ライフサイエンスコーパス: Gitelman

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1 including hypokalaemic metabolic alkalosis; Gitelman's syndrome represents the predominant subset of

2 requently observed disorders are Bartter and Gitelman syndrome, which affect salt transport in the th

3 hloride cotransporter gene (NCCT or TSC) and Gitelman's syndrome (GS).

4 contrast, recombinants were observed between Gitelman's syndrome and the flanking markers D16S419 and

5 Na-Cl cotransporter have been shown to cause Gitelman's syndrome.

6 (NCC) of the distal convoluted tubule cause Gitelman's syndrome, an inherited hypokalemic alkalosis

7 utosomal dominant polycystic kidney disease, Gitelman syndrome, Bartter syndrome, autosomal recessive

8 r's and Bartter's-like syndromes, especially Gitelman's, has come largely as a result of the advances

9 lood pressure can be divided into two groups-Gitelman's syndrome, featuring hypocalciuria, hypomagnes

10 ercalciuria, and/or polyuria), and 26.0% had Gitelman-like syndrome (fortuitous discovery of hypokale

11 nt; and (3) the hypocalciuric-hypomagnesemic Gitelman variant.

12 enal salt wasting with arterial hypotension (Gitelman syndrome).

13 -K-2Cl cotransporter (NKCC2) are involved in Gitelman and Bartter syndrome, respectively, autosomal r

14 of Mg2+ and Ca2+ are altered, as observed in Gitelman's syndrome.

15 nt in WNK4(-/-) mice, which exhibited a mild Gitelman-like syndrome, with normal blood pressure, incr

16 splay hypomagnesemia, which sometimes mimics Gitelman syndrome.

17 findings demonstrate the molecular basis of Gitelman's syndrome.

18 ain knock-in mice showed typical features of Gitelman Syndrome with mild hypokalaemia, hypomagnesaemi

19 We now demonstrate complete linkage of Gitelman's syndrome to the locus encoding the renal thia

20 olume homeostasis and in the pathogenesis of Gitelman's syndrome, we used gene targeting to prepare a

21 be responsible for the clinical phenotype of Gitelman's syndrome, a variant of Bartter's syndrome.

22 hypocalciuria and hypercalcemia, suggesting Gitelman syndrome (GS).

23 re were no recombinants observed between the Gitelman's syndrome phenotype and inheritance of D16S408

24 e clinical phenotype of PHAII is opposite to Gitelman syndrome, a disease caused by dysfunction of th

25 Mutations in NCC also give rise to Gitelman syndrome, a hereditary salt-wasting disorder th

26 the latter is defective in this kindred with Gitelman's syndrome.

27 Patients with Gitelman syndrome (GS), an inherited salt-losing tubulop

28 transporter (NCC) is common in patients with Gitelman's syndrome (GS).

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