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

Abstract

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 (n=18) or without dialysis treatment (control group; n=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 (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. 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.