Sections

Medication

Medication Summary

Aldosterone antagonists are indicated for the treatment of hyperaldosteronism. Hypokalemia and hypertension are also addressed with medications as needed.

Class Summary

Aldosterone antagonists are used to lower the blood pressure, normalize serum potassium, and minimize postoperative hypoaldosteronism.

Spironolactone (Aldactone)

View full drug information

Spironolactone is the agent most commonly used to treat hyperaldosteronism because it directly antagonizes aldosterone effects at the distal tubule.

Eplerenone (Inspra)

View full drug information

Weaker than spironolactone but with very little cross-reactivity with the androgen receptor. The drug usually is given twice a day.

Class Summary

Management of hypokalemia associated with hyperaldosteronism when spironolactone is contraindicated.

Triamterene inhibits reabsorption of sodium ions in exchange for potassium and hydrogen ions at the segment of the distal tubule that is under the control of adrenal mineralocorticoids (especially aldosterone). This activity is not directly related to aldosterone secretion or antagonism, and it is a result of a direct effect on the renal tubule.

The fraction of filtered sodium reaching this distal tubular exchange site is relatively small, and the amount that is exchanged depends on the level of mineralocorticoid activity; thus, the degree of natriuresis and diuresis produced by inhibition of the exchange mechanism is necessarily limited.

Increasing the amount of available sodium and the level of mineralocorticoid activity by using more proximally acting diuretics increases the degree of diuresis and potassium conservation. Triamterene may occasionally cause increases in serum potassium, which can result in hyperkalemia. It does not produce alkalosis, because it does not cause excessive excretion of titratable acid and ammonium.

Amiloride

View full drug information

Amiloride is an antikaliuretic drug with weak natriuretic, diuretic, and antihypertensive activity. It decreases the enhanced urinary excretion of magnesium that occurs when a thiazide or loop diuretic is used alone. It exerts a potassium-conserving effect in patients receiving kaliuretic diuretic agents.

Class Summary

Treatment of hypertension should be designed to lower blood pressure and reduce other risk factors of coronary heart disease. Pharmacologic therapy should be individualized on the basis of the patient’s age, race, known pathophysiologic variables, and concurrent conditions. Treatment should be aimed not only at lowering blood pressure safely and effectively but also at preventing or reversing hyperlipidemia, glucose intolerance, and left ventricular hypertrophy.

Nifedipine (Adalat, Procardia XL, Nifedical XL, Nifediac CC)

View full drug information

Nifedipine is a calcium channel blocker that produces vasodilation with antianginal and antihypertensive effects. It is available in both short-acting and sustained-release preparations.

Nifedipine acts by blocking postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the activation of adenosine triphosphatase (ATPase) on myofibril contraction. The overall effect is reduced intracellular calcium levels in cardiac and smooth muscle cells of the coronary and peripheral vasculature, resulting in dilatation of coronary and peripheral arteries.

Amlodipine (Norvasc)

View full drug information

Amlodipine is a calcium channel blocker that produces vasodilation with antianginal and antihypertensive effects. It acts by blocking the postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the activation of ATPase on myofibril contraction. The overall effect is reduced intracellular calcium levels in cardiac and smooth muscle cells of the coronary and peripheral vasculature, resulting in dilatation of coronary and peripheral arteries.

Diltiazem (Cardizem, Cardizem CD, Dilacor XR, Tiazac)

View full drug information

During depolarization, diltiazem inhibits calcium ions from entering the slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It is a nondihydropyridine appropriate for prophylaxis of variant angina.

Nicardipine (Cardene)

View full drug information

Nicardipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.

Verapamil (Calan, Calan SR, Covera HS, Isoptin, Verelan)

View full drug information

Verapamil is a nondihydropyridine that is appropriate for prophylaxis of variant angina. During depolarization, verapamil inhibits the entry of calcium ions into slow channels or voltage-sensitive areas of the vascular smooth muscle and myocardium.

