Torres Vicente E, Abebe Kaleab Z, Schrier Robert W, Perrone Ronald D, Chapman Arlene B, Yu Alan S, Braun William E, Steinman Theodore I, Brosnahan Godela, Hogan Marie C, Rahbari Frederic F, Grantham Jared J, Bae Kyongtae T, Moore Charity G, Flessner Michael F
Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Kidney Int. 2017 Feb;91(2):493-500. doi: 10.1016/j.kint.2016.10.018. Epub 2016 Dec 16.
The CRISP study of polycystic kidney disease (PKD) found that urinary sodium excretion associated with the rate of total kidney volume increase. Whether sodium restriction slows the progression of Autosomal Dominant PKD (ADPKD) is not known. To evaluate this we conducted a post hoc analysis of the HALT-PKD clinical trials of renin-angiotensin blockade in patients with ADPKD. Linear mixed models examined whether dietary sodium affected rates of total kidney volume or change in estimated glomerular filtration rate (eGFR) in patients with an eGFR over 60 ml/min/1.73 m (Study A) or the risk for a composite endpoint of 50% reduction in eGFR, end-stage renal disease or death, or the rate of eGFR decline in patients with an eGFR 25-60 ml/min/1.73 m (Study B) all in patients initiated on an under100 mEq sodium diet. During the trial urinary sodium excretion significantly declined by an average of 0.25 and 0.41 mEq/24 hour per month in studies A and B, respectively. In Study A, averaged and time varying urinary sodium excretions were significantly associated with kidney growth (0.43%/year and 0.09%/year, respectively, for each 18 mEq urinary sodium excretion). Averaged urinary sodium excretion was not significantly associated with faster eGFR decline (-0.07 ml/min/1.73m/year for each 18 mEq urinary sodium excretion). In Study B, the averaged but not time-varying urinary sodium excretion significantly associated with increased risk for the composite endpoint (hazard ratio 1.08 for each 18 mEq urinary sodium excretion) and a significantly faster eGFR decline (-0.09 ml/min/1.73m/year for each mEq 18 mEq urinary sodium excretion). Thus, sodium restriction is beneficial in the management of ADPKD.
多囊肾病(PKD)的CRISP研究发现,尿钠排泄与总肾体积增加速率相关。钠限制是否能减缓常染色体显性多囊肾病(ADPKD)的进展尚不清楚。为了评估这一点,我们对ADPKD患者肾素-血管紧张素阻断的HALT-PKD临床试验进行了事后分析。线性混合模型检查了饮食钠是否影响总肾体积变化率或估算肾小球滤过率(eGFR)超过60 ml/min/1.73 m²的患者的eGFR变化(研究A),或eGFR为25 - 60 ml/min/1.73 m²的患者中eGFR降低50%、终末期肾病或死亡的复合终点风险,或eGFR下降速率(研究B),所有患者均采用钠摄入量低于100 mEq的饮食。在试验期间,研究A和B的尿钠排泄量分别平均每月显著下降0.25和0.41 mEq/24小时。在研究A中,平均和随时间变化的尿钠排泄量与肾脏生长显著相关(每18 mEq尿钠排泄量分别为每年0.43%和0.09%)。平均尿钠排泄量与更快的eGFR下降无显著相关性(每18 mEq尿钠排泄量为每年 - 0.07 ml/min/1.73m²)。在研究B中,平均而非随时间变化的尿钠排泄量与复合终点风险增加显著相关(每18 mEq尿钠排泄量的风险比为1.08),且eGFR下降显著更快(每18 mEq尿钠排泄量为每年 - 0.09 ml/min/1.73m²)。因此,钠限制对ADPKD的管理有益。