南方医科大学学报

南方医科大学学报 ›› 2021, Vol. 41 ›› Issue (2): 264-271.doi: 10.12122/j.issn.1673-4254.2021.02.15

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盐摄入量对腹膜透析大鼠残余肾功能的影响

康 瀚，王 羽，钟晓红，殷 伟，李 芳，蒋建平   

  • 发布日期:2021-02-05

Effect of salt intake on residual renal function in rats receiving peritoneal dialysis

  • Published:2021-02-05

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摘要：

目的 观察盐摄入量对大鼠残余肾功能的影响，探索盐对残余肾功能影响的可能机制。方法 将5/6肾切除慢性肾衰SD大鼠分为腹透组（n=18，给予腹膜透析治疗4周）和对照组（n=18未给予腹膜透析治疗）。腹透组和对照组组内再分别分为3个亚组，分别给低盐（0.02%NaCl）、正常盐（0.4%NaCl）、高盐（4%NaCl）饲料喂养。分别在8周和12周后，检测大鼠血压，血液、尿液、腹透液的肌酐、钠等生化指标水平；评估肾小球硬化和肾小管间质纤维化的程度；检测肾皮质组织RAS组分（ACE-1、AGT、AT-1）的蛋白表达水平。结果 在8周和12周后，大鼠残余肾功能均出现了下降，其中高盐摄入组大鼠残余肾功能最明显。腹透组中，与正常盐摄入组大鼠相比，高盐摄入组大鼠肾小管间质纤维化评分（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）、肾脏AGT、ACE-1、AT1（P<0.05）的表达水平明显升高。同为高盐饮食喂养的大鼠，腹透组大鼠肾间质纤维化评分、肾小球硬化指数、舒张压上升幅度、肾脏AGT、ACE-1表达水平低于对照组大鼠（P<0.05）。大鼠残余肾功能下降程度与摄钠量存在正相关。结论 高盐饮食的摄入促使肾脏RAS系统激活、血压升高、肾纤维化加重，加速慢性肾衰大鼠残余肾功能下降。腹膜透析通过对钠的清除，部分减轻了高钠饮食对慢性肾衰大鼠残余肾功能的损伤。

关键词:

Abstract: Objective To assess the effect of salt intake on residual renal function in rats and explore the possible mechanism. Methods SD rats were 5/6-nephrectomized to induce chronic renal failure followed by peritoneal dialysis for 4 weeks (n=18) or without dialysis treatment (control group; n=18). In both groups, the rats were divided into 3 subgroups and were given low-salt 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. Results The residual renal function of the rats all decreased especially in rats with high salt intake for 8 and 12 weeks. In peritoneal dialysis group, the rats with high-salt diet showed signficiantly increased renal interstitial fibrosis score (P=0.036), glomerular sclerosis index (P=0.045), systolic blood pressure (P=0.004), diastolic blood pressure (P=0.048), and renal expressions of AGT, ACE-1, and AT1 (P<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 (P<0.05). A positive correlation was noted between the reduction of residual renal function and sodium intake in the rats. Conclusion 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.

Key words: salt intake; peritoneal dialysis; residual renal function; rat models