Doxazosin (Cardura, Cardura XL)

View full drug information

Doxazosin is an alpha1-adrenergic antagonist, which causes vasodilation of veins and arterioles. These effects result in decreased peripheral resistance and blood pressure.

Prazosin (Minipress)

View full drug information

Prazosin is a postsynaptic alpha1-adrenergic antagonist. It causes vasodilation of veins and arterioles. These effects result in decreased peripheral resistance and blood pressure.

Follow-up

Dominguez A, Muppidi V, Gupta S. Hyperaldosteronism. StatPearls. 2020 Jan. [QxMD MEDLINE Link]. [Full Text].
Cobb A, Aeddula NR. Primary Hyperaldosteronism. StatPearls. 2020 Jan. [QxMD MEDLINE Link]. [Full Text].
Kasifoglu T, Akalin A, Cansu DU, Korkmaz C. Hypokalemic paralysis due to primary hyperaldosteronism simulating Gitelman's syndrome. Saudi J Kidney Dis Transpl. 2009 Mar. 20(2):285-7. [QxMD MEDLINE Link].
Korzynska W, Jodkowska A, Gosławska K, Bogunia-Kubik K, Mazur G. Genetic aspects of primary hyperaldosteronism. Adv Clin Exp Med. 2018 Aug. 27 (8):1149-1158. [QxMD MEDLINE Link]. [Full Text].
Aronova A, Iii TJ, Zarnegar R. Management of hypertension in primary aldosteronism. World J Cardiol. 2014 May 26. 6(5):227-33. [QxMD MEDLINE Link]. [Full Text].
Weisbrod AB, Webb RC, Mathur A, Barak S, Abraham SB, Nilubol N, et al. Adrenal histologic findings show no difference in clinical presentation and outcome in primary hyperaldosteronism. Ann Surg Oncol. 2013 Mar. 20(3):753-8. [QxMD MEDLINE Link]. [Full Text].
Funder JW. The genetic basis of primary aldosteronism. Curr Hypertens Rep. 2012 Apr. 14(2):120-4. [QxMD MEDLINE Link].
Lifton RP, Dluhy RG, Powers M, Rich GM, Cook S, Ulick S, et al. A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature. 1992 Jan 16. 355(6357):262-5. [QxMD MEDLINE Link].
Torpy DJ, Gordon RD, Lin JP, Huggard PR, Taymans SE, Stowasser M, et al. Familial hyperaldosteronism type II: description of a large kindred and exclusion of the aldosterone synthase (CYP11B2) gene. J Clin Endocrinol Metab. 1998 Sep. 83(9):3214-8. [QxMD MEDLINE Link].
Lafferty AR, Torpy DJ, Stowasser M, Taymans SE, Lin JP, Huggard P, et al. A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 (7p22). J Med Genet. 2000 Nov. 37(11):831-5. [QxMD MEDLINE Link]. [Full Text].
Choi M, Scholl UI, Yue P, Björklund P, Zhao B, Nelson-Williams C, et al. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Science. 2011 Feb 11. 331(6018):768-72. [QxMD MEDLINE Link]. [Full Text].
Scholl UI, Nelson-Williams C, Yue P, Grekin R, Wyatt RJ, Dillon MJ, et al. Hypertension with or without adrenal hyperplasia due to different inherited mutations in the potassium channel KCNJ5. Proc Natl Acad Sci U S A. 2012 Feb 14. 109(7):2533-8. [QxMD MEDLINE Link]. [Full Text].
Charmandari E, Sertedaki A, Kino T, Merakou C, Hoffman DA, Hatch MM, et al. A novel point mutation in the KCNJ5 gene causing primary hyperaldosteronism and early-onset autosomal dominant hypertension. J Clin Endocrinol Metab. 2012 Aug. 97(8):E1532-9. [QxMD MEDLINE Link]. [Full Text].
