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When Less or More Isn't Enough: Renal Maldevelopment Arising From Disequilibrium in the Renin-Angiotensin System
Lucas Ferreira de Almeida1, Terezila Machado Coimbra1
1Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Insights
Maternal vitamin D deficiency or renin-angiotensin system (RAS) antagonists during fetal development can impair kidney function long-term. These factors disrupt kidney development, increasing risks for adult kidney disease and hypertension.
Area of Science:
- Developmental biology
- Nephrology
- Endocrinology
Background:
- Fetal and neonatal environmental/nutritional factors impact adult kidney health.
- The renin-angiotensin system (RAS) is crucial for kidney development and regulation.
- Vitamin D (VitD) deficiency and RAS antagonists have significant effects on fetal kidney development.
Purpose of the Study:
- To review mechanisms linking fetal RAS antagonists and VitD deficiency to kidney disturbances.
- To explore how maternal RAS imbalance affects fetal kidney development and adult health.
Main Methods:
- Literature review of studies on RAS, VitD, and kidney development.
- Analysis of potential mechanisms of kidney structure and function disturbances.
- Exploration of pathways impacting fetal development and long-term consequences.
Main Results:
- RAS antagonists during fetal development are linked to adult hypertension and renal dysfunction.
- VitD deficiency may inappropriately activate the RAS, affecting blood pressure and renin activity.
- RAS antagonists and VitD deficiency appear to have opposing roles in developmental regulation.
Conclusions:
- Disruptions in fetal kidney development due to RAS antagonists or VitD deficiency have lasting impacts.
- Understanding these mechanisms is crucial for preventing adult kidney disease.
- Maternal RAS status is critical for healthy fetal kidney development.
Abstract:
Environmental and nutritional factors during fetal and neonatal life can have long-lasting effects on renal functions and physiology and susceptibility to kidney disease in adulthood. All components of the renin-angiotensin system (RAS) are highly expressed in the kidneys during the period of renal development. The RAS plays a central role in the regulation of various cellular growth factors and stimulates adhesion molecules and cellular migration. The use of antagonists of this system during fetal development represents a major risk factor for hypertension, renal vascular dysfunction, and kidney medulla atrophy in adulthood. The inappropriate activation of the RAS by vitamin D (VitD) deficiency has been studied in recent years. Clinical and experimental studies have demonstrated an inverse relationship between circulating VitD levels and blood pressure, plasma and renin activity, and an increase in angiotensin II and the receptor AT1. These data raise new questions about the importance of the integrity of the RAS during development since RAS pathway inhibitors and VitD deficiency have opposing functions. This is a literature review on the possible mechanisms by which antagonists of the RAS and VitD deficiency during fetal development provoke disturbances in kidney structure and function. Potential mechanisms are presented and discussed, and the possible pathways by which an imbalanced maternal RAS may negatively impact fetal development and have consequences in adulthood are also explored.