These findings show that albuminuria in kidney transplant recipients is associated with hypertension, ability of urine to proteolytically activate ENaC current, and increased abundance of γENaC.
Of the total 766 patients, those with rare variants in exon 13 of either SCNN1B or SCNN1G had a significantly earlier onset of hypertension (24.7 ± 7.5 vs. 29.0 ± 7.7 years, P = 0.015) and lower serum potassium (3.57 ± 0.59 vs. 3.96 ± 0.41 mmol/l, P = 0.007) than those without rare variants.
We screened the C-terminus of SCNN1B and SCNN1G in an adolescent with poorly controlled hypertension who was clinically diagnosed as having Liddle syndrome.
Mutations in the alpha-, beta- and gamma-ENaC subunit genes (SCNN1A, SCNN1B and SCNN1G) are associated with multi-system pseudohypoaldosteronism (PHA), and mutations in the PY motif of carboxy-terminal region of beta and gamma subunits are associated with Liddle syndrome of hereditary hypertension.
The purpose of this study was to determine whether mutations of SCNN1B or SCNN1G were present in a patient clinically suspected to have Liddle syndrome with no familial history of hypertension.
Common variants of the beta and gamma subunits of the epithelial sodium channel and their relation to plasma renin and aldosterone levels in essential hypertension.
The roles of these missense mutations in the SCNN1B or SCNN1G gene identified in hypertensive patients are not clear in the pathogenesis of hypertension and the regulation of electrolytes.
The roles of these missense mutations in the SCNN1B or SCNN1G gene identified in hypertensive patients are not clear in the pathogenesis of hypertension and the regulation of electrolytes.