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1

Freel, Ellen Marie. "Primary Aldosteronism or Not Primary Aldosteronism." Hypertension 69, no. 5 (May 2017): 780–81. http://dx.doi.org/10.1161/hypertensionaha.117.09050.

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2

Funder, John W. "Primary Aldosteronism." Hypertension 77, no. 3 (March 3, 2021): 900–903. http://dx.doi.org/10.1161/hypertensionaha.120.16585.

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3

Subbarao, Kakarla. "Primary Aldosteronism." Hypertension Journal 2, no. 3 (2016): 178–79. http://dx.doi.org/10.5005/jp-journals-10043-0051.

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4

Wrenn, Sean M., Anand Vaidya, and Carrie C. Lubitz. "Primary aldosteronism." Gland Surgery 9, no. 1 (February 2020): 14–24. http://dx.doi.org/10.21037/gs.2019.10.23.

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5

Bravo, Emmanuel L. "Primary Aldosteronism." Urologic Clinics of North America 16, no. 3 (August 1989): 481–86. http://dx.doi.org/10.1016/s0094-0143(21)01830-9.

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6

Ghannam, Nadia. "Primary Aldosteronism." Annals of Saudi Medicine 5, no. 1 (January 1985): 51–53. http://dx.doi.org/10.5144/0256-4947.1985.51.

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7

HELLEM, ARVID J. "Primary Aldosteronism." Acta Medica Scandinavica 155, no. 4 (April 24, 2009): 271–74. http://dx.doi.org/10.1111/j.0954-6820.1956.tb14374.x.

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8

Pillai, Padma Raghavan, Mindy Griffith, Monica D. Schwarcz, and Irene A. Weiss. "Primary Aldosteronism." Cardiology in Review 28, no. 2 (2020): 84–91. http://dx.doi.org/10.1097/crd.0000000000000281.

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9

Lo, Chung Yau, Po Chor Tam, Annie W. C. Kung, Karen S. L. Lam, and John Wong. "Primary Aldosteronism." Annals of Surgery 224, no. 2 (August 1996): 125–30. http://dx.doi.org/10.1097/00000658-199608000-00003.

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10

YOUNG, WILLIAM F. "Primary Aldosteronism." Cardiology in Review 7, no. 4 (July 1999): 207–14. http://dx.doi.org/10.1097/00045415-199907000-00012.

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11

Stowasser, Michael, Richard D. Gordon, Terry J. Tunny, Shelley A. Klemm, Wendy L. Finn, and Anton L. Krek. "Primary aldosteronism." Journal of Hypertension 9, no. 6 (December 1991): S266. http://dx.doi.org/10.1097/00004872-199112000-00116.

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12

Stowasser, Michael, Richard D. Gordon, Terry J. Tunny, Shelley A. Klemm, Wendy L. Finn, and Anton L. Krek. "Primary aldosteronism." Journal of Hypertension 9 (1991): S266. http://dx.doi.org/10.1097/00004872-199112006-00116.

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13

Byrd, James Brian, Adina F. Turcu, and Richard J. Auchus. "Primary Aldosteronism." Circulation 138, no. 8 (August 21, 2018): 823–35. http://dx.doi.org/10.1161/circulationaha.118.033597.

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14

YOUNG, WILLIAM F. "Primary Aldosteronism." Annals of the New York Academy of Sciences 970, no. 1 (September 2002): 61–76. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04413.x.

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15

Ganguly, Arunabha. "Primary Aldosteronism." New England Journal of Medicine 339, no. 25 (December 17, 1998): 1828–34. http://dx.doi.org/10.1056/nejm199812173392507.

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16

Gomez-Sanchez, Celso E. "Primary Aldosteronism." Hypertension 63, no. 4 (April 2014): 668–69. http://dx.doi.org/10.1161/hypertensionaha.113.02335.

