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Studies on the site of renal tubular defect in Bartter's syndrome
Author(s) -
KIKUCHI MASAHIRO,
SATO MARIKO,
CHIBA AKIKO,
CHIBA YASUSHI,
NAGAO KAZUYA,
SUZUKI TOSHIYUKI,
FUJIGAKI YOKO,
HOSHINO HISAO
Publication year - 1997
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.1997.tb03753.x
Subject(s) - medicine , bartter syndrome , bartter's syndrome , endocrinology , urology , hypokalemia
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 (C H2O /C H2O + C Cl ) 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.