Abstract
This study was performed to demonstrate urinary angiotensinogen as a potential prognostic marker of the albuminuria reduction effects of olmesartan in patients with metabolic syndrome. In 24 patients (eight women, 57.88 ± 2.00 years), 5–40 mg/day of olmesartan were given. Urinary concentrations of albumin and angiotensinogen (normalized by urinary concentrations of creatinine) and plasma renin activity were measured before and after the 12- and 24-week marks of olmesartan treatment. Olmesartan treatment increased plasma renin activity and decreased urinary albumin and urinary angiotensinogen significantly (p < 0.05). Based on the % change in urinary albumin, patients were divided into two groups, responders (<−50%) and non-responders (≥−50%), and a logistic analysis of urinary angiotensinogen before treatment showed the area under the curve as 0.694. When the cutoff value of urinary angiotensinogen before the treatment of 13.9 µg/g Cr was used, the maximum Youden index (0.500, specificity: 11/12 = 91.7% and sensitivity: 7/12 = 58.3%) was obtained. When all patients were re-divided into two groups, those with higher values of urinary angiotensinogen before the treatment (Group H, n = 16) and those with lower values, Group H showed significantly decreased urinary albumin (p < 0.05). Therefore, urinary angiotensinogen could be a prognostic marker of the albuminuria reduction effects of olmesartan in patients with metabolic syndrome.
Highlights
Obesity is a risk factor for a variety of diseases [1,2], including the development and progression of chronic kidney disease (CKD) [3]
This study suggests that in metabolic syndrome patients with activated intrarenal renin-angiotensin system (RAS), angiotensin II receptor blocker (ARB) has albuminuria reduction effects
We previously reported that the olmesartan treatment decreased intrarenal AGT mRNA/protein levels, as well as urinary AGT levels in angiotensin II-infused rats [41]
Summary
Obesity is a risk factor for a variety of diseases [1,2], including the development and progression of chronic kidney disease (CKD) [3]. Metabolic syndrome contributes to the development of type 2 diabetes, hypertension, cardiovascular disease [4] and CKD [5]. Type 2 diabetes and hypertension are widely recognized as risk factors for CKD [6]. There are many reports indicating that an increase in intrarenal angiotensinogen (AGT) and the activation of the renin-angiotensin system (RAS) are involved in CKD [7,8,9,10,11]. The intrarenal RAS is activated in obesity [3,12,13]
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