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hypokalemia/proline
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Patients with hypokalemia develop WNK bodies in the distal convoluted tubule of the kidney.
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Hypokalemia contributes to the progression of chronic kidney disease, while a definitive pathophysiogical theory to explain this remains to be established. K+ deficiency results in profound alterations of renal epithelial transport. These include an increase of salt reabsorption via the
Mg2+ restriction downregulates NCC through NEDD4-2 and prevents its activation by hypokalemia.
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Hypomagnesemia is associated with reduced kidney function and life-threatening complications and sustains hypokalemia. The distal convoluted tubule (DCT) determines final urinary Mgp>2+ p> excretion and, via activity of the Nap>+ p>-Clp>- p> cotransporter (NCC), also plays a key
WNK bodies cluster WNK4 and SPAK/OSR1 to promote NCC activation in hypokalemia.
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Kp>+ p> deficiency stimulates renal salt reuptake via the Nap>+ p>-Clp>- p>-cotransporter (NCC) of the distal convoluted tubule (DCT), thereby reducing Kp>+ p> losses in downstream nephron segments while increasing NaCl retention and blood pressure. NCC activation is mediated
Effects of K+-deficient diets with and without NaCl supplementation on Na+, K+, and H2O transporters' abundance along the nephron.
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Dietary potassium (K(+)) restriction and hypokalemia have been reported to change the abundance of most renal Na(+) and K(+) transporters and aquaporin-2 isoform, but results have not been consistent. The aim of this study was to reexamine Na(+), K(+) and H(2)O transporters' pool size regulation in
SPAK-knockout mice manifest Gitelman syndrome and impaired vasoconstriction.
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Polymorphisms in the gene encoding sterile 20/SPS1-related proline/alanine-rich kinase (SPAK) associate with hypertension susceptibility in humans. SPAK interacts with WNK kinases to regulate the Na(+)-K(+)-2Cl(-) and Na(+)-Cl(-) co-transporters [collectively, N(K)CC]. Mutations in WNK1/4 and N(K)CC
Basolateral Kir4.1 activity in the distal convoluted tubule regulates K secretion by determining NaCl cotransporter activity.
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Renal potassium (K) secretion plays a key role in maintaining K homeostasis. The classic mechanism of renal K secretion is focused on the connecting tubule and cortical collecting duct, in which K is uptaken by basolateral Na-K-ATPase and is secreted into the lumen by apical ROMK (Kir1.1) and
Association of a mutation in thiazide-sensitive Na-Cl cotransporter with familial Gitelman's syndrome.
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Gitelman's syndrome is a variant of Bartter's syndrome, characterized by hypokalemia, hypomagnesemia, hypocalciuria, and hypovolemia. We have observed familial cases of Gitelman's syndrome, and a possible mutation in thiazide-sensitive Na-Cl cotransporter was investigated in this kindred. The
Congenital adrenal hyperplasia with 11 beta-hydroxylase deficiency.
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A rare form of congenital adrenal hyperplasia (CAH), 11 beta-hydroxylase deficiency, may be misdiagnosed as 21-hydroxylase deficiency, the most common form of CAH, because of similar clinical presentations at times and elevated level of 17-hydroxyprogesterone in both conditions. We report a case of
A novel mutation in the beta-subunit of the epithelial sodium channel gene (SCNN1B) in a Thai family with Liddle's syndrome.
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Liddle's syndrome is a rare form of autosomal dominant hypertension with early penetrance and cardiovascular sequelae. It is caused by missense or frameshift mutations in the epithelial sodium channel (ENaC) gene resulting in excessive salt and water resorption from the distal nephron, volume
Molecular genetics of Liddle's syndrome.
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Liddle's syndrome, an autosomal dominant form of monogenic hypertension, is characterized by salt-sensitive hypertension with early penetrance, hypokalemia, metabolic alkalosis, suppression of plasma rennin activity and aldosterone secretion, and a clear-cut response to epithelial sodium channel
A compound heterozygous mutation in the CYP17 (17alpha-hydroxylase/17,20-lyase) gene in a Chinese subject with congenital adrenal hyperplasia.
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Mutations in the CYP17 gene impair steroid biosynthesis in the adrenals and gonads, resulting in 17alpha-hydroxylase/17,20-lyase (P450c17) deficiency, leading to amenorrhea, sexual infantilism, hypokalemia, and hypertension. To date, more than 50 mutations in the CYP17 gene associated with
Analysis of claudin genes in pediatric patients with Bartter's syndrome.
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Bartter's syndrome is a constellation of symptoms characterized by hyper-reninemic hypokalemia, metabolic alkalosis, elevated renin and aldosterone, low or normal blood pressure, and hyperplasia of the juxtaglomerular apparatus. So far, five gene mutations in proteins regulating the sodium chloride
Impaired phosphorylation of Na(+)-K(+)-2Cl(-) cotransporter by oxidative stress-responsive kinase-1 deficiency manifests hypotension and Bartter-like syndrome.
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Na(+)-K(+)-2Cl(-) cotransporters (NKCCs), including NKCC1 and renal-specific NKCC2, and the Na(+)-Cl(-) cotransporter (NCC) play pivotal roles in the regulation of blood pressure (BP) and renal NaCl reabsorption. Oxidative stress-responsive kinase-1 (OSR1) is a known upstream regulator of N(K)CCs.
The expression, regulation, and function of Kir4.1 (Kcnj10) in the mammalian kidney.
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Kir4.1 is an inwardly rectifying potassium (K(+)) channel and is expressed in the brain, inner ear, and kidney. In the kidney, Kir4.1 is expressed in the basolateral membrane of the late thick ascending limb (TAL), the distal convoluted tubule (DCT), and the connecting tubule (CNT)/cortical
Caveolin-1 Deficiency Inhibits the Basolateral K+ Channels in the Distal Convoluted Tubule and Impairs Renal K+ and Mg2+ Transport.
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Kcnj10 encodes the inwardly rectifying K(+) channel Kir4.1 in the basolateral membrane of the distal convoluted tubule (DCT) and is activated by c-Src. However, the regulation and function of this K(+) channel are incompletely characterized. Here, patch-clamp experiments in Kcnj10-transfected HEK293
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