Can renal tubular hypokalemic disorders be accurately diagnosed on the basis of the diuretic response to thiazide? Commentary

Nature Clinical Practice Nephrology

Volumn 3, Issue 10, 2007, Pages 528-529

  Sassen, Martin C ^a   Jeck, Nikola ^a   Klaus, Günter ^a  

^a PHILIPPS UNIVERSITY MARBURG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

CHLORIDE; CLCNKB PROTEIN; CREATININE; HYDROCHLOROTHIAZIDE; KCNJ1 PROTEIN; PEPTIDE TRANSPORTER 1; POTASSIUM; PROTEIN; SODIUM CHLORIDE COTRANSPORTER; THIAZIDE DIURETIC AGENT; UNCLASSIFIED DRUG;

ADOLESCENT; ADULT; BARTTER SYNDROME; BLOOD SAMPLING; CLINICAL TRIAL; CONTROLLED CLINICAL TRIAL; CONTROLLED STUDY; FEMALE; GENE MUTATION; GENETIC SCREENING; GITELMAN SYNDROME; HUMAN; HYPOKALEMIA; KIDNEY TUBULE DISORDER; MAJOR CLINICAL STUDY; MALE; NOTE; PRIORITY JOURNAL;

EID: 34748855516     PISSN: 17458323     EISSN: 17458331     Source Type: Journal    
DOI: 10.1038/ncpneph0576     Document Type: Note

References (4)

1. Kockerling A et al. (1996) Impaired response to furosemide in hyperprostaglandin E syndrome: evidence for a tubular defect in the loop of Henle. J Pediatr 129: 519-528
2. Reinalter SC et al. (2004) Pharmacotyping of hypokalaemic saltlosing tubular disorders. Acta Physiol Scand 181: 513-521
3. Riveira-Munoz E et al. (2007) Transcriptional and functional analyses of SLC12A3 mutations: new clues for the pathogenesis of Gitelman syndrome. J Am Soc Nephrol 18: 1271-1283
4. Konrad M et al. (2000) Mutations in the chloride channel gene CLCNKB as a cause of classic Bartter syndrome. J Am Soc Nephrol 11: 1449-1459