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Secondary hyperaldosteronism, caused by abnormalities of the renal vessels, in clinical endocrinologist

Abstract

Aldosterone levels increase in clinical practice may be due to primary or secondary hyperaldosteronism. Secondary hyperaldosteronism (CAA) is a clinical syndrome caused by increased synthesis of renin juxtaglomerular apparatus of the kidneys in response to lower perfusion pressure in the afferent glomerular arteriole. This mechanism leads to activation of the renin-angiotensin-aldosterone system with a consequent increase in systemic blood pressure. Clinically manifested CAA secondary (systemic) arterial hypertension, the most common form of parenchymal renal disease and renal vascular lesions. Renovascular diseases are a heterogeneous group of pathologies, which includes atherosclerosis of renal arteries, the most common cause; fibromuscular dysplasia (FMD); other more rare diseases, accompanied by a narrowing of the lumen of the renal vessels. Some authors consider the possibility of including a group of renovascular disease presence of multiple renal arteries. Тhe article presents the clinical cases of secondary hyperaldosteronism, caused by FMD and abnormal amounts of the renal arteries, manifested hypertension and increased levels of aldosterone in the blood. Carrying out a detailed search of the diagnostic determination of the ratio of aldosterone to plasma renin helped eliminate endocrine genesis of the disease and to identify the true cause of aldosteronism.

About the Authors

Tatjana N. Markova
City Clinical Hospital №52; Moscow State University of Medicine and Dentistry named after A.I. Evdokimov
Russian Federation
MD, PhD
Competing Interests:

No conflict of interest



Vasilij V. Parshin
City Clinical Hospital №52
Russian Federation
MD
Competing Interests:

No conflict of interest



Nadezhda K. Mishchenko
City Clinical Hospital №52; Moscow State University of Medicine and Dentistry named after A.I. Evdokimov
Russian Federation
MD
Competing Interests:

No conflict of interest



References

1. Бельцевич Д.Г. Первичный гиперальдостеронизм. Клинические рекомендации. // Эндокринная хирургия. – 2008. – Т.2. – №2 – С. 6–10. [Bel’tsevich DG. Pervichnyy giperal’dosteronizm. Klinicheskie rekomendatsii. Endocrine Surgery. 2008;2(2):6-10. (In Russ.)]. doi: 10.14341/2306-3513-2008-2-6-20.

2. Эндокринология: национальное руководство. Под ред. Дедова И.И., Мельниченко Г.А. – М.: ГЭОТАР-Медиа; 2013. – С. 686–687. [Dedov II, Melnichenko GA, editors. Endocrinology. National Guidelines. Moscow: GEOTAR-Media; 2013. P.686-687. (In Russ.)].

3. Диагностика и лечение артериальной гипертензии [архив]. Доступно по: http://www.scardio.ru/content/Guidelines/recommendation-ag-2010.pdf. Ссылка активна на 15.10.2015. [Diagnostika i lechenie arterial'noi gipertenzii[arkhiv]. Available on URL: http://www.scardio.ru/content/Guidelines/recommendation-ag-2010.pdf. Access date: 15.10.2015. (In Russ.)].

4. AbuRahma AF, Srivastava M, Mousa AY, et al. Critical analysis of renal duplex ultrasound parameters in detecting significant renal artery stenosis. J. Vasc. Surg. 2012;56(4):1052-1060.e1051. doi: 10.1016/j.jvs.2012.03.036.

5. Dieter R, Weber B. Renal artery stenosis: epidemiology and treatment. Int. J. Nephrol. Renovasc. Dis. 2014:169. doi: 10.2147/ijnrd.s40175.

6. Фомин В.В., Куприянов И.Е., Разуваева М.А. Множественные почечные артерии – эпифеномен или возможная причина артериальной гипертензии? // Клиническая нефрология. – 2012. – №5-6. – С. 64–67. [Fomin VV,Kupriyanov IE, Razuvaeva MA. Multiple renal arteries – an epiphenomena or potential cause of arterial hypertension? Klinicheskaia nefrologiia. 2012;(5-6):64-67. (In Russ.)].

7. Gokalp G, Hakyemez B, Erdogan C. Vascular anomaly in bilateral ectopic kidney: a case report. Cases Journal. 2010;3(1):5. doi: 10.1186/1757-1626-3-5.

8. Olin JW, Sealove BA. Diagnosis, management, and future developments of fibromuscular dysplasia. J. Vasc. Surg. 2011;53(3):826-836.e821. doi: 10.1016/j.jvs.2010.10.066.

9. Shejul YK, Viswanathan MK, Jangale P, Kulkarni A. Fibromuscular dysplasia: a cause of secondary hypertension. The Korean Journal of Internal Medicine. 2014;29(6):840. doi: 10.3904/kjim.2014.29.6.840.

10. Olin JW, Gornik HL, Bacharach JM, et al. Fibromuscular dysplasia: State of the science and critical unanswered questions: A scientific statement from the American Heart Association. Circulation. 2014;129(9):1048-1078.doi: 10.1161/01.cir.0000442577.96802.8c.

11. Rao TR. Aberrant renal arteries and its clinical significance: a case report. International journal of anatomical variations. 2011;4:37-39.

12. Aristotle S, Sundarapandian, Felicia C. Anatomical study of variations in the blood supply of kidneys. J Clin Diagn Res. 2013;7(8):1555-1557. doi: 10.7860/JCDR/2013/6230.3203.

13. Munn S, Cari. The CARI guidelines. Assessment of donor kidney anatomy. Nephrology. 2010;15(Suppl1):S96-98. doi: 10.1111/j.1440-1797.2009.01215.x.

14. Granata A, Fiorini F, Andrulli S, et al. Doppler ultrasound and renal artery stenosis: An overview. J Ultrasound. 2009;12(4):133-143. doi: 10.1016/j.jus.2009.09.006.


Supplementary files

1. Fig. CT of the renal vessels with contrast
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Type Исследовательские инструменты
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Markova T.N., Parshin V.V., Mishchenko N.K. Secondary hyperaldosteronism, caused by abnormalities of the renal vessels, in clinical endocrinologist. Endocrine Surgery. 2016;10(1):28-34. (In Russ.)

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ISSN 2306-3513 (Print)
ISSN 2310-3965 (Online)