Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Primary Aldosteronism Medication

  • Author: Gabriel I Uwaifo, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Jun 30, 2016
 

Medication Summary

In nonsurgical primary aldosteronism, medical therapy is the treatment of choice. The drug that is the treatment of first choice for most variants of nonsurgical primary aldosteronism is spironolactone, which is used to achieve normoaldosteronism and to assist with blood pressure control. Potassium supplementation should not be routinely administered with spironolactone because of the potential for the development of hyperkalemia.

In patients who are unable to tolerate spironolactone, other potassium-sparing diuretics, such as amiloride and triamterene, can be used, although these are considered less ideal options.[35]

Glucocorticoid-remediable aldosteronism (GRA) is treated with small doses of glucocorticosteroids (ie, hydrocortisone, prednisone). At optimal doses, glucocorticosteroids normalize aldosterone and blood pressure.

Various antihypertensives may be added to achieve adequate blood pressure control. The dihydropyridine calcium channel blockers (eg, nifedipine) directly inhibit aldosterone production; however, while producing significant improvement in patients with hypertension (HTN), they do not address pathophysiology. Plasma renin activity (PRA), aldosterone levels, plasma volume, and serum potassium concentrations remain essentially unchanged with nifedipine use.

Other second-step agents for blood pressure control include thiazide diuretics, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor blockers.[23]

A sodium-restricted diet (< 80 mEq or < 2 g of sodium daily), maintenance of ideal body weight, and regular aerobic exercise contribute substantially to the success of pharmacologic treatment.

Next

Aldosterone Antagonists, Selective

Class Summary

These agents compete with aldosterone receptor sites, reducing edema and ascites.

Spironolactone (Aldactone)

 

Spironolactone competitively binds receptors at the aldosterone-dependent sodium-potassium exchange site in the distal convoluted renal tubule. It provides diuretic and antihypertensive effects, causing increased excretion of sodium and water, while retaining potassium. Spironolactone is administered alone or with a diuretic agent that acts on the proximal renal tubule. Spironolactone may block the effects of aldosterone on arteriolar smooth muscles.

Eplerenone (Inspra)

 

Eplerenone selectively blocks aldosterone at the mineralocorticoid receptors in epithelial (eg, kidney) and nonepithelial (eg, heart, blood vessels, brain) tissues, thus decreasing blood pressure and sodium reabsorption.

Previous
Next

Potassium-Sparing Diuretics

Class Summary

These agents are used as second-line medication for the treatment of primary aldosteronism due to nonlateralizing disease and/or lateralizing disease for which surgery is otherwise contraindicated or refused. They often must be used with other antihypertensives to achieve the best blood pressure control, because they are not potent antihypertensives.

Triamterene (Dyrenium)

 

Triamterene is a potassium-sparing diuretic with relatively weak natriuretic properties. It exerts a diuretic effect on the distal renal tubule to inhibit reabsorption of sodium in exchange for potassium and hydrogen. Triamterene increases sodium excretion and reduces the excessive loss of potassium and hydrogen associated with hydrochlorothiazide. It is not a competitive antagonist of mineralocorticoids; its potassium-conserving effect is observed in patients with Addison disease (ie, without aldosterone).

The onset and duration of activity with triamterene are similar to those of hydrochlorothiazide. No predictable antihypertensive effect is demonstrated. It is rapidly absorbed following oral administration, and peak plasma levels are achieved within 1 hour of dosing. Triamterene is primarily metabolized to a sulfate conjugate of hydroxytriamterene. Plasma and urine levels of this metabolite greatly exceed triamterene levels.

Amiloride

 

Amiloride is a pyrazine-carbonyl-guanidine unrelated chemically to other known antikaliuretic or diuretic agents. It is a potassium-conserving (antikaliuretic) drug that, compared with thiazide diuretics, possesses weak natriuretic, diuretic, and antihypertensive activity. Amiloride's effects have been partially additive to the effects of thiazide diuretics in some clinical studies. When it is administered with a thiazide or loop diuretic, it has been shown to decrease the enhanced urinary excretion of magnesium that occurs when a thiazide or loop diuretic is used alone.

