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Hyperaldosteronism Follow-up

  • Author: George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London); Chief Editor: Stephen Kemp, MD, PhD  more...
 
Updated: Dec 10, 2015
 

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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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 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

Stephen Kemp, MD, PhD Former 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, Southern 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.

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Steroid biosynthetic pathway.
Physiologic regulation of the renin-angiotensin-aldosterone axis.
Table 1. Factors affecting interpretation of ARR results
False Negative Results
FactorAldosteroneReninARR
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 cyclePRA: 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 syndromeNormal
 



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
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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