The review examines the nature of the course of arterial hypertension (AH) in case of tumor and hyperplastic changes in the adrenal cortex, leading to the development of low-renin hyperaldosteronism. The severity and nature of the course of AH were analyzed, it was shown that in most cases high stable hypertension develops, and resistance to multidrug antihypertensive therapy is observed. Attention is drawn to the features of the course of AH: options for hypertensive crisis, as well as cases of a moderately elevated and even normal level of blood pressure. Possible pathogenetic mechanisms that determine the characteristics of the course of AH are considered. Based on the results of the studies, including our own data, the importance of analyzing the individual characteristics of the course of the disease in order to select preferable methods of treatment and reduce the risk of undiagnosed aldosteromas is substantiated.
Key words: low-renin hyperaldosteronism, resistant arterial hypertension, hypertensive crises, normotensive patients.
For citation: Chikhladze N.M. The nature of the course of arterial hypertension in low-renin hyperaldosteronism. Systemic Hypertension. 2019; 16 (4):
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2. Chikhladze N.M. Symptomatic (secondary) arterial hypertension. Diagnosis and treatment. Biblioteka FGBU "NMITs kardiologii" Minzdrava Rossii. Moscow: MIA, 2018 (in Russian).
3. Conn JW. Primary aldosteronism: a new clinical syndrome. J Lab Clin Med 1955; 45: 3–17.
4. Baer L, Sommers SC, Krakoff LR et al. Pseudoprimary aldosteronism: an entity distinct from true primary aldosteronism. Circ Res 1970; 27 (Suppl. 1): 203–20.
5. Pignatelli D, Falcao H, Coimara-Pixoto A, Cruz F. Unilateral adrenal hyperplasia. South Med J 1994; 87: 664–7.
6. Omura M, Sasano H, FujiwaraT et al. Unique Cases of Unilateral Hyperaldosteronemia Due to Multiple Adrenocortical Micronodules, Which Can Only be Detected by Selective Adrenal Venous Sampling. Metabolism 2002; 51 (3): 350–5.
7. Stowasser M, Gartside MG, Gordon RD. A PCR-based method of sсreening individuals of all ages, from neonates to the elderly, for familial hyperaldosteronism type I. Aust NZJ 1997; 27: 685–90.
8. Chikhladze N.M., Favorova O.O., Chazova I.E. Semeinaia forma giperal'dosteronizma I tipa: klinicheskoe nabliudenie i obzor literatury. Therapeutic Archive. 2018; 9: 115–22 (in Russian).
9. Young WF. Primary aldosteronism: renaissance of a syndrome. Clin Endocrinol 2007; 66: 607–18.
10. Ruilope LM. Aldosterone, Hypertension, and cardiovascular disease. Hypertension 2008; 52: 207.
11. Knoz FG, Burnett JC, Kohan DE et al. Escape from the sodium-retaining effects of mineralocorticoids. Kidney Intern 1980; 17: 263–76.
12. Shkhvatsabaia I.K., Chikhladze N.M. Hyperaldosteronism and arterial hypertension. Moscow: Medi-tsina, 1984 (in Russian).
13. Mosso L, Carvajal C, González A et al. Primary aldosteronism and hypertensive disease. Hypertension 2003; 42: 161–5.
14. Monticone S, Burrello J, Tizzani D et al. Prevalence and clinical manifestations of primary aldosteronism encountered in primary care practice. J Am Coll Cardiol 2017; 69: 1811–20.
15. Strauch B, Zelinka T, Hampf M et al. Prevalence of primary hyperaldosteronism in moderate to severe hypertension in the central Europe region. J Hum Hypertens 2003; 17: 349–52.
16. Samedova Kh.F., Chikhladze N.M., Blinova E.V. et al. Otsenka funktsional'nogo sostoianiia miokarda u bol'nykh arterial'noi gipertoniei na fone giperal'dosteronizma s ispol'zovaniem ortogonal'noi elektrokardiografii. Kardiovaskuliarnaia terapiia i profilaktika. 2006; 5 (2): 15–9 (in Russian).
17. Cushman WC, Ford CE, Cutler JA et al; for the ALLHAT Collaborative Research Group: Success and predictors of blood pressure control in diverse North American settings. The Antihypertensive and Lipid-Lowering and Treatment to Prevent Heart Attack Trial (ALLHAT). J Clin Hypertens 2002; 4: 393–404.
18. Calhoun DA. Aldosteronism and hypertension. Clin J Am Soc Nephrol 2006; 1 (5): 1039–45.
19. Douma S, Petidis K, Doumas M et al. Prevalence of primary hyperaldosteronism in resistant hypertension: a retrospective observational study. Lancet 2008; 371 (9628): 1921–6.
20.Chikhladze N.M., Bronshtein M.E., Kazeev K.N., Arabidze G.G. Krizovoe techenie arterial'noi gipertonii u bol'nykh s pervichnym giperal'dosteronizmom. Kardiologiia. 1989; 11: 95–9 (in Russian).
21. Stowasser M, Bachmann AW, Huggard PR et al. Severity of hypertension in familial hyperaldosteronism type I: relationship to gender and degree of biochemical disturbance. J Clin Endocrinol Metab 2000; 85 (6): 2160–6.
22. Mulatero P, Tizzani D, Viola A et al. Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in TOrino-GENetic forms). Hypertension 2011; 58 (5): 797–803.
23. Ito Y, Takeda R, Karashima S et al. Prevalence of primary aldosteronism among prehypertensive and stage 1 hypertensive subjects. Hypertens Res 2011; 34: 98–102.
24. Moradi S, Shafiepour M, Amirbaigloo A. A woman with normotensive primary hyperaldosteronism. Acta Medica Iranica 2016; 54 (2): 156–8.
25. Ito Y, Takeda R, Takeda Y. Subclinical primary aldosteronism. Best Pract Res Clin Endocrinol Metab 2012; 26: 485–95.
26. Médeau V, Moreau F, Trinquart L et al. Clinical and biochemical characteristics of normotensive patients with primary aldosteronism: a comparison with hypertensive cases. Clin Endocrinol 2008; 69 (1): 20–8.
27. Vantyghem M-C, Ronci N, Provost F et al. Aldosterone-producing adenoma without hypertension: a report of two cases. Eur J Endocrinol 1999; 141: 279–85.
28. Nishimiya T, Kikuchi K, Oimatsu H et al. A case of normotensive primary aldosteronism – comparison with 13 previously experienced cases with hypertension. Endocrinol Jpn 1984; 31 (2): 159–64.
29. Rossi GP. Does primary aldosteronism exist in normotensive and mildly hypertensive patients, and should we look for it? Hypertens Res 2011; 34: 43–6.
For citation:Chikhladze N.M. The nature of the course of arterial hypertension in low-renin hyperaldosteronism. Systemic Hypertension. 2019; 16 (4): DOI: 10.26442/2075082X.2019.4.190574