Amiloride has potassium-conserving activity in patients receiving kaliuretic-diuretic agents. Amiloride is not an aldosterone antagonist, and its effects are observed in the absence of aldosterone. It exerts its potassium-sparing effect through the inhibition of sodium reabsorption at the distal convoluted tubule, cortical collecting tubule, and collecting duct. This decreases the net negative potential of the tubular lumen and reduces potassium and hydrogen secretion and their subsequent excretions.

Amiloride usually begins to act within 2 hours after an oral dose. Its effect on electrolyte excretion reaches a peak between 6-10 hours and lasts about 24 hours. Peak plasma levels are obtained in 3-4 hours, and the drug's plasma half-life varies between 6 and 9 hours.

Amiloride is not metabolized by the liver; it is instead excreted unchanged by the kidneys. Within 72 hours, about 50% of a dose of amiloride is excreted in urine and 40% in stool. The drug has little effect on the glomerular filtration rate or on renal blood flow. Because the liver does not metabolize amiloride hydrochloride, drug accumulation is not anticipated in patients with hepatic dysfunction; however, accumulation can occur if hepatorenal syndrome develops.

Amiloride should rarely be used alone. Used as single agents, potassium-sparing diuretics, including amiloride, result in an increased risk of hyperkalemia (approximately 10% with amiloride). Amiloride should be used alone only when persistent hypokalemia has been documented and only with careful titration of the dose and close monitoring of serum electrolyte levels.

Previous
Next

Thiazide Diuretics

Class Summary

Thiazide diuretics inhibit the reabsorption of sodium in the distal tubules, increasing the excretion of sodium, water, and potassium and hydrogen ions. They have been effective in treating hypertension of various etiologies. Besides diminishing sodium reabsorption, they also appear to diminish the sensitivity of blood vessels to circulating vasopressor substances. In all patients treated with diuretics, electrolyte levels should be monitored. Examples of thiazide diuretics are hydrochlorothiazide and chlorthalidone.

Hydrochlorothiazide (Microzide)

 

Hydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as of potassium and hydrogen ions.

Chlorthalidone (Thalitone)

 

Chlorthalidone inhibits the reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as of potassium and hydrogen ions.

Previous
Next

Calcium channel Blockers

Class Summary

Calcium channel blockers affect blood pressure by decreasing vascular peripheral resistance. With short-acting calcium channel blockers, the cardiac response to this action is variable and tachycardia can occur. Long-acting preparations may cause a decrease in heart rate.

Calcium channel blockers are classified by their structure and have different degrees of selectivity in their effects on vascular smooth muscle. The dihydropyridines do not exert electrophysiologic effects and are commonly used to manage hypertension. Facial flushing may occur. Examples of calcium channel blockers include amlodipine and isradipine.

Amlodipine (Norvasc)

 

Amlodipine is generally regarded as a dihydropyridine, although experimental evidence suggests that it also may bind to nondihydropyridine binding sites. It is appropriate for the prophylaxis of variant angina and has antianginal and antihypertensive effects. Amlodipine blocks the postexcitation release of calcium ions into cardiac and vascular smooth muscle, thereby inhibiting the action of adenosine triphosphatase (ATPase) on myofibril contraction.

The overall effect of amlodipine 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 also increases myocardial oxygen delivery in patients with vasospastic angina, and it may potentiate angiotensin-converting enzyme (ACE) inhibitor effects.

During depolarization, amlodipine inhibits the entrance of calcium ions into slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. It has a substantially longer half-life than nifedipine and diltiazem and is administered once daily.

Felodipine

 

Felodipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. It benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. It can be used during pregnancy if clinically indicated.

Calcium channel blockers potentiate ACE inhibitor effects. Renal protection is not proven, but these agents reduce morbidity and mortality rates in congestive heart failure. Calcium channel blockers are indicated in patients with diastolic dysfunction. They are effective as monotherapy in black patients and elderly patients.

Isradipine (DynaCirc CR)

 

Isradipine is a dihydropyridine calcium channel blocker. It inhibits the entrance of calcium into select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization. This causes relaxation of coronary vascular smooth muscle, which results in coronary vasodilation. Vasodilation reduces systemic resistance and blood pressure, with a small increase in resting heart rate. Isradipine also has negative inotropic effects.

