摘要
Background Cardiovascular disease （CVD） is the leading cause of death in patients with end-stage renal disease （ESRD）. We explored the relationship between CVD, plasma brain natriuretic peptide （BNP） and copeptin in non-dialysis patients with chronic kidney disease （CKD）. Methods BNP and copeptin were measured using ELISA in 86 non-dialysis patients with different degrees of CKD and in 20 control patients. The effects of BNP, copeptin levels and other biochemical indices on carotid ultrasound echocardiography and CVD history were determined using correlation analysis. Results BNP and copeptin levels were significantly higher in the CKD group than in the control group. Both indices increased progressively, in parallel with the decline in glomerular filtration rate （GFR）. BNP levels were （184.25±65.18） ng/L in early phase CKD, （975.245±354.09） ng/L in middle phase CKD, and （1463.51±614.92） ng/ml in end phase CKD compared with levels of （101.56±42.76） ng/L in the control group （all P 〈0.01）. Copeptin levels in the middle phase （（20.36±9.47） pmol/L） and end phase groups （（54.26±18.23） pmol/L were significantly higher than in the control group （（9.21±2.64） pmol/L; both P 〈0.01）. There was no difference in copeptin levels between early phase CKD （（10.09±5.23） pmol/L） and control patients. Stepwise multiple regression analysis identified GFR, intima-media thickness （IMT）, left ventricular hypertrophy （LVH）, and previous history of CVD as independent risk factors for elevated BNP and copeptin levels. Conclusion BNP and copeptin appear to provide sensitive biological markers for the evaluation of atherosclerosis in non-dialysis patients with CKD.
Background Cardiovascular disease （CVD） is the leading cause of death in patients with end-stage renal disease （ESRD）. We explored the relationship between CVD, plasma brain natriuretic peptide （BNP） and copeptin in non-dialysis patients with chronic kidney disease （CKD）. Methods BNP and copeptin were measured using ELISA in 86 non-dialysis patients with different degrees of CKD and in 20 control patients. The effects of BNP, copeptin levels and other biochemical indices on carotid ultrasound echocardiography and CVD history were determined using correlation analysis. Results BNP and copeptin levels were significantly higher in the CKD group than in the control group. Both indices increased progressively, in parallel with the decline in glomerular filtration rate （GFR）. BNP levels were （184.25±65.18） ng/L in early phase CKD, （975.245±354.09） ng/L in middle phase CKD, and （1463.51±614.92） ng/ml in end phase CKD compared with levels of （101.56±42.76） ng/L in the control group （all P 〈0.01）. Copeptin levels in the middle phase （（20.36±9.47） pmol/L） and end phase groups （（54.26±18.23） pmol/L were significantly higher than in the control group （（9.21±2.64） pmol/L; both P 〈0.01）. There was no difference in copeptin levels between early phase CKD （（10.09±5.23） pmol/L） and control patients. Stepwise multiple regression analysis identified GFR, intima-media thickness （IMT）, left ventricular hypertrophy （LVH）, and previous history of CVD as independent risk factors for elevated BNP and copeptin levels. Conclusion BNP and copeptin appear to provide sensitive biological markers for the evaluation of atherosclerosis in non-dialysis patients with CKD.
