Renal Handling of Calcium

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Abstract

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.

S. Sanjad, Fiona Karet Frankl, Leila Hamdan … (1996)

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.

Fiona Karet Frankl, Ron Simon, J Soriano … (1996)

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.

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Author and article information

Journal

Journal ID (publisher-id): NEF

Journal ID (nlm-ta): Nephron

Journal ID (doi): 10.1159/issn.1660-8151

Title: Nephron

Publisher: S. Karger AG

ISBN: 978-3-8055-6818-0

ISBN: 978-3-318-00390-1

ISSN (Print): 1660-8151

ISSN (Electronic): 2235-3186

Publication date Subscription-year: 1999

Publication date (Print): December 1998

Publication date (Electronic): 24 December 1998

Volume: 81

Issue: Suppl 1

Pages: 2-7

Affiliations

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Tex., USA

Article

Publisher ID: 46292 Other ID: Nephron 1999;81(suppl 1):2–7

DOI: 10.1159/000046292

PubMed ID: 9873208

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Page count

Figures: 7, References: 11, Pages: 6

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