Objective. To determine the frequency of markers of chronic kidney disease (CKD) in hypertensive patients, and to assess their relationship with the circadian blood pressure (BP) profile and intrarenal vascular resistance.Design and Methods. We studied 70 patients with medically-controlled hypertension (63,2 ± 8,3 years, m — 48,6 %, office BP was 130,5 ± 13,7 / 78,1 ± 8,5 mm Hg), 40 patients were recruited from the Russian multicentre program CHRONOGRAF. Measurement of the office BP, ambulatory BP monitoring were performed. Glomerular filtration rate (GFR) was calculated using the CKD-EPI formula, and albuminuria (AU) was determined as albumin/creatinine (A/Cr) ratio in the morning portion of urine (n = 40) or 24-hour urinary albumin excretion (UAE) (n = 22). Intrarenal vascular resistance was estimated by renal duplex Doppler ultrasound. The resistive index (RI) levels in the main renal arteries (MRA) and intrarenal arteries (IRA) were calculated.Results. Markers of CKD (GFR < 60 ml/min/1,73 m2and/or A/Cr > 30 mg/g and/or UAE > 30 mg/day) were detected in 31,4 % of patients with well-medically-controlled hypertension: average values of BP-day and BP-night were normal. The frequency of markers of CKD was 44,4 % in patients with BP-night ≥ 120/70 mm Hg (40,9 %) and 28,2 % in patients with BP-night < 120/70 mm Hg (58,1 %). A/Cr ratio was positively associated (Rs = 0,3550, р = 0,0266), GFR was negatively associated (Rs = –0,3795, р = 0,002) with systolic BP-night. RI in the segmental intrarenal arteries correlated with GFR (Rs = –0,4232, p = 0,0005). Renal RI were higher in CKD-patients vs. non-CKD-patients. During the ROC-analysis, the threshold value of RI in segmental IRA 0,725 to the detection of CKD markers (sensitivity of 71,4 %, specificity of 68,9 %, AUC = 0,699) was established. Among the diabetic patients, there were more marked disturbances of renal hemodynamic in the presence of CKD markers: RI in arcuate IRA reached 0,73 (0,68–0,75).Conclusions. The high frequency of markers of CKD (31,4 %) was identified even in patients with well-medically-controlled hypertension, it was associated with systolic BP-night. The negative correlation was found between GFR and RI. Renal hemodynamics was significantly disturbed in the presence of CKD markers, especially in patients with type 2 diabetes mellitus. The cut-off point of RI in segmental IRA indicating the CKD markers is 0,725.

Aim. To study interconnections between epicardial adipose tissue thickness (EATt), parameters of glucose metabolism/insulin, C-reactive protein (hsCRP), serum adipokines and severity of coronary artery disease (CAD) depending on the presence of diabetes mellitus type 2 (DM 2); to determine significant markers of CAD severity in patients with DM 2. Materials and methods. The study involved 106 patients with CAD (m/f 64/42, 60.96.8 years), including patients with DM 2 (group 1, n=35) and non-diabetic patients (group 2, n=71). Severity of CAD was evaluated according to angiography data with calculation of Gensini Score (GS). EATt was assessed via echocardiography. Serum levels of glucose/insulin metabolism parameters, lipid fractions, hsCRP and adipokines were evaluated. Clinical parameters, including GS, did not differ between groups. Results. EAT thickness median was elevated in gr.1 (5.1 mm vs. 4.4 mm in group 2), while adiponectin levels were decreased (6.55 g/ml vs. 7.71 g/ml). Linear regression of body mass index and resistin levels on EATt was revealed in gr.1; in gr.2 EATt linearly increased with waist circumference increment when EATt6 mm. Linear regression of EATt on GS was revealed in gr.1 when EATt8 mm, while linear regression in the whole GS range was obtained for HDL-C and hsCRP levels. Conclusion. Study results demonstrate differences in mechanisms of deposition and functioning of epicardial and abdominal adipose tissue depending on the presence or absence of diabetic status. Patients with DM2 are characterized by the excessive EAT deposition and decrease of serum adiponectin levels compared to non-diabetic patients in the equal conditions. Independent markers of CAD severity in DM 2 are decreased HDL-C and increased hsCRP levels, but not EATt.