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1 with a complex phenotype that includes renal salt wasting.
2 antidiuretic hormone secretion and cerebral salt wasting.
3 sh these possibilities, focusing on cerebral salt wasting.
4 antidiuretic hormone secretion and cerebral salt wasting.
5 rientation and cleavage of ENaC, despite the salt wasting.
6 /Cl(-) cotransporter (NCC) manifest profound salt wasting.
8 w a similar phenotype to Bartter syndrome of salt wasting and dehydration due to reduced Na-K-2Cl-cot
11 Pendrin/NCC double KO mice displayed severe salt wasting and sharp increase in urine output under ba
12 uncommon inherited disorder characterized by salt-wasting and end-organ unresponsiveness to mineraloc
13 us died; the other two had transient massive salt-wasting and polyuria reminiscent of antenatal Bartt
14 th kinases would lead to polyuria and severe salt-wasting, and generated SPAK/OSR1 double knockout mi
15 lls and with purified enzymes differed among salt-wasting- and nonclassical-associated variants, but
16 ting both kinases causes severe polyuria and salt-wasting by generating SPAK/OSR1 double knockout (DK
21 mutations to these subunits can lead to the salt wasting disease pseudohypoaldosteronism type I, ass
22 hannel defective in gating that leads to the salt-wasting disease pseudohypoaldosteronism type I, was
25 th chronic renal failure caused by polyuric, salt-wasting diseases may be hampered if ongoing sodium
27 give rise to Gitelman syndrome, a hereditary salt-wasting disorder thought in most cases to arise fro
28 hydroxylase deficiency (25 children with the salt-wasting form and 13 with the simple virilizing form
30 yperplasia (CAH) owing to low sensitivity in salt-wasting forms and a high rate of recall (ie, a posi
32 erited hypokalaemic alkalosis resulting from salt-wasting has proved fertile ground for identificatio
34 orption, cause Bartter's syndrome, featuring salt wasting, hypokalaemic alkalosis, hypercalciuria and
39 tion of Kir4.1 in these mice led to moderate salt wasting, low BP, and profound potassium wasting.
40 characterized by hypokalaemic alkalosis with salt-wasting, low blood pressure, normal magnesium and h
43 le deletion of pendrin or NCC does not cause salt wasting or excessive diuresis under basal condition
44 ve P450 21A2 variants associated with either salt-wasting or nonclassical forms of CAH were expressed
45 tations can be associated either with severe salt-wasting or simple virilizing phenotypes or with mil
46 CaR mutations with a Bartter syndrome-like, salt-wasting phenotype, but the precise mechanism for th
47 with one of three known forms of CAH, namely salt wasting, simple virilizing, or nonclassical CAH.
49 oss-of-function mutations of NCC cause renal salt wasting with arterial hypotension (Gitelman syndrom
50 I (PHA1) is characterized by neonatal renal salt wasting with dehydration, hypotension, hyperkalaemi
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