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Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Early metabolic and hemodynamic indicators of kidney dysfunction in mice offspring from parental low protein diet
Fabiola Diniz1, Francesca Edgington-Giordano1, Samir S El-Dahr1
1Section of Pediatric Nephrology, Department of Pediatrics, Tulane University School of Medicine, New Orleans, LA, 70112, USA.
Insights
Maternal low-protein diet (LPD) causes kidney damage in offspring before blood pressure changes. Early metabolic alterations signal kidney damage, highlighting the need for monitoring in offspring of malnourished parents.
Area of Science:
- Nephrology
- Developmental Biology
- Nutritional Science
Background:
- Maternal malnutrition, specifically a low-protein diet (LPD), leads to offspring oligonephropathy, increasing risks for hypertension and chronic kidney disease.
- Subclinical kidney function alterations in offspring are often overlooked, delaying diagnosis and intervention.
- This study investigates early kidney morphology changes in offspring exposed to maternal LPD before significant functional decline.
Purpose of the Study:
- To examine the initial impact of a maternal low-protein diet (LPD) on kidney morphology and function in offspring.
- To identify early indicators of kidney damage in the first filial (F1) generation.
- To establish a link between parental LPD and offspring kidney development.
Main Methods:
- Histological analysis of kidney morphology.
- Assessment of kidney metabolic and hemodynamic panels.
- Utilized Linear Discriminant Analysis (LDA) and Principal Component Analysis (PCA) for statistical evaluation.
- Studied 12-week-old F1 mice from parents (F0) fed either LPD or normal-protein diet (NPD).
Main Results:
- Offspring (F1) from LPD-fed parents exhibited reduced body and kidney weight at birth and P20, with normalized body weight but persistent low kidney weight at 12 weeks.
- Abnormal kidney morphology, including dilated tubules, oligonephropathy, and cysts, was observed and worsened with age.
- Early metabolic changes included increased urine albumin, plasma creatinine, urea, and BUN, strongly correlated with parental LPD.
- While hemodynamics were largely unchanged, some male offspring showed altered systolic blood pressure, indicating potential sex-specific effects.
Conclusions:
- Significant kidney damage occurs in offspring of LPD-fed parents before detectable blood pressure changes.
- Subtle alterations in kidney metabolic function serve as early indicators of kidney damage.
- These findings underscore the importance of monitoring kidney health in offspring exposed to maternal malnutrition, with implications for both animal models and human health.
Background:
Parental malnutrition, particularly a low-protein diet (LPD), causes oligonephropathy at birth and predisposes offspring to hypertension and chronic kidney disease later in life. The onset of adult kidney disease varies based on genetics and environmental factors, often with subclinical alterations in kidney function being overlooked. This study aimed to examine changes in kidney morphology before significant kidney function decline in the offspring of mice fed a low-protein diet.
Methods:
Using a combination of histological analysis, kidney metabolic and hemodynamic panel assessments, and advanced statistical techniques such as Linear Discriminant Analysis (LDA) and Principal Component Analysis (PCA), we investigated the initial impact of a maternal low-protein diet (LPD) on kidney development and function. Our study utilized 12-week-old F1 mice from F0 parents fed either a low-protein diet (LPD) or a normal-protein diet (NPD) before the onset of hypertension.
Results:
The offspring (F1 generation) of parents (F0 generation) fed an LPD show reduced body weight from birth to P20. The kidney weight was also reduced compared to F1 offspring from parents fed an NPD. At 12 weeks of age, body weight normalized, but kidney weight remained low. Offspring of parents fed an LPD displayed abnormal kidney morphology, including dilated tubules, oligonephropathy, and fluid-filled cysts which had worsened with age. A kidney metabolic panel analysis at 12 weeks revealed a slight but consistent increase in urine albumin, plasma creatinine, mean urea, and BUN concentrations. Although no significant changes in hemodynamic variables were observed, 2/12 mice, both males, showed alterations in systolic blood pressure, suggesting sex-specific effects when comparing F1 mice from F0 fed either diet. Overall, kidney metabolic changes were strongly correlated to parental LPD.
Conclusion:
Our findings indicate that significant kidney damage must accumulate in the F1 generation from parents fed an LPD before any detectable changes in blood pressure occur. Our study suggests that small variations in kidney metabolic function may point to early kidney damage and should not be overlooked in the offspring of these malnourished mice and likely humans.
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