Division of Epidemiology, Department of Public Health Sciences, University of Miami, Miami, Florida, USA.
Division of Epidemiology, Department of Public Health Sciences, University of Miami, Miami, Florida, USA.
Kidney Int. 2020 Jul;98(1):187-194. doi: 10.1016/j.kint.2020.02.037. Epub 2020 Apr 21.
The association between dietary sodium and potassium intake with the development of kidney disease remains unclear, particularly among younger individuals. Here, we determined whether dietary sodium and potassium intake are associated with incident chronic kidney disease (CKD) using data from 1,030 adults (age 23-35 in 1990-1991) from the Coronary Artery Risk Development In Young Adults study, based on repeated measurements of estimated glomerular filtration rate (eGFR) and urinary albumin to creatinine ratio (ACR) from 1995 through 2015. Urinary sodium and potassium excretion (mg/day), calculated from three 24-hour urine collections in 1990-1991, were averaged to measure sodium and potassium intake. Serum creatinine was used to calculate eGFR using the CKD EPI equation; spot urine albumin and creatinine were used to calculate ACR, each at five visits from 1995-1996 through 2015-2016. CKD was defined as decreased eGFR (under 60 ml/min/1.73m) or the development of albuminuria (ACR over 30 mg/g). We used log binomial regression models adjusted for socio-demographic, behavioral, and clinical factors to determine whether sodium and potassium intake were associated with incident CKD (decreased eGFR or developed albuminuria) among those free of CKD in 1995. Dietary sodium intake was not significantly associated with incident CKD. However, every 1,000 mg/day increment of potassium intake in 1990 was significantly associated with a 29% lower risk of incident albuminuria (relative risk 0.71, 95% confidence interval 0.53, 0.95), but not eGFR. Thus, higher dietary potassium intake may protect against the development of kidney damage, particularly albuminuria.
饮食钠和钾摄入量与肾脏疾病的发展之间的关系尚不清楚,特别是在年轻人中。在这里,我们使用来自冠状动脉风险发展在年轻人研究中的 1030 名成年人(1990-1991 年年龄为 23-35 岁)的数据,根据 1995 年至 2015 年期间重复测量估计肾小球滤过率(eGFR)和尿白蛋白与肌酐比(ACR),来确定饮食钠和钾摄入量是否与慢性肾脏病(CKD)的发生有关。通过 1990-1991 年的三次 24 小时尿液收集计算尿钠和钾排泄量(mg/天),并将其平均以测量钠和钾的摄入量。使用 CKD EPI 方程根据血清肌酐计算 eGFR;在 1995-1996 年至 2015-2016 年期间的五次就诊中,使用点尿白蛋白和肌酐计算 ACR。CKD 定义为 eGFR 降低(<60ml/min/1.73m)或蛋白尿发展(ACR 超过 30mg/g)。我们使用对数二项式回归模型调整了社会人口统计学、行为和临床因素,以确定 1995 年无 CKD 的人群中钠和钾摄入量是否与 CKD 的发生(eGFR 降低或蛋白尿发展)有关。饮食钠摄入量与 CKD 的发生无显著相关性。然而,1990 年钾摄入量每增加 1000mg/天,与发生蛋白尿的风险降低 29%显著相关(相对风险 0.71,95%置信区间 0.53,0.95),但与 eGFR 无关。因此,较高的饮食钾摄入量可能有助于预防肾脏损害,特别是蛋白尿。