Nifedipine, extended-release (Adalat CC, Nifedical XL, Procardia XL)

 

Extended-release nifedipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery.

Previous
Next

ACE Inhibitors

Class Summary

Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and lower aldosterone secretion. They are effective and well-tolerated drugs with no adverse effects on plasma lipid levels or glucose tolerance. They prevent the progression of diabetic nephropathy and other forms of glomerulopathies but appear to be less effective in black patients than in white patients. ACE inhibitors are contraindicated in pregnancy.

Patients with high plasma renin activity (PRA) may have an excessive hypotensive response to ACE inhibitors. Patients with bilateral renal vascular disease or with a single kidney, whose renal perfusion is maintained by high levels of angiotensin II, may develop irreversible acute renal failure when treated with ACE inhibitors, and caution should be exercised with their use in these patients. Interestingly, although primary aldosteronism is a condition associated with low plasma renin, aldosterone secretion seems to be exquisitely sensitive to even subnormal concentrations of angiotensin II. This phenomenon seems to be the basis for the efficacy of ACE inhibitors in primary aldosteronism (specifically idiopathic adrenal hyperplasia [IAH]).

Cough and angioedema are less common with newer members of this class than with captopril. Serum potassium and serum creatinine concentrations should be monitored for the development of hyperkalemia and azotemia. Agents in this class include captopril, lisinopril, and enalapril.

Captopril

 

Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. It is rapidly absorbed, but bioavailability is significantly reduced with food intake. Captopril achieves a peak concentration in 1 hour and has a short half-life. The drug is cleared by the kidney; impaired renal function requires reduction of the dosage. Captopril is absorbed well orally.

Give captopril at least 1 hour before meals. If it is added to water, use it within 15 minutes. The dose can be low initially, then titrated upward as needed and as tolerated by the patient.

Enalapril (Vasotec)

 

Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. The drug helps to control blood pressure and proteinuria. Enalapril decreases the pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance.

Enalapril has a favorable clinical effect when administered over a long period. Because it helps to prevent potassium loss in the distal tubules, enalapril reduces the amount of oral potassium supplementation needed by the patient.

Lisinopril (Prinivil, Zestril)

 

Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Benazepril (Lotensin)

 

Benazepril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

When pediatric patients are unable to swallow tablets or the calculated dose does not correspond with tablet strength, an extemporaneous suspension can be compounded. Combine 300 mg (15 tabs of 20 mg strength) in 75 mL of Ora-Plus suspending vehicle and shake well for at least 2 minutes. Let the tablets sit and dissolve for at least 1 hour, then shake again for 1 minute. Add 75 mL of Ora-Sweet. The final concentration is 2 mg/mL, with a total volume of 150 mL. The expiration time is 30 days with refrigeration.

Fosinopril

 

Fosinopril is a competitive ACE inhibitor. It prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.

Quinapril (Accupril)

 

Quinapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion.

Ramipril (Altace)

 

Ramipril inhibits partially inhibits both tissue and circulating ACE activity, therefore reducing the formation of angiotensin II in the tissue and plasma. Ramipril has an antihypertensive effect even in patients with low-renin hypertension.

Previous
Next

Angiotensin II Receptor Blockers

Class Summary

Angiotensin II receptor blockers lower blood pressure by blocking the final receptor (ie, angiotensin II) in the renin-angiotensin axis. Like angiotensin-converting enzyme (ACE) inhibitors, they are contraindicated in pregnancy. Serum electrolyte and creatinine levels should be monitored. Irbesartan and losartan are examples of angiotensin II receptor blockers (ARBs). Interestingly, although primary aldosteronism is a condition associated with low plasma renin, aldosterone secretion seems to be exquisitely sensitive to even subnormal concentrations of angiotensin II. This phenomenon seems to be the basis for the efficacy of ARBs in primary aldosteronism (specifically idiopathic adrenal hyperplasia [IAH]).

Irbesartan (Avapro)

 

Irbesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II at the tissue receptor site. It may induce a more complete inhibition of the renin-angiotensin system than do ACE inhibitors. In addition, irbesartan does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema.

Losartan (Cozaar)

 

Losartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, losartan does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema. It is suitable for patients who are unable to tolerate ACE inhibitors.

