Primary hyperaldosteronism natural history, complications and prognosis

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

Overview

If left untreated, patients with primary hyperaldosteronism may progress to develop stroke, coronary artery disease, and renal insufficiency with associated proteinuria. Aldosterone producing adenomas (APAs) continue to grow slowly over time. The aldosterone production likely correlates with the size of the adenoma. It is a progressive disease and its common complications include left ventricular hypertrophy due to chronic hypertension, atrial fibrillation, myocardial infarction, stroke, proteinuria, and metabolic syndrome. The prognosis of primary hyperaldosteronism is good with treatment. Without treatment, primary hyperaldosteronism will result in hypertension with resultant hypertension-related complications, which may be a major cause of morbidity and mortality among patients.

Natural History, Complications, and Prognosis

Natural History

Complications

Primary aldosteronism is characterized by the development of the following complications:[3][4][5][6][7][8]

Cardiovascular complications

Neurological complications

Renal complications

Metabolic complications

Prognosis

  • The prognosis of primary hyperaldosteronism is good with treatment. Without treatment, primary hyperaldosteronism will result in hypertension with resultant hypertension-related complications, which may be a major cause of morbidity and mortality among patients.
  • Adrenalectomy lowers long-term all-cause mortality from primary hyperaldosteronism.[14][15][16]

Patients undergoing unilateral adrenalectomy for unilateral adenoma

Patients receiving aldosterone antagonist medications

Patients with FH-I undergoing treatment with glucocorticoid medications

References

  1. Gordon RD (1997). "Primary aldosteronism: a new understanding". Clin. Exp. Hypertens. 19 (5–6): 857–70. PMID 9247760.
  2. "Cardiovascular complications in patients with primary aldosteronism - ScienceDirect".
  3. Nishimura M, Uzu T, Fujii T, Kuroda S, Nakamura S, Inenaga T, Kimura G (1999). "Cardiovascular complications in patients with primary aldosteronism". Am. J. Kidney Dis. 33 (2): 261–6. PMID 10023636.
  4. Giacchetti G, Turchi F, Boscaro M, Ronconi V (2009). "Management of primary aldosteronism: its complications and their outcomes after treatment". Curr Vasc Pharmacol. 7 (2): 244–49. PMID 19356005.
  5. 5.0 5.1 Reincke M, Meisinger C, Holle R, Quinkler M, Hahner S, Beuschlein F, Bidlingmaier M, Seissler J, Endres S (2010). "Is primary aldosteronism associated with diabetes mellitus? Results of the German Conn's Registry". Horm. Metab. Res. 42 (6): 435–9. doi:10.1055/s-0029-1246189. PMID 20119885.
  6. Hanslik G, Wallaschofski H, Dietz A, Riester A, Reincke M, Allolio B, Lang K, Quack I, Rump LC, Willenberg HS, Beuschlein F, Quinkler M, Hannemann A (2015). "Increased prevalence of diabetes mellitus and the metabolic syndrome in patients with primary aldosteronism of the German Conn's Registry". Eur. J. Endocrinol. 173 (5): 665–75. doi:10.1530/EJE-15-0450. PMID 26311088.
  7. 7.0 7.1 Gordon RD (1995). "Primary aldosteronism". J. Endocrinol. Invest. 18 (7): 495–511. doi:10.1007/BF03349761. PMID 9221268.
  8. 8.0 8.1 "Prevalence and Characteristics of the Metabolic Syndrome in Primary Aldosteronism | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic".
  9. Wu VC, Kuo CC, Wang SM, Liu KL, Huang KH, Lin YH, Chu TS, Chang HW, Lin CY, Tsai CT, Lin LY, Chueh SC, Kao TW, Chen YM, Chiang WC, Tsai TJ, Ho YL, Lin SL, Wang WJ, Wu KD (2011). "Primary aldosteronism: changes in cystatin C-based kidney filtration, proteinuria, and renal duplex indices with treatment". J. Hypertens. 29 (9): 1778–86. doi:10.1097/HJH.0b013e3283495cbb. PMID 21738054.
  10. Novello M, Catena C, Nadalini E, Colussi GL, Baroselli S, Chiuch A, Lapenna R, Bazzocchi M, Sechi LA (2007). "Renal cysts and hypokalemia in primary aldosteronism: results of long-term follow-up after treatment". J. Hypertens. 25 (7): 1443–50. doi:10.1097/HJH.0b013e328126855b. PMID 17563567.
  11. Fallo F, Federspil G, Veglio F, Mulatero P (2007). "The metabolic syndrome in primary aldosteronism". Curr. Hypertens. Rep. 9 (2): 106–11. PMID 17442220.
  12. "Metabolic syndrome in primary aldosteronism and essential hypertension: Relationship to adiponectin gene variants - ScienceDirect".
  13. Ronconi V, Turchi F, Rilli S, Di Mattia D, Agostinelli L, Boscaro M, Giacchetti G (2010). "Metabolic syndrome in primary aldosteronism and essential hypertension: relationship to adiponectin gene variants". Nutr Metab Cardiovasc Dis. 20 (2): 93–100. doi:10.1016/j.numecd.2009.03.007. PMID 19481913.
  14. "Long term outcome of Aldosteronism after target treatments | Scientific Reports".
  15. "Treatment strategy and outcome with primary aldosteronism: a nationwide longitudinal cohort based study".
  16. Celen O, O'Brien MJ, Melby JC, Beazley RM (1996). "Factors influencing outcome of surgery for primary aldosteronism". Arch Surg. 131 (6): 646–50. PMID 8645073.
  17. 17.0 17.1 Stowasser M, Gordon RD, Gunasekera TG, Cowley DC, Ward G, Archibald C, Smithers BM (2003). "High rate of detection of primary aldosteronism, including surgically treatable forms, after 'non-selective' screening of hypertensive patients". J. Hypertens. 21 (11): 2149–57. doi:10.1097/01.hjh.0000098141.70956.53. PMID 14597859.
  18. 18.0 18.1 Stowasser M, Gordon RD (2004). "Primary aldosteronism--careful investigation is essential and rewarding". Mol. Cell. Endocrinol. 217 (1–2): 33–9. doi:10.1016/j.mce.2003.10.006. PMID 15134798.
  19. Stowasser M, Gordon RD, Rutherford JC, Nikwan NZ, Daunt N, Slater GJ (2001). "Diagnosis and management of primary aldosteronism". J Renin Angiotensin Aldosterone Syst. 2 (3): 156–69. doi:10.3317/jraas.2001.022. PMID 11881117.
  20. Stowasser M, Gartside MG, Gordon RD (1997). "A PCR-based method of screening individuals of all ages, from neonates to the elderly, for familial hyperaldosteronism type I". Aust N Z J Med. 27 (6): 685–90. PMID 9483237.

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