摘要
目的研究高盐对肥胖相关性高血压患者醛固酮的影响。方法收集2016年12月至2017年6月第三军医大学大坪医院住院的高血压患者301例,按照体重指数分成正常体重组和超重肥胖组,对两组患者一般资料及24 h尿醛固酮及摄盐量等临床资料进行比较分析。结果与正常体重的高血压患者相比较,超重肥胖的高血压患者摄盐量显著升高,同时其24 h尿醛固酮排泄量也显著增加。通过对血脂、血糖、尿酸等因素进行多变量校正后,超重肥胖的高血压患者较正常体重的高血压患者24 h尿醛固酮水平增加0.577μg、日均摄盐量增加1.754 g。对超重肥胖的高血压患者按照摄盐量(中位数8.66 g/d)分为高摄盐组和低摄盐组,结果高摄盐组的高血压患者较低摄盐组的高血压患者的24 h尿醛固酮水平显著升高,相关分析显示超重肥胖组的高血压患者24 h尿醛固酮排泄与摄盐量呈正相关(r=0.1480,P<0.05)。结论肥胖相关性高血压患者摄盐量和24 h尿醛固酮水平显著升高,且二者显著相关,这可能是导致难治性高血压的原因之一。
Objective To study the effect of high salt intake on urinary aldosterone excretion in obesity-related hypertensive patients. Methods A total of 301 patients with hypertension were randomly divided into normal body weight group and overweight/obese group according to their body mass index(BMI). The general data and 24-hour urine aldosterone excretion were collected and analyzed. Results Compared with hypertensive patients from normal body weight group, the salt intake and 24-hour urinary aldosterone excretion were significantly increased in hypertensive patients of overweight/obesity group. After adjusting for blood fat, sugar, UA and other confounding factors, 24-hour urinary aldosterone excretion of overweight/obesity group was increased by 0.577 ug and salt intake increased by 1.754 g/d, when compared to hypertensive patients of normal body weight group. According to median of salt intake(median 8.66 g/d), overweight/obesity groups was divided into high salt intake group and low salt intake group, and the analysis showed that 24-hour urinary aldosterone excretion was significantly increased in the high salt intake group, and the correlation analysis showed that 24-hour urinary aldosterone excretion was positively correlated with salt intake(r=0.1480, P<0.05). Conclution Obesity-related hypertensive patients have higher salt intake and 24-hour urinary aldosterone excretion level. Salt intake is positively correlated with their 24-hour urinary aldosterone excretion,and it may be one of the causes of refractory hypertension.
引文
[1]Mente A,O'Donnell MJ,Rangarajan S,et al.Association of urinary sodium and potassium excretion with blood pressure[J].N Engl J Med,2014,371(7):601-611.
[2]李若青,陈珏材,何洪波,等.高血压患者肥胖程度及盐摄入量对血压的影响研究[J].中国实用内科杂志,2015,35(4):338-341.
[3]中华医学会心血管病学分会高血压学组.肥胖相关性高血压管理的中国专家共识[J].中华心血管病杂志,2016,44(3):212-219.
[4]Bentley-Lewis R,Adler GK,Perlstein T,et al.Body mass index predicts aldosterone production in normotensive adults on a high-salt diet.[J].JClin Endocrinol Meta,2007,92(11):4472.
[5]刘力生.中国高血压防治指南2010[J].中华心血管病杂志,2011,39(7):701-708.
[6]Cobb LK,Anderson CA,Elliott P,et al.Methodological issues in cohort studies that relate sodium intake to cardiovascular disease outcomes:a science advisory from the American Heart Association[J].Circulation,2014,129(10):1173-1186.
[7]He FJ,Marrero NM,Macgregor GA.Salt intake is related to soft drink consumption in children and adolescents:a link to obesity?[J].Hypertension,2008,51(6):e54;author reply e55.
[8]中华人民共和国卫生部疾病控制司.中国成人超重和肥胖症预控制指南[M].人民卫生出版社,2006.
[9]Ma Y,He FJ,Macgregor GA.High Salt Intake:Independent Risk Factor for Obesity?[J].Hypertension,2015,66(4):843-849.
[10]Harada E,Mizuno Y,Katoh D,et al.Increased urinary aldosterone excretion is associated with subcutaneous not visceral,adipose tissue area in obese individuals:a possible manifestation of dysfunctional subcutaneous adipose tissue.[J].Clin Endocrinol,2013,79(4):510-516.
[11]Ames MK,Atkins CE,Lantis AC,et al.Evaluation of subacute change in RAAS activity(as indicated by urinary aldosterone:creatinine,after pharmacologic provocation)and the response to ACE inhibition.[J].JRenin Angiotensin Aldosterone Syst,2016,17(1):1470320316633897.
[12]Achard V,Boulluciocca S,Desbriere R,et al.Renin receptor expression in human adipose tissue.[J].Am J Physiol Regul Integr Comp Physiol,2007,292(1):R274.
[13]Henegar JR,Bigler SA,Henegar LK,et al.Functional and structural changes in the kidney in the early stages of obesity[J].J Am Soc Nephrol,2001,12(6):1211-1217.
[14]Catena C,Colussi G,Sechi LA.Aldosterone,organ damage and dietary salt.[J].Clin Exp Pharmacol Physiol,2013,40(12):922-928.