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Effect of low birth weight on impaired renal development and function and hypertension in rat model
Zongde Xie1, Qingyi Dong, Jianfang Ge
1Institute of Pediatrics, The Second Xiangya Hospital, Central South University, Changsha, PR China. xiezd9099@yahoo.com.cn
Insights
Low birth weight (LBW) in rats, caused by a maternal low-protein diet, leads to abnormal kidney development and renal dysfunction. A reduced glomerular number in LBW offspring is a risk factor for developing hypertension.
Area of Science:
- Nephrology
- Developmental Biology
- Cardiovascular Physiology
Background:
- Low birth weight (LBW) is linked to adult hypertension.
- LBW may impair kidney development, leading to renal dysfunction and hypertension.
Purpose of the Study:
- To investigate the impact of maternal low-protein diet on kidney development and function in Sprague-Dawley rats.
- To determine if impaired kidney development in LBW offspring is associated with hypertension.
Main Methods:
- Rats were fed isocaloric diets with 21% (control) or 10% (LBW) protein during pregnancy.
- Offspring renal function and structure were assessed from birth to 3 months.
- Measurements included urine protein, serum and urine creatinine, creatinine clearance, glomerular number, and blood pressure.
Main Results:
- LBW rats showed increased urine protein volume at 3 months and lower urine creatinine at 2 and 3 months.
- Creatinine clearance rate (Ccr) was significantly lower in LBW rats at all time points.
- LBW rats had fewer glomeruli and increased blood pressure at 2 months, with a negative correlation between blood pressure and glomerular number.
Conclusions:
- Maternal low-protein diet causes abnormal kidney development and renal dysfunction in LBW rats.
- Reduced glomerular number in LBW offspring is a potential risk factor for hypertension.
Background/Aim:
Epidemiological studies have shown that low birth weight (LBW) is associated with a higher incidence of hypertension in adulthood. LBW may affect the kidney development, which in turn leads to impaired renal function and hypertension.
Methods:
Sprague-Dawley rats were fed isocaloric diets containing either 21% (w/w) (control group) or 10% (w/w) (LBW group) protein throughout pregnancy and chow during lactation. Renal function and structure of the offspring were measured from birth to 3 months.
Results:
At 3 weeks and 2 months, there was no difference in the volume of 24 h urine protein between the two groups. However, the volume was higher (117.17 ± 10.40 vs. 79.28 ± 14.26, p < 0.01) in LBW group at 3 months. Maternal protein intake did not alter serum creatinine in this study, but urine creatinine was lower in LBW group at 2 and 3 months. The creatinine clearance rate (Ccr) was significantly lower in LBW group than in control group at all time points. Glomerular number was reduced significantly in LBW group (22,720 ± 639 vs. 28,520 ± 526, p < 0.01) at 2 months, which was accompanied by an increase in blood pressure. There was a statistically significant negative correlation between the blood pressure and the glomerular number at 2 months (r = -0.919, p = 0.008).
Conclusions:
These data showed that abnormal kidney development and renal dysfunction occurred in LBW rats due to a maternal low-protein diet. Possessing a decreased glomerular number might be a risk factor for hypertension in LBW rats.
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