Boulkroun S, Beuschlein F, Rossi GP, Golib-Dzib JF, Fischer E, Amar L, et al. Prevalence, clinical, and molecular correlates of KCNJ5 mutations in primary aldosteronism. Hypertension. 2012 Mar. 59(3):592-8. [QxMD MEDLINE Link].
Taguchi R, Yamada M, Nakajima Y, Satoh T, Hashimoto K, Shibusawa N, et al. Expression and mutations of KCNJ5 mRNA in Japanese patients with aldosterone-producing adenomas. J Clin Endocrinol Metab. 2012 Apr. 97(4):1311-9. [QxMD MEDLINE Link].
Monticone S, Hattangady NG, Nishimoto K, Mantero F, Rubin B, Cicala MV, et al. Effect of KCNJ5 mutations on gene expression in aldosterone-producing adenomas and adrenocortical cells. J Clin Endocrinol Metab. 2012 Aug. 97(8):E1567-72. [QxMD MEDLINE Link]. [Full Text].
Azizan EA, Lam BY, Newhouse SJ, Zhou J, Kuc RE, Clarke J, et al. Microarray, qPCR, and KCNJ5 sequencing of aldosterone-producing adenomas reveal differences in genotype and phenotype between zona glomerulosa- and zona fasciculata-like tumors. J Clin Endocrinol Metab. 2012 May. 97(5):E819-29. [QxMD MEDLINE Link].
Al-Salameh A, Cohen R, Desailloud R. Overview of the genetic determinants of primary aldosteronism. Appl Clin Genet. 2014. 7:67-79. [QxMD MEDLINE Link]. [Full Text].
Markou A, Sertedaki A, Kaltsas G, et al. Stress-induced Aldosterone Hyper-Secretion in a Substantial Subset of Patients With Essential Hypertension. J Clin Endocrinol Metab. 2015 Aug. 100 (8):2857-64. [QxMD MEDLINE Link]. [Full Text].
Escher G. Hyperaldosteronism in pregnancy. Ther Adv Cardiovasc Dis. 2009 Apr. 3(2):123-32. [QxMD MEDLINE Link].
Fuller PJ. Adrenal Diagnostics: An Endocrinologist's Perspective focused on Hyperaldosteronism. Clin Biochem Rev. 2013 Nov. 34(3):111-6. [QxMD MEDLINE Link]. [Full Text].
Prejbisz A, Warchol-Celinska E, Lenders JW, Januszewicz A. Cardiovascular Risk in Primary Hyperaldosteronism. Horm Metab Res. 2015 Dec. 47 (13):973-80. [QxMD MEDLINE Link].
Holland OB, Brown H, Kuhnert L, Fairchild C, Risk M, Gomez-Sanchez CE. Further evaluation of saline infusion for the diagnosis of primary aldosteronism. Hypertension. 1984 Sep-Oct. 6(5):717-23. [QxMD MEDLINE Link].
Ignatowska-Switalska H, Chodakowska J, Januszewicz W, Feltynowski T, Adamczyk M, Lewandowski J. Evaluation of plasma aldosterone to plasma renin activity ratio in patients with primary aldosteronism. J Hum Hypertens. 1997 Jun. 11(6):373-8. [QxMD MEDLINE Link].
Galati SJ, Hopkins SM, Cheesman KC, Zhuk RA, Levine AC. Primary aldosteronism: emerging trends. Trends Endocrinol Metab. 2013 Sep. 24(9):421-30. [QxMD MEDLINE Link].
Guichard JL, Clark D 3rd, Calhoun DA, Ahmed MI. Aldosterone receptor antagonists: current perspectives and therapies. Vasc Health Risk Manag. 2013. 9:321-31. [QxMD MEDLINE Link]. [Full Text].
Weiner ID. Endocrine and hypertensive disorders of potassium regulation: primary aldosteronism. Semin Nephrol. 2013 May. 33(3):265-76. [QxMD MEDLINE Link]. [Full Text].
Harvey AM. Hyperaldosteronism: diagnosis, lateralization, and treatment. Surg Clin North Am. 2014 Jun. 94(3):643-56. [QxMD MEDLINE Link].
Lai S, Petramala L, Mastroluca D, et al. Hyperaldosteronism and cardiovascular risk in patients with autosomal dominant polycystic kidney disease. Medicine (Baltimore). 2016 Jul. 95 (29):e4175. [QxMD MEDLINE Link].
