Liddle syndrome in a newborn infant

Farahnak K. Assadi*, Robert E. Kimura, Uma Subramanian, Sameer Patel

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


A 10-week-old female infant developed hypertension. The elevated blood pressure was associated with metabolic alkalosis and urinary chloride wastage. The family history was unremarkable. Her urinalysis, blood urea nitrogen (BUN), and serum creatinine concentrations were all normal. A renal ultrasound was normal. A technetium-99m diethylenetriaminopentoacetic acid (DTPA) renal scan with captopril showed normal blood flow bilaterally. The head ultrasound and echocardiogram were normal. Blood epinephrine, norepinephrine, catecholamines, thyroxine, and steroid levels were also normal. Treatment with various combinations of labetalol, hydralazine, captopril, methyldopa, nifedipine, and spironolactone, all at high doses, failed to control the elevated blood pressure. Serum aldosterone level and peripheral plasma renin activity were low. The lack of therapeutic response to spironolactone, with a good response to amiloride and recurrence of hypertension and metabolic alkalosis after amiloride cessation that was subsequently treated with amiloride, established the diagnosis of Liddle syndrome. To our knowledge, this is the youngest patient with Liddle syndrome that has been reported in the literature.

Original languageEnglish (US)
Pages (from-to)609-611
Number of pages3
JournalPediatric Nephrology
Issue number8
StatePublished - 2002


  • Amiloride
  • Liddle syndrome
  • Metabolic alkalosis
  • Neonatal hypertension
  • Spironolactone

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Nephrology


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