Under normal conditions, most of the sodium chloride filteredby the kidney (often more than 99 percent) is reabsorbed, andone can think of the tubular functions that permit this reabsorptionas involving salt (solute) and water (solvent). When salt islost, water goes along with it, and the various salt-losingtubulopathies are often very difficult to control. These conditionscan be distinguished by their symptoms and biochemical characteristics,which has been helpful in their management.
Hypokalemic salt-losing tubulopathies (called Bartter's syndromes)are a group of clinically and genetically distinct inheritedrenal disorders.1 In 1962, Bartter and colleagues detailed the. . . [Full Text of this Article]
Source Information
From the Department of Medicine and the Membrane Protein Study Group, University of Montreal (D.G.B.); and the Department of Human Genetics and Medicine, McGill University (T.M.F.) — both in Montreal.
This article has been cited by other articles:
Sands, J. M., Bichet, D. G.
(2006). Nephrogenic Diabetes Insipidus. ANN INTERN MED
144: 186-194
[Full Text]
Fujiwara, T. M., Bichet, D. G.
(2005). Molecular Biology of Hereditary Diabetes Insipidus. J. Am. Soc. Nephrol.
16: 2836-2846
[Abstract][Full Text]
Lin, S.-H., Shiang, J.-C., Huang, C.-C., Yang, S.-S., Hsu, Y.-J., Cheng, C.-J.
(2005). Phenotype and Genotype Analysis in Chinese Patients with Gitelman's Syndrome. J. Clin. Endocrinol. Metab.
90: 2500-2507
[Abstract][Full Text]
Kotchen, T. A.
(2005). Contributions of Sodium and Chloride to NaCl-Induced Hypertension. Hypertension
45: 849-850
[Full Text]
Previous
