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Hypertension and kidney alterations in rat offspring from low protein pregnancies
Veronica C Villar-Martini1, Jorge J Carvalho, Mario F Neves
1Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Insights
Maternal low protein intake during gestation impairs kidney development, leading to fewer nephrons and structural damage. This increases the risk of kidney disease later in life.
Area of Science:
- Nephrology
- Developmental Biology
- Nutritional Science
Background:
- Low birth weight is linked to early-onset end-stage renal disease.
- Maternal nutrition during gestation significantly impacts offspring kidney development.
Purpose of the Study:
- To investigate early and late glomerular structural changes in Wistar rats.
- To assess the effects of gestational low protein intake on offspring kidney development.
Main Methods:
- Wistar rats were fed either normal (19%) or low (5%) protein diets during gestation.
- Offspring were studied at birth (day 0), day 10, day 90, and day 180.
- Kidney structure, glomerular basement membrane (GBM) thickness, and podocyte morphology were analyzed.
Main Results:
- Low protein offspring exhibited delayed glomerulogenesis and fewer renal corpuscles (nephrons) compared to controls.
- In adulthood, low protein offspring showed higher blood pressure, thickened GBM, and podocyte structural abnormalities.
- Immature glomeruli were present at day 10 only in low protein offspring, indicating impaired nephrogenesis.
Conclusions:
- Gestational low protein diet causes glomerulogenesis retardation and reduced nephron number.
- Structural alterations, including GBM thickening and podocyte damage, persist into adulthood.
- These findings highlight the long-term renal consequences of maternal nutritional deficiencies.
Objective:
Low birth weight contributes to the early onset of end-stage renal disease. Therefore, this study was undertaken to investigate early and late glomerular structural alterations in both sexes of Wistar rat offspring from dams submitted to severe low protein intake during gestation.
Methods:
Offspring from dams fed normal protein (19% of protein) or low protein (5% of protein) were studied at days 0, 10, 90 and 180 of age.
Results:
Inner cortical structure showed immature (comma-shaped and S-shaped forms) and mature corpuscles in different proportions in low protein offspring (less maturity) and normal protein offspring (more maturity). At day 10 (end of the nephrogenesis period), immature corpuscles were observed only in low protein offspring. In adulthood, low protein offspring had higher blood pressure, and showed thicker glomerular basement membrane (GBM) with effacement of the pedicles, and slit diaphragm absent with some podocytes directly adhering to the basal membrane with pedicles absent. The number of renal corpuscles was lower in low protein offspring than in normal protein offspring of the same sex, all age groups (P < 0.001). No interaction was observed between sex and maternal nutrition for the same sex and all age groups.
Conclusion:
Gestational low protein leads to glomerulogenesis retardation and consequently a lower nephron number with thick GBM and structural alterations in the pedicles of podocytes.
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