摘要
Essential hypertension is a difficult diagnosis in children and the gene of the renal-epithelial chloride channel ClC-Kb is potentially predisposing. In vitro studies have shown that a common ClC-Kb threonine481serine (T481S) polymorphism leads to enhanced chloride channel activity and may predispose for hypertension (HT). We therefore analysed children at risk for HT for the T481S polymorphism and associated genotype with blood pressure (BP) status. A total of 48 children with essential hypertension (mean age 14.4 ±2.7 years, 26 male;22 female;mean BP 143.4 ±7.5/88 ±5.8 mmHg) were compared with 78 children with white-coat HT (WCHT), who showed occasionally hypertensive BP values, which were not confirmed by ambulatory blood pressure monitoring (mean age 13.7 ±2.5 years, 49 male, 29 female;mean BP 122.4 ±4.3/68.2 ±3.5 mmHg). Other causes of HT were excluded. Allelic frequencies of hypertensive patients were not significantly different from those with WCHT (HT: A 0.84;T 0.16 vs. WCHT: A 0.85;T 0.15). However, the T-allele was observed more frequently in WCHT subjects with systolic and diastolic BP exceeding the 90th percentile (A 0.71;T 0.29, n = 34, p 【0.05, considered as borderline hypertensive). The preliminary data suggest that children with WCHT carry the ClC-Kb T481S polymorphism more often and that this variant may predispose for development of arterial HT.
Essential hypertension is a difficult diagnosis in children and the gene of the renal-epithelial chloride channel ClC-Kb is potentially predisposing. In vitro studies have shown that a common ClC-Kb threonine481serine (T481S) polymorphism leads to enhanced chloride channel activity and may predispose for hypertension (HT). We therefore analysed children at risk for HT for the T481S polymorphism and associated genotype with blood pressure (BP) status. A total of 48 children with essential hypertension (mean age 14.4 ±2.7 years, 26 male;22 female;mean BP 143.4 ±7.5/88 ±5.8 mmHg) were compared with 78 children with white-coat HT (WCHT), who showed occasionally hypertensive BP values, which were not confirmed by ambulatory blood pressure monitoring (mean age 13.7 ±2.5 years, 49 male, 29 female;mean BP 122.4 ±4.3/68.2 ±3.5 mmHg). Other causes of HT were excluded. Allelic frequencies of hypertensive patients were not significantly different from those with WCHT (HT: A 0.84;T 0.16 vs. WCHT: A 0.85;T 0.15). However, the T-allele was observed more frequently in WCHT subjects with systolic and diastolic BP exceeding the 90th percentile (A 0.71;T 0.29, n = 34, p <0.05, considered as borderline hypertensive). The preliminary data suggest that children with WCHT carry the ClC-Kb T481S polymorphism more often and that this variant may predispose for development of arterial HT.
