Kang H, Wang Y, Zhong X, Yin W, Li F, Jiang J
Department of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Laboratory Animal Center, Southern Medical University, Guangzhou 510515, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2021 Feb 25;41(2):264-271. doi: 10.12122/j.issn.1673-4254.2021.02.15.
To assess the effect of salt intake on residual renal function in rats and explore the possible mechanism.
SD rats were 5/6-nephrectomized to induce chronic renal failure followed by peritoneal dialysis for 4 weeks (=18) or without dialysis treatment (control group; =18). In both groups, the rats were divided into 3 subgroups and were given lowsalt diet (0.02% NaCl), normal salt diet (0.4% NaCl), and high-salt diet (4% NaCl). After 8 and 12weeks, blood pressure and creatinine and sodium levels in the blood, urine, and peritoneal dialysate of the rats were examined. Glomerular sclerosis, tubulointerstitial fibrosis, and protein expression levels of RAS components (ACE-1, AGT, and AT-1) in renal cortical tissue of the rats were evaluated.
The residual renal function of the rats all decreased especially in rats with high salt intake for 8and 12 weeks. In peritoneal dialysis group, the rats with high-salt diet showed signficiantly increased renal interstitial fibrosis score (=0.036), glomerular sclerosis index (=0.045), systolic blood pressure (=0.004), diastolic blood pressure (=0.048), and renal expressions of AGT, ACE-1, and AT1 ( < 0.05) as compared with those with normal salt intake. In the rats fed the same high-salt diet, the renal interstitial fibrosis score, glomerular sclerosis index, diastolic blood pressure increase, and renal AGT and ACE-1 expression levels were significantly lower in the peritoneal dialysis group than in the control group ( < 0.05). A positive correlation was noted between the reduction of residual renal function and sodium intake in the rats.
In rats with chronic renal failure, high salt intake promotes the activation of the renal RAS system, increases blood pressure, and agrevates renal fibrosis to accelerate the decline of residual renal function, and peritoneal dialysis partially reduces the damage of residual renal function induced by high-salt diets by removing excessive sodium.
评估盐摄入量对大鼠残余肾功能的影响并探讨其可能机制。
将SD大鼠进行5/6肾切除以诱导慢性肾衰竭，随后一组进行4周的腹膜透析（n = 18），另一组不进行透析治疗（对照组；n = 18）。在两组中，大鼠均被分为3个亚组，并分别给予低盐饮食（0.02% NaCl）、正常盐饮食（0.4% NaCl）和高盐饮食（4% NaCl）。8周和12周后，检测大鼠的血压、血液、尿液及腹膜透析液中的肌酐和钠水平。评估大鼠肾皮质组织中的肾小球硬化、肾小管间质纤维化以及肾素 - 血管紧张素系统（RAS）成分（ACE - 1、AGT和AT - Ⅰ）的蛋白表达水平。
大鼠的残余肾功能均下降，尤其是高盐摄入8周和12周的大鼠。在腹膜透析组中，与正常盐摄入的大鼠相比，高盐饮食的大鼠肾间质纤维化评分（P = 0.036）、肾小球硬化指数（P = 0.045）、收缩压（P = 0.004）、舒张压（P = 0.048）以及肾组织中AGT、ACE - 1和AT1的表达均显著增加（P < 0.05）。在喂食相同高盐饮食的大鼠中，腹膜透析组的肾间质纤维化评分、肾小球硬化指数、舒张压升高幅度以及肾组织中AGT和ACE - 1的表达水平均显著低于对照组（P < 0.05）。大鼠残余肾功能的降低与钠摄入量之间呈正相关。
在慢性肾衰竭大鼠中，高盐摄入促进肾RAS系统激活，升高血压，加重肾纤维化，加速残余肾功能下降，而腹膜透析通过清除过多的钠部分减轻高盐饮食对残余肾功能的损害。