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17

Funder, John W. "Primary Aldosteronism." Hypertension 74, no. 3 (September 2019): 458–66. http://dx.doi.org/10.1161/hypertensionaha.119.12935.

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18

Yang, Yuhong, Celso E. Gomez-Sanchez, Diana Jaquin, Elke Tatjana Aristizabal Prada, Lucie S. Meyer, Thomas Knösel, Holger Schneider, Felix Beuschlein, Martin Reincke, and Tracy Ann Williams. "Primary Aldosteronism." Hypertension 74, no. 4 (October 2019): 809–16. http://dx.doi.org/10.1161/hypertensionaha.119.13476.

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19

Funder, John W. "Primary Aldosteronism." Hypertension 76, no. 2 (August 2020): 325–26. http://dx.doi.org/10.1161/hypertensionaha.120.15456.

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20

Stowasser, Michael, and Richard D. Gordon. "Primary aldosteronism." Best Practice & Research Clinical Endocrinology & Metabolism 17, no. 4 (December 2003): 591–605. http://dx.doi.org/10.1016/s1521-690x(03)00050-2.

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21

Corry, Dalila B., and Michael L. Tuck. "Secondary Aldosteronism." Endocrinology and Metabolism Clinics of North America 24, no. 3 (September 1995): 511–30. http://dx.doi.org/10.1016/s0889-8529(18)30029-x.

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22

Litchfield, W. Reid, and Robert G. Dluhy. "Primary Aldosteronism." Endocrinology and Metabolism Clinics of North America 24, no. 3 (September 1995): 593–612. http://dx.doi.org/10.1016/s0889-8529(18)30033-1.

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23

Young, William F., and George G. Klee. "Primary Aldosteronism." Endocrinology and Metabolism Clinics of North America 17, no. 2 (June 1988): 367–95. http://dx.doi.org/10.1016/s0889-8529(18)30425-0.

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24

Travers, S., A. Blanchard, E. Cornu, C. Faucard, L. Baffalie, M. Azizi, P. Houillier, L. Amar, and S. Baron. "PRIMARY ALDOSTERONISM." Journal of Hypertension 37 (July 2019): e30. http://dx.doi.org/10.1097/01.hjh.0000570660.50840.c1.

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25

Pego, M., J. Maldonado, B. Ponces, F. Alves, P. Almeida, F. J. Oliveira, and E. Castro Sousa. "PRIMARY ALDOSTERONISM." Journal of Hypertension 18 (June 2000): S34. http://dx.doi.org/10.1097/00004872-200006001-00103.

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26

Stowasser, Michael, and Richard D. Gordon. "Primary aldosteronism." Journal of Hypertension 18, no. 9 (September 2000): 1165–76. http://dx.doi.org/10.1097/00004872-200018090-00002.

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27

Stewart, Paul, and William Young. "Primary Aldosteronism." Journal of Clinical Endocrinology & Metabolism 92, no. 12 (December 1, 2007): E1. http://dx.doi.org/10.1210/jcem.92.12.9996.

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28

Ansari, Azam. "Primary aldosteronism." Lancet 360, no. 9333 (August 2002): 617. http://dx.doi.org/10.1016/s0140-6736(02)09785-4.

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29

Bravo, Emmanuel L. "Primary Aldosteronism." Cardiology Clinics 6, no. 4 (November 1988): 509–15. http://dx.doi.org/10.1016/s0733-8651(18)30473-9.

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30

Galati, Sandi-Jo. "Primary Aldosteronism." Endocrinology and Metabolism Clinics of North America 44, no. 2 (June 2015): 355–69. http://dx.doi.org/10.1016/j.ecl.2015.02.010.

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31

Rossi, Gian Paolo. "Primary Aldosteronism." Journal of the American College of Cardiology 74, no. 22 (December 2019): 2799–811. http://dx.doi.org/10.1016/j.jacc.2019.09.057.

