Literature DB >> 28705920

Nephron Remodeling Underlies Hyperkalemia in Familial Hyperkalemic Hypertension.

James A McCormick1, David H Ellison2,3.   

Abstract

Entities:  

Keywords:  Gordon Syndrome; chloride; hyperkalemia; sodium; thiazide

Mesh:

Year:  2017        PMID: 28705920      PMCID: PMC5576953          DOI: 10.1681/ASN.2017060660

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


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Review 3.  Mammalian distal tubule: physiology, pathophysiology, and molecular anatomy.

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4.  Luminal influences on potassium secretion: sodium concentration and fluid flow rate.

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5.  Wnk4 controls blood pressure and potassium homeostasis via regulation of mass and activity of the distal convoluted tubule.

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7.  Molecular pathogenesis of pseudohypoaldosteronism type II: generation and analysis of a Wnk4(D561A/+) knockin mouse model.

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8.  Constitutively Active SPAK Causes Hyperkalemia by Activating NCC and Remodeling Distal Tubules.

Authors:  P Richard Grimm; Richard Coleman; Eric Delpire; Paul A Welling
Journal:  J Am Soc Nephrol       Date:  2017-04-25       Impact factor: 10.121

9.  Acute inhibition of NCC does not activate distal electrogenic Na+ reabsorption or kaliuresis.

Authors:  Robert W Hunter; Eilidh Craigie; Natalie Z M Homer; John J Mullins; Matthew A Bailey
Journal:  Am J Physiol Renal Physiol       Date:  2014-01-08

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1.  Familial hyperkalemic hypertension: hyperkalemia not hypertension defines dominant KLHL3 disease and may permit earlier recognition and tailored therapy.

Authors:  Meenakshi Sambharia; Jyothsna Gattineni; Lama Noureddine; M Adela Mansilla; Christie P Thomas
Journal:  J Nephrol       Date:  2022-01-08       Impact factor: 4.393

Review 2.  The Mineralocorticoid Receptor in Salt-Sensitive Hypertension and Renal Injury.

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