Objective·To analyze the influencing factors of left ventricular mass index(LVMI)in patients with essential hypertension,and explore the relationship between aldosterone levels and left ventricular hypertrophy(LVH).Methods·A total of 155 patients with essential hypertension,hospitalized in the Hypertension Department of the Northern Campus of Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,from January 2013 to December 2019,and excluded from primary aldosteronism by saline load test(post-saline suppression plasma aldosterone<60 pg/mL),were enrolled.General clinical data(age,gender,smoking status,duration of hypertension,etc.),physical examination data(blood pressure and body mass index),blood biochemistry(renal function,electrolytes,fasting blood glucose,and lipids),urinary sodium,and relevant hormones(basal and activated aldosterone,basal and activated renin,urinary aldosterone,post-saline suppression aldosterone,etc.)were collected.LVMI was evaluated by echocardiography.Pearson correlation analysis was used to assess the linear association between LVMI and each variable.Binary Logistic regression models were applied to screen independent risk factors for LVH.Multiple linear regression models were used to assess the impact of variables on LVMI.Results·The mean age of the 155 patients was(46.85±11.08)years,with 51.6%being male.Pearson correlation analysis showed that LVMI was significantly positively correlated with post-saline suppression aldosterone(r=0.334,P<0.001),age(r=0.184,P=0.032),duration of hypertension(r=0.241,P=0.005),systolic blood pressure(r=0.280,P=0.001),and pulse pressure(r=0.339,P<0.001).No significant correlations were found with diastolic blood pressure,body mass index,fasting blood glucose,total cholesterol,low-density lipoprotein cholesterol,triglyceride,high-density lipoprotein cholesterol,urinary sodium,basal aldosterone,activated aldosterone,or urinary aldosterone.After adjusting for confounders,including gender,smoking history,age,duration of hypertension,body mass index,pulse pressure,systolic blood pressure,fasting blood glucose,and total cholesterol,binary Logistic regression showed that each 1 pg/mL increase in post-saline suppression aldosterone was associated with a 5.1%increased risk of LVH(OR=1.051,95%CI 1.016?1.088,P=0.004).Multiple linear regression identified suppressed aldosterone(β=0.359,P<0.001),duration of hypertension(β=0.168,P=0.046),and pulse pressure(β=0.226,P=0.008)as independent influencing factors for LVMI.Conclusion·Suppressed aldosterone is an independent influencing factor for LVH in patients with essential hypertension.

Objective·To analyze the influencing factors of left ventricular mass index(LVMI)in patients with essential hypertension,and explore the relationship between aldosterone levels and left ventricular hypertrophy(LVH).Methods·A total of 155 patients with essential hypertension,hospitalized in the Hypertension Department of the Northern Campus of Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,from January 2013 to December 2019,and excluded from primary aldosteronism by saline load test(post-saline suppression plasma aldosterone<60 pg/mL),were enrolled.General clinical data(age,gender,smoking status,duration of hypertension,etc.),physical examination data(blood pressure and body mass index),blood biochemistry(renal function,electrolytes,fasting blood glucose,and lipids),urinary sodium,and relevant hormones(basal and activated aldosterone,basal and activated renin,urinary aldosterone,post-saline suppression aldosterone,etc.)were collected.LVMI was evaluated by echocardiography.Pearson correlation analysis was used to assess the linear association between LVMI and each variable.Binary Logistic regression models were applied to screen independent risk factors for LVH.Multiple linear regression models were used to assess the impact of variables on LVMI.Results·The mean age of the 155 patients was(46.85±11.08)years,with 51.6%being male.Pearson correlation analysis showed that LVMI was significantly positively correlated with post-saline suppression aldosterone(r=0.334,P<0.001),age(r=0.184,P=0.032),duration of hypertension(r=0.241,P=0.005),systolic blood pressure(r=0.280,P=0.001),and pulse pressure(r=0.339,P<0.001).No significant correlations were found with diastolic blood pressure,body mass index,fasting blood glucose,total cholesterol,low-density lipoprotein cholesterol,triglyceride,high-density lipoprotein cholesterol,urinary sodium,basal aldosterone,activated aldosterone,or urinary aldosterone.After adjusting for confounders,including gender,smoking history,age,duration of hypertension,body mass index,pulse pressure,systolic blood pressure,fasting blood glucose,and total cholesterol,binary Logistic regression showed that each 1 pg/mL increase in post-saline suppression aldosterone was associated with a 5.1%increased risk of LVH(OR=1.051,95%CI 1.016?1.088,P=0.004).Multiple linear regression identified suppressed aldosterone(β=0.359,P<0.001),duration of hypertension(β=0.168,P=0.046),and pulse pressure(β=0.226,P=0.008)as independent influencing factors for LVMI.Conclusion·Suppressed aldosterone is an independent influencing factor for LVH in patients with essential hypertension.

Objective To investigate the effects of fluvastatin on the tubulointerstitium damage in progressive diabetic kidney disease. Methods A rat model of type 2 diabetic nephropathy (DN) was developed successfully by combination of dietary induced insulin resistance and low dose STZ induced hyperglycemia after unilateral nephrectomy. Female SD rats were randomly divided into three groups: control rats, type 2 diabetic rats and type 2 diabetic rats treated with fluvastatin (2mg/kg/d). After 6 weeks, blood glucose, serum insulin, serum triglyceride and cholesterol, serum creatinine, and urinary protein were measured respectively. The protein expressions of c Jun and tansforming growth factor (TGF) ? 1 were studied by immunohistochemistry. TGF ? 1 gene expression was studied with a RT PCR technique. Results Fluvastatin at lower doses, which did not influence blood glucose and blood lipid level, significantly inhibited expression of c Jun protein(0 2536?0 0180 vs 0 5855?0 0314, P