Rossi GP, Cesari M, Cuspidi C, Maiolino G, Cicala MV, Bisogni V, et al. Long-term control of arterial hypertension and regression of left ventricular hypertrophy with treatment of primary aldosteronism. Hypertension. 2013 Jul. 62(1):62-9. [QxMD MEDLINE Link].
Fourkiotis V, Vonend O, Diederich S, Fischer E, Lang K, Endres S, et al. Effectiveness of eplerenone or spironolactone treatment in preserving renal function in primary aldosteronism. Eur J Endocrinol. 2013 Jan. 168(1):75-81. [QxMD MEDLINE Link].
Rossi GP, Maiolino G, Flego A, et al. Adrenalectomy Lowers Incident Atrial Fibrillation in Primary Aldosteronism Patients at Long Term. Hypertension. 2018 Apr. 71 (4):585-591. [QxMD MEDLINE Link]. [Full Text].
Künzel HE. Psychopathological symptoms in patients with primary hyperaldosteronism--possible pathways. Horm Metab Res. 2012 Mar. 44(3):202-7. [QxMD MEDLINE Link].
Schmiemann G, Gebhardt K, Hummers-Pradier E, Egidi G. Prevalence of hyperaldosteronism in primary care patients with resistant hypertension. J Am Board Fam Med. 2012 Jan-Feb. 25(1):98-103. [QxMD MEDLINE Link].
Kumar B, Swee M. Aldosterone-renin ratio in the assessment of primary aldosteronism. JAMA. 2014 Jul. 312(2):184-5. [QxMD MEDLINE Link].
Gouli A, Kaltsas G, Tzonou A, Markou A, Androulakis II, Ragkou D, et al. High prevalence of autonomous aldosterone secretion among patients with essential hypertension. Eur J Clin Invest. 2011 Nov. 41(11):1227-36. [QxMD MEDLINE Link].
Lucatello B, Benso A, Tabaro I, Capello E, Caprino MP, Marafetti L, et al. Long-term re-evaluation of primary aldosteronism after medical treatment reveals high proportion of normal mineralocorticoid secretion. Eur J Endocrinol. 2013 Apr. 168(4):525-32. [QxMD MEDLINE Link].
Wu CH, Yang YW, Hu YH, Tsai YC, Kuo KL, Lin YH, et al. Comparison of 24-h urinary aldosterone level and random urinary aldosterone-to-creatinine ratio in the diagnosis of primary aldosteronism. PLoS One. 2013. 8(6):e67417. [QxMD MEDLINE Link]. [Full Text].
Piaditis GP, Kaltsas GA, Androulakis II, Gouli A, Makras P, Papadogias D, et al. High prevalence of autonomous cortisol and aldosterone secretion from adrenal adenomas. Clin Endocrinol (Oxf). 2009 Dec. 71(6):772-8. [QxMD MEDLINE Link].
Gordon RD. Primary aldosteronism. J Endocrinol Invest. 1995 Jul-Aug. 18(7):495-511. [QxMD MEDLINE Link].
Gordon RD, Stowasser M, Klemm SA, Tunny TJ. Primary aldosteronism--some genetic, morphological, and biochemical aspects of subtypes. Steroids. 1995 Jan. 60(1):35-41. [QxMD MEDLINE Link].
Markou A, Pappa T, Kaltsas G, Gouli A, Mitsakis K, Tsounas P, et al. Evidence of primary aldosteronism in a predominantly female cohort of normotensive individuals: a very high odds ratio for progression into arterial hypertension. J Clin Endocrinol Metab. 2013 Apr. 98(4):1409-16. [QxMD MEDLINE Link].
Papanastasiou L, Markou A, Pappa T, Gouli A, Tsounas P, Fountoulakis S, et al. Primary aldosteronism in hypertensive patients: clinical implications and target therapy. Eur J Clin Invest. 2014 Aug. 44(8):697-706. [QxMD MEDLINE Link].
