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Gitelman syndrome

variant of Bartter's syndrome with hypomagnesemia & hypocalciuria Genetics: - autosomal recessive - mutation in the thiazide-sensitive Na+Cl- cotransporter of the distal tubule (SLC12A3) Clinical manifestations: - patients generally present in late adolescence or early adulthood [4] - patients are often asymptomatic - transient periods of muscular weakness & tetany, usually accompanied by abdominal pain, vomiting & fever - normal blood pressure - phenotype is highly heterogeneous in terms of age at onset & severity - laboratory features might also change during life - overlapping features with Bartter syndrome Laboratory: - arterial blood gas, serum K+: hypokalemic metabolic alkalosis - serum magnesium: hypomagnesemia - serum Ca+2 may be high normal - urine Ca+2: hypocalciuria - urine chloride > 20 meq/L [4] - plasma renin activity increased - SLC12A3 gene mutation

Interactions

disease interactions

Related

Bartter syndrome hyperaldosteronism solute carrier family 12 member 3; thiazide-sensitive Na+Cl- cotransporter; Na+Cl- symporter (SLC12A3, TSC)

General

genetic disease of the kidney genetic syndrome (multisystem disorder)

Database Correlations

OMIM correlations MORBIDMAP 600968

References

  1. OMIM :accession 263800
  2. UniProt :accession P55017
  3. Nakhoul F, Nakhoul N, Dorman E, Berger L, Skorecki K, Magen D. Gitelman's syndrome: a pathophysiological and clinical update. Endocrine. 2012 Feb;41(1):53-7. Review. PMID: 22169961
  4. Medical Knowledge Self Assessment Program (MKSAP) 19. American College of Physicians, Philadelphia 2021 - Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022