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32

Shuto, Yujin. "Primary Aldosteronism." Journal of Nippon Medical School 68, no. 5 (2001): 447–49. http://dx.doi.org/10.1272/jnms.68.447.

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33

Wu, Vin-Cent, Chin-Chi Kuo, Shuo-Meng Wang, Kao-Lang Liu, Kuo-How Huang, Yen-Hung Lin, Tzong-Shinn Chu, et al. "Primary aldosteronism." Journal of Hypertension 29, no. 9 (September 2011): 1778–86. http://dx.doi.org/10.1097/hjh.0b013e3283495cbb.

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34

Kaplan, Norman M. "Primary aldosteronism." Journal of Hypertension 30, no. 10 (October 2012): 1899–902. http://dx.doi.org/10.1097/hjh.0b013e3283559a03.

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35

LINS, PER-ERIC, and ULF ADAMSON. "Primary Aldosteronism." Acta Medica Scandinavica 221, no. 3 (April 24, 2009): 275–82. http://dx.doi.org/10.1111/j.0954-6820.1987.tb00894.x.

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36

Kim, Sang Wan. "Primary Aldosteronism." Korean Journal of Medicine 82, no. 4 (2012): 396. http://dx.doi.org/10.3904/kjm.2012.82.4.396.

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37

Carey, Robert M. "Primary Aldosteronism." Hormone Research in Paediatrics 71, no. 1 (2009): 8–12. http://dx.doi.org/10.1159/000178029.

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38

Bergman, B. O. "Primary aldosteronism." Urology 35, no. 5 (May 1990): 393–98. http://dx.doi.org/10.1016/0090-4295(90)80079-3.

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39

Gordon, R. D. "Primary aldosteronism." Journal of Endocrinological Investigation 18, no. 7 (July 1995): 495–511. http://dx.doi.org/10.1007/bf03349761.

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40

Pitt, Bertram, and James Brian Byrd. "Primary Aldosteronism." JACC: Cardiovascular Imaging 13, no. 10 (October 2020): 2160–61. http://dx.doi.org/10.1016/j.jcmg.2020.06.025.

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41

Satoh, Fumitoshi, Ryo Morimoto, Yoshitsugu Iwakura, Yoshikiyo Ono, Masataka Kudo, Kei Takase, and Sadayoshi Ito. "Primary aldosteronism." Reviews in Endocrine and Metabolic Disorders 12, no. 1 (February 9, 2011): 11–14. http://dx.doi.org/10.1007/s11154-011-9161-9.

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42

Gröndal, S., and B. Hamberger. "Primary aldosteronism." British Journal of Surgery 79, no. 6 (June 1992): 484–85. http://dx.doi.org/10.1002/bjs.1800790604.

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43

Auchus, Richard J., and Fiemu E. Nwariaku. "Primary aldosteronism." Current Cardiology Reports 9, no. 6 (November 2007): 447–52. http://dx.doi.org/10.1007/bf02938388.

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44

Carey, Robert M. "Primary aldosteronism." Journal of Surgical Oncology 106, no. 5 (July 17, 2012): 575–79. http://dx.doi.org/10.1002/jso.23206.

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45

Moraitis, Andreas, and Constantine Stratakis. "Adrenocortical Causes of Hypertension." International Journal of Hypertension 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/624691.

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Primary aldosteronism is the most common cause of secondary hypertension. In the past, screening for primary aldosteronism was offered only in patients with hypertension associated with hypokalemia. Recent studies showed that hypokalemia is seen in only 25% of the patients with primary aldosteronism, which has increased the prevalence of primary aldosteronism to 10–15% of all cases with new onset hypertension.
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46

Hundemer, Gregory L., and Anand Vaidya. "MANAGEMENT OF ENDOCRINE DISEASE: The role of surgical adrenalectomy in primary aldosteronism." European Journal of Endocrinology 183, no. 6 (December 2020): R185—R196. http://dx.doi.org/10.1530/eje-20-0863.