Mussa A, Camilla R, Monticone S, Porta F, Tessaris D, Verna F, et al. Polyuric-polydipsic syndrome in a pediatric case of non-glucocorticoid remediable familial hyperaldosteronism. Endocr J. 2012 Jun 30. 59(6):497-502. [QxMD MEDLINE Link].
Rossi GP, Auchus RJ, Brown M, Lenders JW, Naruse M, Plouin PF, et al. An expert consensus statement on use of adrenal vein sampling for the subtyping of primary aldosteronism. Hypertension. 2014 Jan. 63(1):151-60. [QxMD MEDLINE Link].
Rossitto G, Regolisti G, Rossi E, Negro A, Nicoli D, Casali B, et al. Elevation of angiotensin-II type-1-receptor autoantibodies titer in primary aldosteronism as a result of aldosterone-producing adenoma. Hypertension. 2013 Feb. 61(2):526-33. [QxMD MEDLINE Link].
Di Martino M, Garcia Sanz I, Munoz de Nova JL, Marin Campos C, Martinez Martin M, Dominguez Gadea L. NP-59 test for preoperative localization of primary hyperaldosteronism. Langenbecks Arch Surg. 2017 Mar. 402 (2):303-8. [QxMD MEDLINE Link].
Spyridonidis TJ, Apostolopoulos DJ. Is there a role for Nuclear Medicine in diagnosis and management of patients with primary aldosteronism?. Hell J Nucl Med. 2013 May-Aug. 16(2):134-9. [QxMD MEDLINE Link].
Chen Cardenas SM, Santhanam P. ¹¹C-metomidate PET in the diagnosis of adrenal masses and primary aldosteronism: a review of the literature. Endocrine. 2020 Sep 4. [QxMD MEDLINE Link].
Feldman RD. Aldosterone and blood pressure regulation: recent milestones on the long and winding road from electrocortin to KCNJ5, GPER, and beyond. Hypertension. 2014 Jan. 63(1):19-21. [QxMD MEDLINE Link].
Scholl UI, Goh G, Stölting G, de Oliveira RC, Choi M, Overton JD, et al. Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism. Nat Genet. 2013 Sep. 45(9):1050-4. [QxMD MEDLINE Link]. [Full Text].
Cerny MA. Progress towards clinically useful aldosterone synthase inhibitors. Curr Top Med Chem. 2013. 13(12):1385-401. [QxMD MEDLINE Link].
Araujo-Castro M, Paja Fano M, Gonzalez Boillos M, et al. Evolution of the cardiometabolic profile of primary hyperaldosteronism patients treated with adrenalectomy and with mineralocorticoid receptor antagonists: results from the SPAIN-ALDO Registry. Endocrine. 2022 Jun. 76 (3):687-96. [QxMD MEDLINE Link].
Sacks BA, Sacks AC, Faintuch S. Radiofrequency ablation treatment for aldosterone-producing adenomas. Curr Opin Endocrinol Diabetes Obes. 2017 Feb 28. [QxMD MEDLINE Link].
Uppot RN, Gervais DA. Imaging-guided adrenal tumor ablation. AJR Am J Roentgenol. 2013 Jun. 200(6):1226-33. [QxMD MEDLINE Link].
Spence JD. Diagnosis of primary aldosteronism: for medical management, not just surgery. J Hypertens. 2009 Jan. 27(1):204-5; author reply 205. [QxMD MEDLINE Link].
Hu YH, Wu CH, Er LK, Lin CD, Liu YB, Chueh SC, et al. Laparoendoscopic single-site adrenalectomy in patients with primary hyperaldosteronism: A prospective study with long-term follow up. Asian J Surg. 2015 Nov 25. [QxMD MEDLINE Link].
Korah HE, Scholl UI. An Update on Familial Hyperaldosteronism. Horm Metab Res. 2015 Oct 7. [QxMD MEDLINE Link].

