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      Renal Handling of Calcium


      S. Karger AG

      Diuretics, Amiloride, Thiazide, Furosemide, Calcium

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          Ca absorption is mediated by both active and passive processes. Absorption in both proximal tubule and thick ascending limb is mainly coupled indirectly to Na absorption and is a passive process through the paracellular pathway. In the distal convoluted tubule, Ca absorption is regulated independently of Na absorption; this is the principal site of action of parathyroid hormone, calcitonin, and 1,25-(OH)<sub>2</sub>D<sub>3</sub>. Models for transport in proximal tubule, thick ascending limb, and distal convoluted tubule afford attractive explanations for the influence on Ca transport of effective arterial blood volume, parathyroid hormone, acid-base balance, genetic disturbances such as Bartter’s and Gitelman’s syndromes, and diuretic action.

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          Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2.

          Inherited hypokalaemic alkalosis with low blood pressure can be divided into two groups-Gitelman's syndrome, featuring hypocalciuria, hypomagnesaemia and milder clinical manifestations, and Bartter's syndrome, featuring hypercalciuria and early presentation with severe volume depletion. Mutations in the renal Na-Cl cotransporter have been shown to cause Gitelman's syndrome. We demonstrate linkage of Bartter's syndrome to the renal Na-K-2Cl cotransporter gene NKCC2, and identify frameshift or non-conservative missense mutations for this gene that co-segregate with the disease. These findings demonstrate the molecular basis of Bartter's syndrome, provide the basis for molecular classification of patients with inherited hypokalaemic alkalosis, and suggest potential phenotypes in heterozygous carriers of NKCC2 mutations.
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            Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK.

            Mutations in the Na-K-2Cl cotransporter (NKCC2), a mediator of renal salt reabsorption, cause Bartter's syndrome, featuring salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pressure. NKCC2 mutations can be excluded in some Bartter's kindreds, prompting examination of regulators of cotransporter activity. One regulator is believed to be ROMK, an ATP-sensitive K+ channel that 'recycles' reabsorbed K+ back to the tubule lumen. Examination of the ROMK gene reveals mutations that co-segregate with the disease and disrupt ROMK function in four Bartter's kindreds. Our findings establish the genetic heterogeneity of Bartter's syndrome, and demonstrate the physiologic role of ROMK in vivo.

              Author and article information

              S. Karger AG
              December 1998
              24 December 1998
              : 81
              : Suppl 1
              : 2-7
              Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Tex., USA
              46292 Nephron 1999;81(suppl 1):2–7
              © 1998 S. Karger AG, Basel

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              Page count
              Figures: 7, References: 11, Pages: 6
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              Cardiovascular Medicine, Nephrology

              Calcium, Furosemide, Amiloride, Diuretics, Thiazide


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