The Unrecognized Prevalence of Primary Aldosteronism
| Autor: | Anand Vaidya, Paul N. Hopkins, Robert M. Carey, Jenifer M Brown, David A. Calhoun, Gordon H. Williams, Mohammed Siddiqui |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
medicine.medical_specialty
Aldosterone business.industry Cross-sectional study 010102 general mathematics General Medicine medicine.disease 01 natural sciences Plasma renin activity Gastroenterology Excretion 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Primary aldosteronism Blood pressure chemistry Internal medicine Renin–angiotensin system Internal Medicine medicine Population study 030212 general & internal medicine 0101 mathematics business |
| Zdroj: | Annals of Internal Medicine. 173:10-20 |
| ISSN: | 1539-3704 0003-4819 |
| DOI: | 10.7326/m20-0065 |
| Popis: | Background Primary aldosteronism is a nonsuppressible renin-independent aldosterone production that causes hypertension and cardiovascular disease. Objective To characterize the prevalence of nonsuppressible renin-independent aldosterone production, as well as biochemically overt primary aldosteronism, in relation to blood pressure. Design Cross-sectional study. Setting 4 U.S. academic medical centers. Participants Participants with normotension (n = 289), stage 1 hypertension (n = 115), stage 2 hypertension (n = 203), and resistant hypertension (n = 408). Measurements Participants completed an oral sodium suppression test, regardless of aldosterone or renin levels, as a confirmatory diagnostic for primary aldosteronism and to quantify the magnitude of renin-independent aldosterone production. Urinary aldosterone was measured in participants in high sodium balance with suppressed renin activity. Biochemically overt primary aldosteronism was diagnosed when urinary aldosterone levels were higher than 12 μg/24 h. Results Every blood pressure category had a continuum of renin-independent aldosterone production, where greater severity of production was associated with higher blood pressure, kaliuresis, and lower serum potassium levels. Mean adjusted levels of urinary aldosterone were 6.5 μg/24 h (95% CI, 5.2 to 7.7 μg/24 h) in normotension, 7.3 μg/24 h (CI, 5.6 to 8.9 μg/24 h) in stage 1 hypertension, 9.5 μg/24 h (CI, 8.2 to 10.8 μg/24 h) in stage 2 hypertension, and 14.6 μg/24 h (CI, 12.9 to 16.2 μg/24 h) in resistant hypertension; corresponding adjusted prevalence estimates for biochemically overt primary aldosteronism were 11.3% (CI, 5.9% to 16.8%), 15.7% (CI, 8.6% to 22.9%), 21.6% (CI, 16.1% to 27.0%), and 22.0% (CI, 17.2% to 26.8%). The aldosterone-renin ratio had poor sensitivity and negative predictive value for detecting biochemically overt primary aldosteronism. Limitation Prevalence estimates rely on arbitrary and conventional thresholds, and the study population may not represent nationwide demographics. Conclusion The prevalence of primary aldosteronism is high and largely unrecognized. Beyond this categorical definition of primary aldosteronism, there is a prevalent continuum of renin-independent aldosterone production that parallels the severity of hypertension. These findings redefine the primary aldosteronism syndrome and implicate it in the pathogenesis of "essential" hypertension. Primary funding source National Institutes of Health. |
| Databáze: | OpenAIRE |
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