Studies on the site of renal tubular defect in Bartter’s syndrome

Masahiro Kikuchi, Mariko Sato, Akiko Chiba, Yasushi Chiba, Kazuya Nagao, Toshiyuki Suzuki, Yoko Fujigaki, Hisao Hoshino

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)


Renal tubular function was studied in an 8-month-old male infant with Bartter’s syndrome, which is characterized by hypokalemic metabolic alkalosis, normotensive hyperreninemic hyperaldosteronism, and reduced pressor response to angiotensin II. Chloride transport along the diluting segment (CH2O/CH2O + CCl) was impaired. Furthermore, furosemide did not elicit normal natriuresis, which suggested impaired chloride reabsorptive capacity at the furosemide-sensitive ascending limb of Henle’s loop. Loss of antidiuretic hormone-mediated urinary concentration was in support of this. These findings pointed to the thick ascending limb of Henle’s loop as the site of the primary defect in this child.

Original languageEnglish
Pages (from-to)358-361
Number of pages4
JournalPediatrics International
Issue number3
Publication statusPublished - 1997 Jun
Externally publishedYes


  • Antidiuretic hormone
  • Bartter’s syndrome
  • Furosemide
  • Renal tubular function

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health


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