コーパス検索結果 (left1)
通し番号をクリックするとPubMedの該当ページを表示します
1 Gitelman syndrome is a salt-losing tubulopathy caused by
2 Gitelman syndrome is a salt-losing tubulopathy character
3 Gitelman syndrome is caused by biallelic pathogenic vari
4 Gitelman syndrome is the most frequent hereditary salt-l
8 including hypokalaemic metabolic alkalosis; Gitelman's syndrome represents the predominant subset of
9 requently observed disorders are Bartter and Gitelman syndrome, which affect salt transport in the th
13 contrast, recombinants were observed between Gitelman's syndrome and the flanking markers D16S419 and
15 (NCC) of the distal convoluted tubule cause Gitelman's syndrome, an inherited hypokalemic alkalosis
17 utosomal dominant polycystic kidney disease, Gitelman syndrome, Bartter syndrome, autosomal recessive
18 r's and Bartter's-like syndromes, especially Gitelman's, has come largely as a result of the advances
19 described for tubulopathies such as Fanconi, Gitelman, and Bartter-like syndromes and renal tubular a
21 lood pressure can be divided into two groups-Gitelman's syndrome, featuring hypocalciuria, hypomagnes
22 ercalciuria, and/or polyuria), and 26.0% had Gitelman-like syndrome (fortuitous discovery of hypokale
26 -K-2Cl cotransporter (NKCC2) are involved in Gitelman and Bartter syndrome, respectively, autosomal r
28 nt in WNK4(-/-) mice, which exhibited a mild Gitelman-like syndrome, with normal blood pressure, incr
31 ain knock-in mice showed typical features of Gitelman Syndrome with mild hypokalaemia, hypomagnesaemi
33 olume homeostasis and in the pathogenesis of Gitelman's syndrome, we used gene targeting to prepare a
34 10 may result in the same renal phenotype of Gitelman syndrome, as they can lead to reduced NCC activ
35 be responsible for the clinical phenotype of Gitelman's syndrome, a variant of Bartter's syndrome.
37 DNA samples from individuals with suspected Gitelman syndrome in whom a single likely pathogenic or
38 re were no recombinants observed between the Gitelman's syndrome phenotype and inheritance of D16S408
39 e clinical phenotype of PHAII is opposite to Gitelman syndrome, a disease caused by dysfunction of th
42 DNA (mtDNA) variants in three families with Gitelman-like electrolyte abnormalities, then investigat
47 testing, approximately 14% of patients with Gitelman syndrome were prediabetic, compared with 5% of
49 med a cross-sectional study of patients with Gitelman syndrome, heterozygous carriers, and healthy no