Media Gallery

Steroid biosynthetic pathway.
Physiologic regulation of the renin-angiotensin-aldosterone axis.

of 2

Table 1. Factors affecting interpretation of ARR results

False Negative Results
Factor	Aldosterone	Renin	ARR
Medications
K-sparing diuretics	↑	↑↑	↓
K-wasting diuretics (Non-K-sparing diuretics, such as thiazides, induce renal potassium losses and reduce plasma potassium concentrations, leading to decreased aldosterone secretion.)	→↑	↑↑	↓
ACE inhibitors	↓	↑↑	↓
Angiotensin receptor blockers	↓	↑↑	↓
DHPs (It is a shared opinion that dihydropyridinic calcium channel blockers do not significantly affect aldosterone secretion, mainly causing an increase in PRA, which rarely gives false negatives.)	→↓	↑	↓
Other conditions
Hypokalemia	↓	→↑	↓
Sodium-restricted diet	↑	↑↑	↓
Pregnancy	↑	↑↑	↓
Renovascular hypertension	↑	↑↑	↓
Malignant hypertension	↑	↑↑	↓
False Positive Results
Beta-adrenergic blockers	↓	↓↓	↑
Central alpha-2 agonists (eg, clonidine, alpha-methyldopa)	↓	↓↓	↑
NSAIDS	↑	↓↓	↑
Other conditions
Potassium loading	↑	→↓	↑
Sodium-loaded diet	↓	↓↓	↑
Advancing age	↓	↓↓	↑
Renal dysfunction	→↑	↓	↑
PHA-2	→	↓	↑
Luteal phase of menstrual cycle	↑	PRA: Unchanged	↑
Antihypertensive Medications With Minimal Effect on the ARR
Prazosin, doxazosin, terazosin			←→
Verapamil, hydralazine			←→
Other medications
Renin inhibitors (Renin inhibitors raise the ARR if renin is measured as PRA [false positive] and lower it if measured as DAR concentration [false negative.])	↓	↑↓	↑↓
SSRIs	↑	↑	↓
OCPs (OCPs have little effect on ARR when renin is measured as PRA. Use of immunometric measurements of DAR rather than PRA may give false positive results. Subdermal etonogestrel has no effect on ARR.)	↑	↓DAR	↑
Liddle syndrome	↓	↓	Normal
ARR, aldosterone-renin ratio; NSAIDs, non-steroidal anti-inflammatory drugs; K, potassium; ACE, angiotensin converting enzyme; ARBs, angiotensin II type 1 receptor blockers; DHPs, dihydropyridines; PHA-2, pseudohypoaldosteronism type 2; PRA, plasma renin activity; DAR, direct active renin; OCPs, oral contraceptive agents; SSRIs, selective serotonin reuptake inhibitors

Table 2. Drugs Used in the Management of Idiopathic Hyperaldosteronism in Children

Drug	Class	Pediatric Dose
Spironolactone	Aldosterone antagonist	0-10 kg: 6.25 mg/dose PO q12h 11-20 kg: 12.5 mg/dose PO q12h 21-40 kg: 25 mg/dose PO q12h >40 kg: 25 mg PO q8h
Potassium canrenoate	Aldosterone antagonist	3-8 mg/kg IV qd; not to exceed 400 mg
Amiloride	Potassium-sparing diuretic	0.2 mg/kg q12h
Triamterene	Potassium-sparing diuretic	2 mg/kg/dose q8-24h
Nifedipine	Dihydropyridine calcium channel antagonist	0.25-0.5 mg/kg PO q6-8h
Amlodipine	Calcium channel antagonist	0.05-0.2 mg/ day PO
Doxazosin	Alpha₁ -specific adrenergic antagonist	0.02-0.1 mg/day; not to exceed 4 mg
Prazosin	Alpha₁ -specific adrenergic antagonist	0.005 mg/kg test dose, then 0.025-0.1 mg/kg/dose q6h; not to exceed 0.5 mg/dose

Back to List

Author

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, American College of Endocrinology

Disclosure: Nothing to disclose.

