Endothelial nitric oxide synthase gene expression is associated with hypertension in autosomal dominant polycystic kidney disease.
نویسندگان
چکیده
BACKGROUND/AIMS Early occurrence of hypertension is the prominent feature of autosomal dominant polycystic kidney disease (ADPKD). The role of angiotensin-converting enzyme (ACE) gene polymorphism and endothelial nitric oxide synthase (eNOS) gene polymorphism in the clinical course of ADPKD is not well understood. However, data about the expression of these genes are lacking. Thus, we aimed to investigate the polymorphisms and expressions of both the ACE and eNOS genes that affect hypertension in ADPKD. METHODS Whole blood samples were obtained from all participants. ACE and eNOS gene polymorphisms and their expressions were analyzed in 78 ADPKD patients and 30 controls. Gene expressions were assessed by quantitative real-time PCR. Twenty-four-hour blood pressure monitoring was performed for the diagnosis of hypertension in all study participants. RESULTS eNOS expression and the estimated glomerular filtration rate were found to be significantly higher in ADPKD patients without hypertension than in those with hypertension. Each unit of increase in eNOS expression led to a 0.88-fold decrease (95% CI: 0.80-0.96) in the risk of hypertension in multiple logistic regression analysis. CONCLUSIONS eNOS gene expression is independently predictive of hypertension in the ADPKD population. This study showed, for the first time, a novel link between eNOS gene expression and hypertension in ADPKD.
منابع مشابه
Nitric oxide synthase and polycystic kidney disease
Polycystic kidney disease (PKD) is a multisystem disorder characterized by the formation of cysts within the kidneys. PKD is mainly caused by the unfolding of its immunoglobulin-like PKD domains. There are two major forms of PKD; autosomal dominant (ADPKD) that caused by mutations of PKD1 and PKD2 (1) and autosomal recessive (ARPKD) caused by mutations in PKHD1 gene (2,3). Although, cellular ch...
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عنوان ژورنال:
- Cardiorenal medicine
دوره 4 3-4 شماره
صفحات -
تاریخ انتشار 2014