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Primary aldosteronism is common and contributes to adverse cardiovascular, kidney, and metabolic outcomes. When instituted early and effectively, targeted therapies can mitigate these adverse outcomes. Surgical adrenalectomy is among the most effective treatments because it has the potential to cure, or attenuate the severity of, pathologic aldosterone excess, resulting in a host of biochemical and clinical changes that improve health outcomes. Herein, we review the role of surgical adrenalectomy in primary aldosteronism while emphasizing the physiologic ramifications of surgical intervention, and compare these to other targeted medical therapies for primary aldosteronism. We specifically review the role of curative adrenalectomy for unilateral primary aldosteronism, the role of non-curative adrenalectomy for bilateral primary aldosteronism, and how these interventions influence biochemical and clinical outcomes in relation to medical therapies for primary aldosteronism.
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47

Gomez-Sanchez, Celso E. "Guía para el manejo del Aldosteronismo Primario." Diagnóstico 61, no. 1 (March 14, 2022): e350. http://dx.doi.org/10.33734/diagnostico.v61i1.350.

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El aldosteronismo primario es la causa de hipertensión secundaria más común que afecta entre 5-24% de los pacientes con hipertensión arterial y está asociada a un incremento de la morbilidad cardiovascular, cerebrovascular y renal comparada con pacientes con hipertensión primaria. El diagnóstico depende de la demostración de una elevación autónoma de la secreción de aldosterona con respecto a un aumento de la ingesta de sal y que no responde al sistema renina-angiotensina. Las causas más comunes del aldosteronism primario son debidos a un adenoma adrenal productor de aldosterona, hiperplasia bilateral idiopática y menos comunes son la hiperplasia unilateral idiopática y el carcinoma adrenal causante de aldosteronismo. El diagnóstico diferencial es realizado usando una tomografía adrenal y especialmente con el muestreo de las venas adrenales. El tratamiento de adenomas es por una adrenalectomíalaparoscópica y en el caso del aldosteronismo bilateral idiopático tratamiento médico con bloqueadores del receptor mineralocorticoide (espirolactonas o eplerenona).
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48

Schirpenbach, Caroline, Lysann Seiler, Christiane Maser-Gluth, Frank Rüdiger, Christian Nickel, Felix Beuschlein, and Martin Reincke. "Confirmatory testing in normokalaemic primary aldosteronism: the value of the saline infusion test and urinary aldosterone metabolites." European Journal of Endocrinology 154, no. 6 (June 2006): 865–73. http://dx.doi.org/10.1530/eje.1.02164.

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Objective: Primary aldosteronism has recently been recognized as the most frequent cause of secondary hypertension. Since most patients are normokalaemic, differentiation to essential hypertension is challenging. As differentiation by baseline aldosterone/renin ratio may be insufficient, diagnosis should be confirmed by additional tests. However, as most confirmatory tests have been evaluated in hypokalaemic primary aldosteronism only, we reassessed the value of the saline infusion test and 24 h urinary aldosterone metabolites as confirmatory tests for both normo- and hypokalaemic primary aldosteronism under current antihypertensive medication. Patients and methods: 25 patients with primary aldosteronism (11 hypokalaemic, 14 normokalaemic), 29 patients with essential hypertension and 47 normotensive subjects were studied. The hypertensives received their usual medication with the exception of spironolactone. All subjects underwent a standard saline infusion test (determination of plasma aldosterone before and after 2.0 liters of isotonic saline for 4 hours i.v.) and collected a 24 h urine sample for examination of urinary tetrahydroaldosterone and aldosterone-18-glucuronide. Results: In hypokalaemic primary aldosteronism the saline infusion test showed a reasonable sensitivity (91%) and specificity (90%). However, the test failed to differentiate sufficiently between essential hypertension and normokalaemic primary aldosteronism (sensitivity 57%, specificity 90%). Similarly, urinary tetrahydroaldosterone had higher sensitivity in hypokalaemic than in normokalaemic primary aldosteronism (sensitivity 64% vs 36%, specificity 100%), whereas for aldosterone-18-glucuronide, no differences in hypo- and normokalaemic primary aldosteronism were found (sensitivity 45% and 43%, specificity 100%). Conclusions: These data show that the saline infusion test as an established test in classical hypokalaemic primary aldosteronism is not a reliable test in the normokalaemic variant of the disease. Due to its low accuracy, determination of urinary aldosterone metabolites did not prove useful in confirming either normo- or hypokalaemic patients. We conclude from our data that these tests should not be used as confirmatory testing in the normokalaemic variant of primary aldosteronism.
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49