Olmesartan (Benicar)

 

Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to angiotensin II type 1 receptors in vascular smooth muscle. Its action is independent of the pathways for angiotensin II synthesis.

Valsartan (Diovan)

 

Valsartan is a prodrug that displaces angiotensin II from angiotensin II type 1 receptors, blocking the vasoconstrictor effects of angiotensin II. Valsartan may also lower blood pressure through its effects on aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.

Valsartan may induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, it does not affect the response to bradykinin and is less likely to be associated with cough and angioedema. Valsartan is suitable for patients who are unable to tolerate ACE inhibitors.

Telmisartan (Micardis)

 

Telmisartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in many tissues, such as vascular smooth muscle and the adrenal gland and therefore reduces blood pressure. There is also an AT2 receptor found in many tissues, but AT2 is not known to be associated with cardiovascular homeostasis and telmisartan has much greater affinity for the AT1 receptor than for the AT2 receptor

Previous
Next

Corticosteroids

Class Summary

This class of agents are therapeutically appropriate only for the GRA subtype of primary aldosteronism. The treatment of choice in GRA is the administration of the lowest possible dose of glucocorticoid that can be used to achieve adequate blood pressure control. Because of the potential adverse effects that can result from even subtle glucocorticoid excess, using short-acting glucocorticoids, such as prednisone and hydrocortisone (rather than dexamethasone), is generally best.

Prednisone

 

Prednisone is a short-acting prodrug that exerts its effects after it undergoes metabolism and is converted to prednisolone. Prednisone mimics naturally occurring cortisol and is used in GRA to rapidly suppress aldosterone levels and resolve the volume expansion and hypertension in this disorder, being generally efficacious within 2 weeks of treatment initiation.

Hydrocortisone (Solu-Cortef, Cortef)

 

Hydrocortisone possesses a molecular similarity to aldosterone and therefore not only binds to the glucocorticoid receptor (thus resulting in resulting in lower aldosterone levels in GRA), but also the mineralocorticoid receptor (MR), thus also providing competitive inhibition of ambient aldosterone levels at the MR level (resulting in decreased physiologic effects of existing ambient aldosterone levels in GRA).

Previous
 
Contributor Information and Disclosures
Author

Gabriel I Uwaifo, MD Associate Professor, Section of Endocrinology, Diabetes and Metabolism, Louisiana State University School of Medicine in New Orleans; Adjunct Professor, Joint Program on Diabetes, Endocrinology and Metabolism, Pennington Biomedical Research Center in Baton Rouge

Gabriel I Uwaifo, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Society of Hypertension, Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Nicholas J Sarlis, MD, PhD, FACP Vice President, Head of Medical Affairs, Incyte Corporation

Nicholas J Sarlis, MD, PhD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American Association for Cancer Research, American Association of Clinical Endocrinologists, American College of Physicians, American Federation for Medical Research, American Head and Neck Society, American Medical Association, American Society for Radiation Oncology, American Thyroid Association, Endocrine Society, New York Academy of Sciences, Royal Society of Medicine, Association for Psychological Science, American College of Endocrinology, European Society for Medical Oncology, American Society of Clinical Oncology

Disclosure: Received salary from Incyte Corporation for employment; Received ownership interest from Sanofi-Aventis for previous employment; Received ownership interest/ stock & stock option (incl. rsu) holder from Incyte Corporation for employment.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS, Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, American Society of Law, Medicine &Ethics, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Serge A Jabbour, MD Associate Professor, Department of Medicine, Division of Endocrinology, Jefferson Medical College of Thomas Jefferson University

Serge A Jabbour, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Thyroid Association, Endocrine Society, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Frederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group

Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, andInternational Society for Clinical Densitometry

Disclosure: Nothing to disclose.

References
  1. Rossi GP, Ragazzo F, Seccia TM, Maniero C, Barisa M, Calò LA, et al. Hyperparathyroidism can be useful in the identification of primary aldosteronism due to aldosterone-producing adenoma. Hypertension. 2012 Aug. 60(2):431-6. [Medline].

  2. Dluhy RG, Lifton RP. Glucocorticoid-remediable aldosteronism. Endocrinol Metab Clin North Am. 1994 Jun. 23(2):285-97. [Medline].

