Renal failure · 2012
The relationship of visfatin levels with insulin resistance and left ventricular hypertrophy in peritoneal dialysis patients.
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Karakan Sebnem, Sezer Siren, Özdemir Acar F Nurhan, Haberal Mehmet
Аннотация
BACKGROUND/OBJECTIVES: Cardiovascular abnormalities are common in patients with chronic kidney disease. Visfatin influences lipid metabolism, insulin sensitivity, and cardiovascular health. The aim of this study was to explore the relation of serum visfatin to cardiovascular risk factors in nondiabetic peritoneal dialysis (PD) patients.
PATIENTS AND METHODS: Eighty-seven nondiabetic patients (mean age 48 ± 15 years, 39 males) under PD were enrolled. Weight, anthropometric measurements, blood pressure, biochemical parameters, and insulin resistance (homeostatic model assessment-insulin resistance-HOMA-IR) were measured. Visfatin was measured and left ventricular mass index (LVMI) was calculated by echocardiography.
RESULTS: LVMI was correlated with body mass index (BMI; r = 0.47, p = 0.01), systolic blood pressure (SBP; r = 0.62, p = 0.04), and serum visfatin levels (r = 0.49, p = 0.03). According to HOMA-IR levels patients were grouped as insulin-resistant (IR) (HOMA-IR ≥2.0, n = 35) and noninsulin-resistant (non-IR) (HOMA-IR <2.0, n = 52) groups. The IR group had longer PD duration and higher BMI, total cholesterol, uric acid, and serum visfatin levels (p < 0.05). The study patients were divided into three groups according to their serum visfatin levels. Group 1 (≤34 ng/mL, n = 22) was considered as the lowest tertile of low visfatin and group 2 (35-42 ng/mL, n = 43) and group 3 (≥43 ng/mL, n = 22) in the upper tertile. Considering the visfatin groups, group 3 patients had significantly higher BMI (p = 0.00), total cholesterol (p = 0.03), C-reactive protein (CRP) (p = 0.03), HOMA-IR (p = 0.03), and LVMI (p = 0.02). In regression analysis, SBP (β = 0.19, p < 0.05) and serum visfatin levels (β = 0.74, p < 0.05) were independent variables affecting LVMI.
CONCLUSION: Serum visfatin might be a sensitive marker than HOMA-IR evaluations for cardiac performance in nondiabetic PD patients.
PATIENTS AND METHODS: Eighty-seven nondiabetic patients (mean age 48 ± 15 years, 39 males) under PD were enrolled. Weight, anthropometric measurements, blood pressure, biochemical parameters, and insulin resistance (homeostatic model assessment-insulin resistance-HOMA-IR) were measured. Visfatin was measured and left ventricular mass index (LVMI) was calculated by echocardiography.
RESULTS: LVMI was correlated with body mass index (BMI; r = 0.47, p = 0.01), systolic blood pressure (SBP; r = 0.62, p = 0.04), and serum visfatin levels (r = 0.49, p = 0.03). According to HOMA-IR levels patients were grouped as insulin-resistant (IR) (HOMA-IR ≥2.0, n = 35) and noninsulin-resistant (non-IR) (HOMA-IR <2.0, n = 52) groups. The IR group had longer PD duration and higher BMI, total cholesterol, uric acid, and serum visfatin levels (p < 0.05). The study patients were divided into three groups according to their serum visfatin levels. Group 1 (≤34 ng/mL, n = 22) was considered as the lowest tertile of low visfatin and group 2 (35-42 ng/mL, n = 43) and group 3 (≥43 ng/mL, n = 22) in the upper tertile. Considering the visfatin groups, group 3 patients had significantly higher BMI (p = 0.00), total cholesterol (p = 0.03), C-reactive protein (CRP) (p = 0.03), HOMA-IR (p = 0.03), and LVMI (p = 0.02). In regression analysis, SBP (β = 0.19, p < 0.05) and serum visfatin levels (β = 0.74, p < 0.05) were independent variables affecting LVMI.
CONCLUSION: Serum visfatin might be a sensitive marker than HOMA-IR evaluations for cardiac performance in nondiabetic PD patients.