eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Pseudohypoaldosteronism: Follow-up

Author: Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Diabetes, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis and St Jude Children's Research Hospital; Lieutenant Colonel (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Coauthor(s): Jose F Pascual-y-Baralt, MD, Chief, Division of Pediatric Nephrology, San Antonio Military Pediatric Center; Clinical Professor, Department of Pediatrics, University of Texas Health Science Campus
Contributor Information and Disclosures

Updated: Jul 11, 2008

Follow-up

Further Inpatient Care

  • Patients should be closely monitored; they require frequent reevaluations.
  • No potassium should be contained in intravenous fluids.
  • Once fluid and sodium deficits are corrected, administer maintenance fluids at 120-160 mL/kg/d and sodium supplementation at 20-40 mEq/kg/d.
  • If differentiating adrenal insufficiency from PHA-I is impossible at presentation, treat patients with glucocorticoids once electrolytes, blood sugar, cortisol, and adrenocorticotropic hormone (ACTH) concentrations are obtained until the diagnosis of PHA-I is confirmed.
  • Monitor weight and fluid intake and output every 12 hours and recalculate infusion rate if fluid balance becomes negative.
  • Monitor blood pressure and serum and urine electrolytes closely, watching for normalization of blood pressure as well as of serum electrolytes.
  • Electrocardiographic monitoring is warranted.

Further Outpatient Care

  • Maintain fluids at 120-160 mL/kg/d.
  • A high-sodium and low-potassium diet should be followed.
  • Sodium supplementation at 20-40 mEq/kg/d until patients are aged 1-2 years may be provided as 20% NaCl (at 3 mEq/mL) every 6 hours and added to patients' feedings.
  • Closely monitor serum electrolytes, blood pressure, weight, and height.
  • Watch for dehydration and hypovolemia.
  • Patients with multiple target organ defects pseudohypoaldosteronism type I (MTOD PHA-I) should be observed for episodes of respiratory distress.

Inpatient & Outpatient Medications

  • Potassium-binding resins
  • Prostaglandin inhibitors
  • Alkalinizing agents
  • Hydrochlorothiazide in PHA-II

Deterrence/Prevention

  • The rare occasions when unintentional salt or fluid restriction is most likely to occur include hospitalization, surgery, major accidental trauma, and life-threatening emergency. Thus, wearing lifelong medical identification (such as a MedicAlert necklace or bracelet) is imperative to provide another way to alert healthcare professionals who are unfamiliar with the patient's rare medical condition.

Complications

  • Severe hyperkalemia and even death may occur as a result of cardiac arrhythmia.
  • Nephrocalcinosis may occur in PHA-I.
  • Nephrolithiasis may occur in PHA-II.
  • Frequent episodes of dehydration may occur.

Prognosis

  • Renal pseudohypoaldosteronism type I
    • The disease tends to be transient, and symptoms resolve in patients older than 2 years. A progressive decrease in urinary salt wastage occurs as the renal tubule matures throughout infancy. Older children may be asymptomatic with normal salt intake, but plasma aldosterone remains elevated. PRA decreases to normal with advancing age. Adult patients with PHA-I have normal serum electrolytes without salt supplementation but may be more vulnerable to electrolyte disturbances under stress. Plasma aldosterone levels remain elevated throughout life. Whether affected adults possess a lifetime higher risk for nephrolithiasis is unclear, thus, annual visits to a nephrologist or informed primary care provider are prudent.
    • Children with early childhood hyperkalemia usually achieve normal height within 6 months; at about 5 years, therapy is no longer needed.
  • MTOD PHA-I: Salt wasting is more severe in this form of PHA. MTOD PHA-I has a poorer outcome than the renal form, and death may ensue during the neonatal period. Improvement with advancing age does not occur as in the isolated renal form. Therapy must be maintained throughout childhood and probably throughout life.
  • PHA-II: Patients with PHA-II require lifelong therapy.
  • Secondary pseudohypoaldosteronism
    • All abnormalities tend to disappear after medical or surgical therapy; however, hyperkalemia may last as long as 3 years. Polyuria and renal sodium loss may transiently become more severe during the early period following relief of obstruction, and some degree of polyuria may persist.
    • Abnormalities improve or disappear following discontinuation of drugs that can impair renin or aldosterone synthesis or cause mineralocorticoid resistance.

Patient Education

  • Watch for dehydration.
  • Avoid foods high in potassium content.
  • Genetic counseling should be provided by a qualified professional.

Miscellaneous

Medicolegal Pitfalls

  • ACE inhibitors should not be used in patients with pseudohypoaldosteronism type II (PHA-II) because these drugs may aggravate hyperkalemia, which may be life threatening.
 


More on Pseudohypoaldosteronism

Overview: Pseudohypoaldosteronism
Differential Diagnoses & Workup: Pseudohypoaldosteronism
Treatment & Medication: Pseudohypoaldosteronism
Follow-up: Pseudohypoaldosteronism
References
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Further Reading

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Keywords

pseudohypoaldosteronism, PHA, pseudohypoaldosteronism type I, PHA-I, Cheek and Perry syndrome, renal pseudohypoaldosteronism type I, AD renal PHA-I, multiple target organ pseudohypoaldosteronism, MTOD PHA-I, autosomal recessive PHA-I, AR PHA-I, early childhood hyperkalemia, renal tubular acidosis subtypes 4 and 5, RTA, pseudohypoaldosteronism type II, PHA-II, Gordon syndrome, adolescent hyperkalemic syndrome, Spitzer-Weinstein syndrome, mineralocorticoid-resistant hyperkalemia, renal tubular acidosis type IV subtype 3, metabolic acidosis, hypervolemia, renal salt wasting, hypotension, hypertension, chloride shunt syndrome, renal tube defects, short stature, urolithiasis, obstructive uropathy, urinary tract infection, tubulointerstitial nephritis, sickle cell nephropathy, systemic lupus erythematosus, amyloidosis, neonatal medullary necrosis, unilateral renal vein thrombosis, failure to thrive, adolescent hyperkalemic syndrome

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Contributor Information and Disclosures

Author

Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Diabetes, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis and St Jude Children's Research Hospital; Lieutenant Colonel (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society
Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching

Coauthor(s)

Jose F Pascual-y-Baralt, MD, Chief, Division of Pediatric Nephrology, San Antonio Military Pediatric Center; Clinical Professor, Department of Pediatrics, University of Texas Health Science Campus
Jose F Pascual-y-Baralt, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, American Society of Pediatric Nephrology, Association of Military Surgeons of the US, and International Society of Nephrology
Disclosure: Nothing to disclose.

Medical Editor

Arlan L Rosenbloom, MD, Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology
Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Florida Pediatric Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Lynne Lipton Levitsky, MD, Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor, Department of Pediatrics, Harvard University 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, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and 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: Genentech, Inc. Honoraria Speaking and teaching; Pfiser, Inc. Honoraria Consulting

 
 
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