  3. Funder JW. The genetic basis of primary aldosteronism. Curr Hypertens Rep. 2012 Apr. 14(2):120-4. [Medline].

  4. Choi M, Scholl UI, Yue P, et al. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Science. 2011 Feb 11. 331(6018):768-72. [Medline]. [Full Text].

  5. Young DB. Quantitative analysis of aldosterone's role in potassium regulation. Am J Physiol. 1988 Nov. 255(5 Pt 2):F811-22. [Medline].

  6. Stowasser M, Klemm SA, Tunny TJ, et al. Plasma aldosterone response to ACTH in subtypes of primary aldosteronism. Clin Exp Pharmacol Physiol. 1995 Jun-Jul. 22(6-7):460-2. [Medline].

  7. Litchfield WR, New MI, Coolidge C, et al. Evaluation of the dexamethasone suppression test for the diagnosis of glucocorticoid-remediable aldosteronism. J Clin Endocrinol Metab. 1997 Nov. 82(11):3570-3. [Medline]. [Full Text].

  8. Mulatero P, Stowasser M, Loh KC, Fardella CE, Gordon RD, Mosso L, et al. Increased diagnosis of primary aldosteronism, including surgically correctable forms, in centers from five continents. J Clin Endocrinol Metab. 2004 Mar. 89(3):1045-50. [Medline].

  9. Born-Frontsberg E, Reincke M, Rump LC, et al. Cardiovascular and cerebrovascular comorbidities of hypokalemic and normokalemic primary aldosteronism: results of the German Conn's Registry. J Clin Endocrinol Metab. 2009 Apr. 94(4):1125-30. [Medline].

  10. Bernini G, Galetta F, Franzoni F, Bardini M, Taurino C, Bernardini M, et al. Arterial stiffness, intima-media thickness and carotid artery fibrosis in patients with primary aldosteronism. J Hypertens. 2008 Dec. 26(12):2399-405. [Medline].

  11. Apostolopoulou K, Künzel HE, Gerum S, Merkle K, Schulz S, Fischer E, et al. Gender differences in anxiety and depressive symptoms in patients with primary hyperaldosteronism: A cross-sectional study. World J Biol Psychiatry. 2012 May 8. [Medline].

  12. Cruz DN, Perazella MA. Hypertension and hypokalemia: unusual syndromes. Conn Med. 1997 Feb. 61(2):67-75. [Medline].

  13. Cesari M, Letizia C, Angeli P, Sciomer S, Rosi S, Rossi GP. Cardiac Remodeling in Patients With Primary and Secondary Aldosteronism: A Tissue Doppler Study. Circ Cardiovasc Imaging. 2016 Jun. 9 (6):[Medline].

  14. Hall JE, Granger JP, Smith MJ Jr. Role of renal hemodynamics and arterial pressure in aldosterone "escape". Hypertension. 1984. 6:1183.

  15. Yokota N, Bruneau BG, Kuroski de Bold ML, et al. Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway. J Clin Invest. 1994 Nov. 94(5):1938-46. [Medline]. [Full Text].

  16. Vallon V, Rieg T. Regulation of renal NaCl and water transport by the ATP/UTP/P2Y2 receptor system. Am J Physiol Renal Physiol. 2011 Sep. 301(3):F463-75. [Medline]. [Full Text].

  17. Schiffrin EL, Chrétien M, Seidah NG, et al. Response of human aldosteronoma cells in culture to the N-terminal glycopeptide of pro-opiomelanocortin and gamma 3-MSH. Horm Metab Res. 1983 Apr. 15(4):181-4. [Medline].

  18. [Guideline] Funder JW, Carey RM, Fardella C, Gomez-Sanchez CE, Mantero F, Stowasser M, et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2008 Sep. 93(9):3266-81. [Medline].

  19. Quamme GA. Control of magnesium transport in the thick ascending limb. Am J Physiol. 1989 Feb. 256(2 Pt 2):F197-210. [Medline].

  20. Seiler L, Rump LC, Schulte-Mönting J, Slawik M, Borm K, Pavenstädt H, et al. Diagnosis of primary aldosteronism: value of different screening parameters and influence of antihypertensive medication. Eur J Endocrinol. 2004 Mar. 150(3):329-37. [Medline].