Coauthor(s)

Amalia Sertedaki, PhD Research Associate, Molecular Endocrinology Laboratory, Division of Endocrinology, Diabetes and Metabolism, First Department of Pediatrics, Aghia Sophia Children's Hospital, University of Athens Medical School, Greece

Disclosure: Nothing to disclose.

Eleni Magdalini Kyritsi, MD, PhD Clinical Resident in Endocrinology, Division of Endocrinology, Metabolism and Diabetes, First Department of Pediatrics, "Aghia Sophia" Children's Hospital, University of Athens Medical School, Greece

Disclosure: Nothing to disclose.

Chief Editor

Robert P Hoffman, MD Professor and Program Director, Department of Pediatrics, Ohio State University College of Medicine; Pediatric Endocrinologist, Division of Pediatric, Endocrinology, Diabetes, and Metabolism, Nationwide Children's Hospital

Robert P Hoffman, MD is a member of the following medical societies: American College of Pediatricians, American Diabetes Association, American Pediatric Society, Christian Medical and Dental Associations, Endocrine Society, Midwest Society for Pediatric Research, Pediatric Endocrine Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Acknowledgements

Antony Lafferty, MB ChB, FRACP Senior Lecturer of Pediatric Endocrinology, Monash University Department of Pediatrics, National Institutes of Health, Bethesda, MD, and Princess Margaret Hospital for Children, Perth, Western Australia

Antony Lafferty, MB ChB, FRACP is a member of the following medical societies: Endocrine Society

Disclosure: Nothing to disclose.

Lynne Lipton Levitsky, MD Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor of Pediatrics, Harvard Medical School

Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Pfizer Grant/research funds P.I.; Tercica Grant/research funds Other; Eli Lily Grant/research funds PI; NovoNordisk Grant/research funds PI; NovoNordisk Consulting fee Consulting; Onyx Heart Valve Consulting fee Consulting

Thomas A Wilson, MD Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Hyperaldosteronism Medication

Medication Summary

Aldosterone Antagonists, Selective

Class Summary

Spironolactone (Aldactone)

Spironolactone (Aldactone)

Eplerenone (Inspra)

Eplerenone (Inspra)

Diuretics, Potassium-Sparing

Class Summary

Triamterene (Dyrenium)

Triamterene (Dyrenium)

Amiloride

Amiloride

Antihypertensives, Other

Class Summary

Nifedipine (Adalat, Procardia XL, Nifedical XL, Nifediac CC)

Nifedipine (Adalat, Procardia XL, Nifedical XL, Nifediac CC)

Amlodipine (Norvasc)

Amlodipine (Norvasc)

Diltiazem (Cardizem, Cardizem CD, Dilacor XR, Tiazac)

Diltiazem (Cardizem, Cardizem CD, Dilacor XR, Tiazac)

Nicardipine (Cardene)

Nicardipine (Cardene)

Verapamil (Calan, Calan SR, Covera HS, Isoptin, Verelan)

Verapamil (Calan, Calan SR, Covera HS, Isoptin, Verelan)

Doxazosin (Cardura, Cardura XL)

Doxazosin (Cardura, Cardura XL)

Prazosin (Minipress)

Prazosin (Minipress)

Hyperaldosteronism Medication

Medication Summary

Aldosterone Antagonists, Selective

Class Summary

Spironolactone (Aldactone)

Eplerenone (Inspra)

Diuretics, Potassium-Sparing

Class Summary

Triamterene (Dyrenium)

Amiloride

Antihypertensives, Other

Class Summary

Nifedipine (Adalat, Procardia XL, Nifedical XL, Nifediac CC)

Amlodipine (Norvasc)

Diltiazem (Cardizem, Cardizem CD, Dilacor XR, Tiazac)

Nicardipine (Cardene)

Verapamil (Calan, Calan SR, Covera HS, Isoptin, Verelan)

Doxazosin (Cardura, Cardura XL)

Prazosin (Minipress)

References

Tables

Contributor Information and Disclosures

What would you like to print?