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PSEUDOHYPOALDOSTERONISM, TYPE IID

Known as: FAMILIAL HYPERKALEMIC HYPERTENSION, FHHT, PHA2D 
 
National Institutes of Health

Related topics

Related topics

5 relations
Autosomal dominant inheritanceAutosomal recessive inheritanceHypertensive diseasePSEUDOHYPOALDOSTERONISM, TYPE IIE

Broader (1)

Pseudohypoaldosteronism, Type II

Papers overview

Semantic Scholar uses AI to extract papers important to this topic.
Highly Cited
2014
Highly Cited
2014
Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3.
Familial hyperkalemic hypertension (FHHt) is a monogenic disease resulting from mutations in genes encoding WNK kinases, the… Expand
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Highly Cited
2013
Highly Cited
2013
WNK1-related Familial Hyperkalemic Hypertension results from an increased expression of L-WNK1 specifically in the distal nephron
Significance Hypertension, one of the most common morbidity factors worldwide, is caused mostly by a deregulation of salt… Expand
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Highly Cited
2012
Highly Cited
2012
KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron
Familial hyperkalemic hypertension (FHHt) is a Mendelian form of arterial hypertension that is partially explained by mutations… Expand
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Review
2011
Review
2011
The WNK kinase network regulating sodium, potassium, and blood pressure.
The relationship between renal salt handling and hypertension is intertwined historically. The discovery of WNK kinases (With No… Expand
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Highly Cited
2010
Highly Cited
2010
Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension
Mutations in WNK1 and WNK4 lead to familial hyperkalemic hypertension (FHHt). Because FHHt associates net positive Na+ balance… Expand
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Highly Cited
2007
Highly Cited
2007
The thiazide-sensitive Na-Cl cotransporter is regulated by a WNK kinase signaling complex.
The pathogenesis of essential hypertension remains unknown, but thiazide diuretics are frequently recommended as first-line… Expand
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2007
2007
WNK1 and WNK4 modulate CFTR activity.
The cystic fibrosis transmembrane conductance regulator (CFTR) is an ATP-gated chloride channel. WNK kinases are widely expressed… Expand
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Highly Cited
2007
Highly Cited
2007
WNK4 enhances TRPV5-mediated calcium transport: potential role in hypercalciuria of familial hyperkalemic hypertension caused by gene mutation of WNK4.
The epithelial Ca(2+) channel TRPV5 serves as a gatekeeper for active Ca(2+) reabsorption in the distal convoluted tubule and… Expand
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Highly Cited
2006
Highly Cited
2006
Dietary electrolyte-driven responses in the renal WNK kinase pathway in vivo.
WNK1 and WNK4 are unusual serine/threonine kinases with atypical positioning of the catalytic active-site lysine (WNK: With-No-K… Expand
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Highly Cited
2005
Highly Cited
2005
Mechanisms of WNK1 and WNK4 interaction in the regulation of thiazide-sensitive NaCl cotransport.
With-no-lysine (WNK) kinases are highly expressed along the mammalian distal nephron. Mutations in either WNK1 or WNK4 cause… Expand
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