  21. Tzanela M, Effremidis G, Vassiliadi D, et al. The aldosterone to renin ratio in the evaluation of patients with incidentally detected adrenal masses. Endocrine. 2007 Oct. 32(2):136-42. [Medline].

  22. Diederich S, Mai K, Bahr V, et al. The simultaneous measurement of plasma-aldosterone- and -renin-concentration allows rapid classification of all disorders of the renin-aldosterone system. Exp Clin Endocrinol Diabetes. 2007 Jul. 115(7):433-8. [Medline].

  23. Wu VC, Chang HW, Liu KL, et al. Primary aldosteronism: diagnostic accuracy of the losartan and captopril tests. Am J Hypertens. 2009 Aug. 22(8):821-7. [Medline].

  24. Burton TJ, Mackenzie IS, Balan K, Koo B, Bird N, Soloviev DV, et al. Evaluation of the sensitivity and specificity of (11)C-metomidate positron emission tomography (PET)-CT for lateralizing aldosterone secretion by Conn's adenomas. J Clin Endocrinol Metab. 2012 Jan. 97(1):100-9. [Medline].

  25. Otsuka F, Otsuka-Misunaga F, Koyama S, et al. Hormonal characteristics of primary aldosteronism due to unilateral adrenal hyperplasia. J Endocrinol Invest. 1998 Sep. 21(8):531-6. [Medline].

  26. Stowasser M, Bachmann AW, Tunny TJ. Production of 18-oxo-cortisol in subtypes of primary aldosteronism. Clin Exp Pharmacol Physiol. 1996 Jun-Jul. 23(6-7):591-3. [Medline].

  27. Hamlet SM, Gordon RD, Gomez-Sanchez CE, et al. Adrenal transitional zone steroids, 18-oxo and 18-hydroxycortisol, useful in the diagnosis of primary aldosteronism, are ACTH-dependent. Clin Exp Pharmacol Physiol. 1988 Apr. 15(4):317-22. [Medline].

  28. McAlister FA, Lewanczuk RZ. Primary hyperaldosteronism and adrenal incidentaloma: an argument for physiologic testing before adrenalectomy. Can J Surg. 1998 Aug. 41(4):299-305. [Medline].

  29. Georgiades CS, Hong K, Geschwind JF, et al. Adjunctive use of C-arm CT may eliminate technical failure in adrenal vein sampling. J Vasc Interv Radiol. 2007 Sep. 18(9):1102-5. [Medline].

  30. Young WF, Stanson AW, Grant CS, et al. Primary aldosteronism: adrenal venous sampling. Surgery. 1996 Dec. 120(6):913-9; discussion 919-20. [Medline].

  31. Webb R, Mathur A, Chang R, Baid S, Nilubol N, Libutti SK, et al. What is the Best Criterion for the Interpretation of Adrenal Vein Sample Results in Patients with Primary Hyperaldosteronism?. Ann Surg Oncol. 2011 Nov 3. [Medline].

  32. Young WF, Stanson AW, Thompson GB, et al. Role for adrenal venous sampling in primary aldosteronism. Surgery. 2004 Dec. 136(6):1227-35. [Medline].

  33. Naruse M, Naruse K, Yoshimoto T, et al. Dopaminergic regulation of aldosterone secretion: its pathophysiologic significance in subsets of primary aldosteronism. Hypertens Res. 1995 Jun. 18 Suppl 1:S59-64. [Medline].

  34. Carey RM. Primary aldosteronism. Horm Res. 2009 Jan. 71 Suppl 1:8-12. [Medline].

  35. Hood SJ, Taylor KP, Ashby MJ, et al. The spironolactone, amiloride, losartan, and thiazide (SALT) double-blind crossover trial in patients with low-renin hypertension and elevated aldosterone-renin ratio. Circulation. 2007 Jul 17. 116(3):268-75. [Medline]. [Full Text].

  36. Ronconi V, Turchi F, Appolloni G, di Tizio V, Boscaro M, Giacchetti G. Aldosterone, Mineralocorticoid Receptor and the Metabolic Syndrome: Role of the Mineralocorticoid Receptor Antagonists. Curr Vasc Pharmacol. 2011 Oct 21. [Medline].

