Hyperaldosteronism Follow-up

  • Author: George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London); Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: May 10, 2012
 

Further Outpatient Care

Frequency and requirement for follow-up depends on the cause of the hyperaldosteronism.

Patients who are treated medically need regular follow-up to ensure adequacy of blood pressure control and treatment of hypokalemia.

In children, doses must be adjusted as patients grow.

In cases with familial hyperaldosteronism, genetic counseling is also important at an age-appropriate level.

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Inpatient & Outpatient Medications

Severe hypokalemia may require intravenous correction if the potassium is less than 2.5 mmol/L or the patient is clinically symptomatic. Once stable, sodium restriction and oral potassium supplements may be used as effectively as or in addition to potassium-sparing diuretics.

Spironolactone is the most effective drug for controlling the effects of hyperaldosteronism, although it may interfere with the progression of puberty. Newer drugs with greater specificity for the mineralocorticoid receptor than spironolactone are becoming available.

Alternative medications for patients in whom aldosterone antagonists are contraindicated include amiloride and triamterene as well as calcium channel antagonists (see Medication), alpha-adrenergic antagonists (especially alpha1-specific agents, eg, prazosin, doxazosin); in patients with angiotensin II–responsive disease, angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists are indicated.

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Transfer

Patients receiving medical treatment for hyperaldosteronism must be transferred to a physician with experience managing such cases. This may be an endocrinologist, a cardiologist, or a nephrologist.

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Complications

Complications of primary hyperaldosteronism can be divided into those due to the primary disease, such as hypertension and hypokalemia, and those arising from treatment.

Hypertension

Hypertension due to hyperaldosteronism can cause damage to many organs and organ systems, including the heart (hypertrophy and myocardial fibrosis), the blood vessels (vascular remodeling with medial and intimal hypertrophy and acceleration of atherogenesis), the eyes (arterial narrowing, retinal ischemia, and papilledema), the kidneys (progressive deterioration with nephrosclerosis), and the brain (hemorrhage).

Aggressive blood pressure control and early diagnosis and treatment of the underlying hyperaldosteronism minimize the risk of these complications.

Hypokalemia

Hypokalemia initially results in weakness, constipation, polyuria, and, if more severe, may cause cardiac arrhythmias.

Patients on cardiac drugs are at greater risk of this complication.

Adrenal venous sampling

Adrenal venous sampling should be performed in centers with appropriate expertise. Adrenal veins are often small, and the right vein is difficult to cannulate.

Performance of adrenal venography is not recommended because this may cause bleeding into the gland.

Specific treatment-related complications

The use of laparoscopic adrenalectomy considerably reduces postoperative recovery time and complication risk. The risk of operative complications is related directly to the experience of the surgeon.

In addition to these complications, following surgical removal of aldosteronoma, a period of hypoadrenalism can occur. If not recognized, this can result in clinically significant hyponatremia and hyperkalemia.

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Prognosis

The age of the patient and the duration of disease before diagnosis are the 2 most important prognostic factors.

Adult studies have shown that hypertension is improved significantly in approximately 70% of cases (see Treatment). This figure is likely to be higher in children because disease duration is shorter and the prevalence of other causes of hypertension is lower.

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Patient Education

Patients with mild hyperaldosteronism must learn how to avoid foods that are high in sodium because this exacerbates their hypertension and increases their tendency to develop hypokalemia.

Patients also need to know that medication can lead to hyperkalemia and hypotension, particularly in the presence of intercurrent illness, and they should be advised to see their pediatrician in these circumstances.

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Contributor Information and Disclosures
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 Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

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.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

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.

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

  2. Escher G. Hyperaldosteronism in pregnancy. Ther Adv Cardiovasc Dis. Apr 2009;3(2):123-32. [Medline].

  3. 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. Sep-Oct 1984;6(5):717-23. [Medline].

  4. 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. Jun 1997;11(6):373-8. [Medline].

  5. Kasifoglu T, Akalin A, Cansu DU, Korkmaz C. Hypokalemic paralysis due to primary hyperaldosteronism simulating Gitelman's syndrome. Saudi J Kidney Dis Transpl. Mar 2009;20(2):285-7. [Medline].

  6. Künzel HE. Psychopathological symptoms in patients with primary hyperaldosteronism--possible pathways. Horm Metab Res. Mar 2012;44(3):202-7. [Medline].

  7. Schmiemann G, Gebhardt K, Hummers-Pradier E, Egidi G. Prevalence of hyperaldosteronism in primary care patients with resistant hypertension. J Am Board Fam Med. Jan-Feb 2012;25(1):98-103. [Medline].

  8. Gordon RD. Primary aldosteronism. J Endocrinol Invest. Jul-Aug 1995;18(7):495-511. [Medline].

  9. Gordon RD, Stowasser M, Klemm SA, Tunny TJ. Primary aldosteronism--some genetic, morphological, and biochemical aspects of subtypes. Steroids. Jan 1995;60(1):35-41. [Medline].

  10. Spence JD. Diagnosis of primary aldosteronism: for medical management, not just surgery. J Hypertens. Jan 2009;27(1):204-5; author reply 205. [Medline].

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Steroid biosynthetic pathway.
Physiologic regulation of the renin-angiotensin-aldosterone axis.
Table. Drugs Used in the Management of Idiopathic Hyperaldosteronism in Children
Drug Class Pediatric Dose
SpironolactoneAldosterone antagonist0-10 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 canrenoateAldosterone antagonist3-8 mg/kg IV qd; not to exceed 400 mg
AmiloridePotassium-sparing diuretic0.2 mg/kg q12h
TriamterenePotassium-sparing diuretic2 mg/kg/dose q8-24h
NifedipineDihydropyridine calcium channel antagonist0.25-0.5 mg/kg PO q6-8h
AmlodipineCalcium channel antagonist0.05-0.2 mg/ day PO
DoxazosinAlpha1 -specific adrenergic antagonist0.02-0.1 mg/day; not to exceed 4 mg
PrazosinAlpha1 -specific adrenergic antagonist0.005 mg/kg test dose, then 0.025-0.1 mg/kg/dose q6h; not to exceed 0.5 mg/dose
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