scholarly journals A case report of Bartter's syndrome associated with possible pseudohypoparathyroidism type II.

1987 ◽  
Vol 76 (4) ◽  
pp. 549-552
Author(s):  
Hirofumi SHIGETA ◽  
Naohiro TASAKI ◽  
Seiji KITAZUMI ◽  
Yoshihiro KITAGAWA ◽  
Takahiro KANATSUNA ◽  
...  
Keyword(s):  
Case Report ◽  
Type Ii ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Pseudohypoparathyroidism Type Ii

scholarly journals A Case of Pseudohypoparathyroidism (PHP) Type II Associated with Bartter's Syndrome-Restoration of Phosphaturic Response to Parathyroid

1992 ◽  
Vol 68 (7) ◽  
pp. 676-687
Author(s):  
Yukihiro BANDO ◽  
Hisatsugu MIYAKOSHI ◽  
Tadasu NAGAOKA ◽  
Kensou OHSAWA ◽  
Ken-ichi KOBAYASHI
Keyword(s):  
Type Ii ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome

scholarly journals Neonatal Pseudo-Bartter's Syndrome with Hypokalemia and ECG Changes Born to a Mother with Eating Disorder: A Case Report

2017 ◽  
Vol 66 (2) ◽  
pp. 153-158
Author(s):  
Yuko AKUTSU ◽  
Yuya HIGASHI ◽  
Yukako NAGAYOSHI ◽  
Manabu SUGIE ◽  
Tsutomu KONDO ◽  
...  
Keyword(s):  
Eating Disorder ◽  
Case Report ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Ecg Changes

scholarly journals ADULT VARIANT BARTTER’S SYNDROME- A CASE REPORT

2017 ◽  
Vol 4 (16) ◽  
pp. 951-953
Author(s):  
Ishwar Sidappa Hasabi ◽  
Mahabaleshwar Mamadapur ◽  
Chandrashekar Kachapur ◽  
Sitaram N ◽  
Kalinga B.E
Keyword(s):  
Case Report ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome

Pregnancy Complicated with Bartter's Syndrome: A Case Report

2001 ◽  
Vol 27 (5) ◽  
pp. 267-274 ◽  
Author(s):  
Tomoyoshi Nohira ◽  
Toshihide Nakada ◽  
Osamu Akutagawa ◽  
Atsuya Fujito ◽  
Kazuhiro Okabe ◽  
...  
Keyword(s):  
Case Report ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome

scholarly journals Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins

2008 ◽  
Vol 294 (6) ◽  
pp. F1373-F1380 ◽  
Author(s):  
Carsten A. Wagner ◽  
Dominique Loffing-Cueni ◽  
Qingshang Yan ◽  
Nicole Schulz ◽  
Panagiotis Fakitsas ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Statistical Significance ◽  
Salt Transport ◽  
Postnatal Life ◽  
Thick Ascending Limb ◽  
Type Ii ◽  
Bartter’S Syndrome ◽  
Wild Type ◽  
Bartter's Syndrome ◽  
Altered Expression

Bartter's syndrome represents a group of hereditary salt- and water-losing renal tubulopathies caused by loss-of-function mutations in proteins mediating or regulating salt transport in the thick ascending limb (TAL) of Henle's loop. Mutations in the ROMK channel cause type II antenatal Bartter's syndrome that presents with maternal polyhydramnios and postnatal life-threatening volume depletion. We have developed a colony of Romk null mice showing a Bartter-like phenotype and with increased survival to adulthood, suggesting the activation of compensatory mechanisms. To test the hypothesis that upregulation of Na+-transporting proteins in segments distal to the TAL contributes to compensation, we studied expression of salt-transporting proteins in ROMK-deficient ( Romk−/−) mice. Plasma aldosterone was 40% higher and urinary PGE2 excretion was 1.5-fold higher in Romk−/− compared with wild-type littermates. Semiquantitative immunoblotting of kidney homogenates revealed decreased abundances of proximal tubule Na+/H+ exchanger (NHE3) and Na+-Pi cotransporter (NaPi-IIa) and TAL-specific Na+-K+-2Cl−-cotransporter (NKCC2/BSC1) in Romk−/− mice, while the distal convoluted tubule (DCT)-specific Na+-Cl− cotransporter (NCC/TSC) was markedly increased. The abundance of the α-,β-, and γ-subunits of the epithelial Na+ channel (ENaC) was slightly increased, although only differences for γ-ENaC reached statistical significance. Morphometry revealed a fourfold increase in the fractional volume of DCT but not of connecting tubule (CNT) and collecting duct (CCD). Consistently, CNT and CD of Romk−/− mice revealed no apparent increase in the luminal abundance of the ENaC compared with those of wild-type mice. These data suggest that the loss of ROMK-dependent Na+ absorption in the TAL is compensated predominately by upregulation of Na+ transport in downstream DCT cells. These adaptive changes in Romk−/− mice may help to limit renal Na+ loss, and thereby, contribute to survival of these mice.

Bartter's Syndrome in Pregnancy: A Case Report and Review

1997 ◽  
Vol 14 (01) ◽  
pp. 55-57 ◽  
Author(s):  
Erin O'Sullivan ◽  
Manju Monga ◽  
William Graves
Keyword(s):  
Case Report ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
In Pregnancy

Case Report: Subclinical Pseudohypoparathyroidism Type II: Evidence for Failure of Physiologic Adjustment in Calcium Metabolism During Pregnancy

1989 ◽  
Vol 297 (4) ◽  
pp. 247-250 ◽  
Author(s):  
Haruhiko Salto ◽  
Masahiko Saito ◽  
Katsuhiko Saito ◽  
Akiko Terauchi ◽  
Takashi Kobayashi ◽  
...  
Keyword(s):  
Case Report ◽  
Calcium Metabolism ◽  
Type Ii ◽  
Pseudohypoparathyroidism Type Ii

scholarly journals Impaired Renal NaCl Absorption in Mice Lacking the ROMK Potassium Channel, a Model for Type II Bartter's Syndrome

2002 ◽  
Vol 277 (40) ◽  
pp. 37871-37880 ◽  
Author(s):  
John N. Lorenz ◽  
Nancy R. Baird ◽  
Louise M. Judd ◽  
William T. Noonan ◽  
Anastasia Andringa ◽  
...  
Keyword(s):  
Potassium Channel ◽  
Type Ii ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Nacl Absorption
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