  37. Minowada S, Fujimura T, Takahashi N, et al. Computed tomography-guided percutaneous acetic acid injection therapy for functioning adrenocortical adenoma. J Clin Endocrinol Metab. 2003 Dec. 88(12):5814-7. [Medline]. [Full Text].

  38. Sukor N, Gordon RD, Ku YK, et al. Role of unilateral adrenalectomy in bilateral primary aldosteronism: a 22-year single center experience. J Clin Endocrinol Metab. 2009 Jul. 94(7):2437-45. [Medline].

  39. Celen O, O'Brien MJ, Melby JC, et al. Factors influencing outcome of surgery for primary aldosteronism. Arch Surg. 1996 Jun. 131(6):646-50. [Medline].

  40. Waldmann J, Maurer L, Holler J, Kann PH, Ramaswamy A, Bartsch DK, et al. Outcome of surgery for primary hyperaldosteronism. World J Surg. 2011 Nov. 35(11):2422-7. [Medline].

  41. Letavernier E, Peyrard S, Amar L, et al. Blood pressure outcome of adrenalectomy in patients with primary hyperaldosteronism with or without unilateral adenoma. J Hypertens. 2008 Sep. 26(9):1816-23. [Medline].

  42. Milsom SR, Espiner EA, Nicholls MG, et al. The blood pressure response to unilateral adrenalectomy in primary aldosteronism. Q J Med. 1986 Dec. 61(236):1141-51. [Medline].

  43. Giacchetti G, Turchi F, Boscaro M, Ronconi V. Management of primary aldosteronism: its complications and their outcomes after treatment. Curr Vasc Pharmacol. 2009 Apr. 7(2):244-49. [Medline].

  44. Amar L, Baguet JP, Bardet S, et al. SFE/SFHTA/AFCE primary aldosteronism consensus: Introduction and handbook. Ann Endocrinol (Paris). 2016 Jun 14. [Medline]. [Full Text].

  45. Baguet JP, Steichen O, Mounier-Vehier C, Gosse P. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 1: Epidemiology of PA, who should be screened for sporadic PA?. Ann Endocrinol (Paris). 2016 Apr 15. 86 (20):1002-8. [Medline]. [Full Text].

  46. Douillard C, Houillier P, Nussberger J, Girerd X. SFE/SFHTA/AFCE Consensus on Primary Aldosteronism, part 2: First diagnostic steps. Ann Endocrinol (Paris). 2016 May 10. [Medline]. [Full Text].

  47. Reznik Y, Amar L, Tabarin A. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 3: Confirmatory testing. Ann Endocrinol (Paris). 2016 Jun 15. [Medline]. [Full Text].

  48. Bardet S, Chamontin B, Douillard C, et al. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 4: Subtype diagnosis. Ann Endocrinol (Paris). 2016 Mar 29. [Medline]. [Full Text].

  49. Zennaro MC, Jeunemaitre X. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 5: Genetic diagnosis of primary aldosteronism. Ann Endocrinol (Paris). 2016 Jun 14. [Medline]. [Full Text].

  50. Steichen O, Amar L, Chaffanjon P, Kraimps JL, Menegaux F, Zinzindohoue F. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 6: Adrenal surgery. Ann Endocrinol (Paris). 2016 Jun 10. [Medline]. [Full Text].

  51. Pechère-Bertschi A, Herpin D, Lefebvre H. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 7: Medical treatment of primary aldosteronism. Ann Endocrinol (Paris). 2016 Jun 14. [Medline]. [Full Text].

 
Previous
Next
 
Magnetic resonance imaging (MRI) scan in a patient with Conn syndrome showing a left adrenal adenoma.
Scintigram obtained by using iodine-131-beta-iodomethyl-norcholesterol (NP-59) in a 59-year-old man with hypertension shows fairly intense radionuclide uptake in the right adrenal tumor. At surgery, a Conn tumor was confirmed.
Effects of main antihypertensives on the renin-angiotensin system.
Potential causes of primary aldosteronism.
Transitional zone adrenocortical steroids.
Algorithm for screening for potential primary aldosteronism.
Algorithm for confirmation of primary aldosteronism.
Algorithm for distinguishing subtypes of primary aldosteronism.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.