Vaidya, Anand, and Robert M. Carey. "Evolution of the Primary Aldosteronism Syndrome: Updating the Approach." Journal of Clinical Endocrinology & Metabolism 105, no. 12 (August 31, 2020): 3771–83. http://dx.doi.org/10.1210/clinem/dgaa606.

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Abstract Context New approaches are needed to address the evolution of the primary aldosteronism syndrome and to increase its recognition. Herein, we review evidence indicating that primary aldosteronism is a prevalent syndrome that is mostly unrecognized, and present a pragmatic and pathophysiology-based approach to improve diagnosis and treatment. Methods Evidence was gathered from published guidelines and studies identified from PubMed by searching for primary aldosteronism, aldosterone, renin, and hypertension. This evidence was supplemented by the authors’ personal knowledge, research experience, and clinical encounters in primary aldosteronism. Interpretation of Evidence Renin-independent aldosterone production is a prevalent phenotype that is diagnosed as primary aldosteronism when severe in magnitude, but is largely unrecognized when milder in severity. Renin-independent aldosterone production can be detected in normotensive and hypertensive individuals, and the magnitude of this biochemical phenotype parallels the magnitude of blood pressure elevation, the risk for incident hypertension and cardiovascular disease, and the likelihood and magnitude of blood pressure reduction with mineralocorticoid receptor antagonist therapy. Expansion of the indications to screen for primary aldosteronism, combined with the use of a pathophysiology-based approach that emphasizes inappropriate aldosterone production in the context of renin suppression, will substantially increase the diagnostic and therapeutic yields for primary aldosteronism. Conclusions The landscape of primary aldosteronism has evolved to recognize that it is a prevalent syndrome of renin-independent aldosterone production that contributes to the pathogenesis of hypertension and cardiovascular disease. Expanding screening indications and simplifying the diagnostic approach will enable implementation of targeted treatment for primary aldosteronism.
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50

Stavropoulos, Konstantinos, Konstantinos Imprialos, Vasilios Papademetriou, Charles Faselis, Kostas Tsioufis, Kyriakos Dimitriadis, and Michael Doumas. "Primary Aldosteronism: Novel Insights." Current Hypertension Reviews 16, no. 1 (February 13, 2020): 19–23. http://dx.doi.org/10.2174/1573402115666190415155512.

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Background: Primary aldosteronism is one of the most common causes of secondary hypertension. Patients with this endocrine syndrome are at increased cardiovascular risk, higher than hypertensive individuals with equal blood pressure levels. Objectives: The study aimed to thoroughly present and critically discuss the novel insights into the field of primary aldosteronism, focusing on the clinically meaningful aspects. Method: We meticulously evaluated existing data in the field of primary aldosteronism in order to summarize future perspectives in this narrative review. Results: Novel data suggests that a subclinical form of primary aldosteronism might exist. Interesting findings might simplify the diagnostic procedure of the disease, especially for the localization of primary aldosteronism. The most promising progress has been noted in the field of the molecular basis of the disease, suggesting new potential therapeutic targets. Conclusion: Several significant aspects are at early stages of evaluation. Future research is essential to investigate these well-promising perspectives.
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