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Reliable, easy-to-read patient information on common medical conditions ā€” written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.

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Primary hyperaldosteronism epidemiology and demographics

Introduction

Overview

Overview

Prevalence of primary hyperaldosteronism is from 1,400-32,000 (median, 8,800) per 100,000 individuals around the world. Primary hyperaldosteronism incidence among patients with newly diagnosed hypertension is 11,200 of per 100,000 individuals. The case-fatality rate of primary hyperaldosteronism is approximately 23.4 per 1,000 individual-years. Patients of all age groups may develop primary hyperaldosteronism. There is no racial predilection for primary hyperaldosteronism.

Epidemiology and Demographics

Epidemiology and Demographics

Prevalence

  • Prevalence of primary hyperaldosteronism varies from 1,400 to 32,000 (median, 8,800) per 100,000 individuals around the world.[1][2]
  • In patients with resistant hypertension, the prevalence of primary hyperaldosteronism is reported to be even higher, ranging from a low of 17,000 per 100,000 patients to a high of 23,000 per 100,000 patients.[3]
  • The prevalence of familial hyperaldosteronism type II ranges from 1.2 to 6% in adult populations of primary hyperaldosteronism.[4]

Incidence

  • Primary hyperaldosteronism incidence among patients with newly diagnosed hypertension is 11,200 of per 100,000 individuals.[5]

Case-Fatality rate

  • The case-fatality rate of primary hyperaldosteronism is approximately 23.4 per 1,000 individual-years.[6]

Age

  • Patients of all age groups may develop primary hyperaldosteronism.

Gender

Race

  • There is no racial predilection for primary hyperaldosteronism.[9]
  • Blacks have been found to have lower plasma renin activity than other populations.[10]
References

References

  1. ā†‘ Rossi GP, Pessina AC, Heagerty AM (2008). “Primary aldosteronism: an update on screening, diagnosis and treatment”. J. Hypertens. 26 (4): 613ā€“21. doi:10.1097/HJH.0b013e3282f4b3e6. PMIDĀ 18327065.
  2. ā†‘ Rossi GP, Seccia TM, Pessina AC (2007). “Clinical use of laboratory tests for the identification of secondary forms of arterial hypertension”. Crit Rev Clin Lab Sci. 44 (1): 1ā€“85. doi:10.1080/10408360600931831. PMIDĀ 17175520.
  3. ā†‘ Stowasser M, Taylor PJ, Pimenta E, Ahmed AH, Gordon RD (2010). “Laboratory investigation of primary aldosteronism”. Clin Biochem Rev. 31 (2): 39ā€“56. PMCĀ 2874431. PMIDĀ 20498828.
  4. ā†‘ Stowasser M, Gordon RD (2000). “Primary aldosteronism: learning from the study of familial varieties”. J. Hypertens. 18 (9): 1165ā€“76. PMIDĀ 10994747.
  5. ā†‘ Rossi GP (2010). “Prevalence and diagnosis of primary aldosteronism”. Curr. Hypertens. Rep. 12 (5): 342ā€“8. doi:10.1007/s11906-010-0134-2. PMIDĀ 20665130.
  6. ā†‘ Wu, Vin-Cent; Wang, Shuo-Meng; Chang, Chia-Hui; Hu, Ya-Hui; Lin, Lian-Yu; Lin, Yen-Hung; Chueh, Shih-Chieh Jeff; Chen, Likwang; Wu, Kwan-Dun (2016). “Long term outcome of Aldosteronism after target treatments”. Scientific Reports. 6 (1). doi:10.1038/srep32103. ISSNĀ 2045-2322.
  7. _The_Journal_of_Clinical_Endocrinology_&_Metabolism_|_Oxford_Academic_7-0|ā†‘ “Evidence for Abnormal Left Ventricular Structure and Function in Normotensive Individuals with Familial Hyperaldosteronism Type I | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic”.
  8. ā†‘ Woo K, Waisman J, Melamed J, Lepor H (2000). “Primary aldosteronism caused by unilateral adrenal hyperplasia”. Rev Urol. 2 (2): 100ā€“4. PMCĀ 1476104. PMIDĀ 16985748.
  9. ā†‘ Calhoun DA, Nishizaka MK, Zaman MA, Thakkar RB, Weissmann P (2002). “Hyperaldosteronism among black and white subjects with resistant hypertension”. Hypertension. 40 (6): 892ā€“6. PMIDĀ 12468575.
  10. ā†‘ Lee MR, Critchley JA, Gordon CJ, Makarananda K, Sriwatanakul K, Balali-Mood M, Boye GL (1990). “Ethnic differences in the renal sodium dopamine relationship. A possible explanation for regional variations in the prevalence of hypertension?”. Am. J. Hypertens. 3 (6 Pt 2): 100Sā€“103S. PMIDĀ 2383374.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]