PAC | … | 1.12 (1.01, 1.27) ‡ | ||
Continuous increment of aldosterone, by renin phenotype in CONPASS | ||||
1‐SD increment of SAC when PRC >15 mIU/L | … | … | 51/1002 | 1.04 (0.78, 1.54) |
1‐SD increment of SAC when PRC ≤15 mIU/L | … | … | 109/1610 | 1.28 (1.10, 1.46) ‡ |
Categories of aldosterone and renin phenotype in CONPASS* | ||||
PAC<10 ng/dL | … | … | 58/1080 | Reference |
PAC ≥10 ng/dL and PRC >15 mIU/L | … | … | 28/568 | 1.43 (0.88, 2.32) |
PAC ≥10 ng/dL and PRC ≤15 mIU/L | … | … | 74/964 | 1.59 (1.10, 2.31) ‡ |
Categories of aldosteronism in CONPASS § | ||||
Normal aldosterone: PAC <10 ng/dL | … | … | 58/1080 | Reference |
Confirmed renin‐dependent aldosteronism by CCT | … | … | 24/575 | 1.78 (0.72, 4.41) |
Confirmed renin‐independent aldosteronism by CCT | … | … | 78/957 | 2.57 (1.13, 5.86) ‡ |
All of these effects are based on the multivariate model, which adjusted for age, sex, body mass index, systolic blood pressure, current smoking status, alcohol consumption, total cholesterol, presence or absence of diabetes, antihypertensive medication use, and sodium status. CCT indicates captopril challenge test; CONPASS, Chongqing Primary Aldosteronism Study; FOS, Framingham Offspring Study; HR, hazard ratio; OR, odds ratio; PAC, plasma aldosterone concentration (ng/dL); PRC, plasma renin concentration (mIU/L); and SAC, serum aldosterone concentration (ng/dL). For SAC, 1 ng/dL = 27 pmol/L.
SAC ≥10 ng dL−1 was suspected as aldosteronism. PRC ≤15 mU/L was considered as low‐renin status. Subjects with PRC ≤15 mU/L and SAC ≥10 ng dL−1 were considered as renin‐independent aldosteronism, and subjects with PRC >15 mU/L and SAC ≥10 ng dL−1 were considered as renin‐dependent aldosteronism.
HR/OR (95% CI): HR (95% CI) for FOS, OR (95% CI) for CONPASS.
P value was <0.05.
PAC <10 ng dL−1 was considered as normal aldosterone. Subjects with PAC ≥10 ng dL−1 at screening and unsuppressed aldosterone secretion in the captopril challenge test (defined as PAC ≥10 ng dL−1 after the test) were confirmed as renin‐independent aldosteronism, while subjects with PAC ≥10 ng dL−1 and suppressed aldosterone secretion in CCT (defined as PAC <10 ng dL−1 after the test) were confirmed as renin‐dependent aldosteronism.