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Estimation of Nephron Number in Whole Kidney using the Acid Maceration Method
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Developmental Origins and Nephron Endowment in Hypertension
Shari Gurusinghe1, Anita Tambay1, Christine B Sethna1
1Department of Pediatrics, Division of Pediatric Nephrology, Cohen Children's Medical Center of New York, New York, NY, United States.
Frontiers in Pediatrics
|July 15, 2017
Summary
A reduced number of nephrons, or kidney functional units, acquired during fetal development is linked to higher blood pressure and kidney disease risk later in life. Improving prenatal conditions may prevent future hypertension.
Area of Science:
- Nephrology
- Developmental Biology
- Cardiovascular Disease
Background:
- Primary hypertension is a major global risk factor for cardiovascular disease.
- The intrauterine environment significantly influences fetal kidney development and long-term health.
- Adverse prenatal conditions can impair nephrogenesis, reducing nephron number.
Purpose of the Study:
- To explore the link between reduced nephron number and the risk of adult hypertension and chronic kidney disease.
- To review evidence supporting the developmental programming of hypertension.
Main Methods:
- Review of epidemiological studies on prenatal factors and kidney development.
- Analysis of animal and human studies investigating the relationship between nephron number and blood pressure.
- Examination of Brenner's hypothesis on reduced nephron complement.
Main Results:
- Numerous studies confirm an inverse association between blood pressure and nephron number.
- Adverse in utero exposures (nutritional deficiencies, toxins) negatively impact nephrogenesis.
- A reduced nephron complement is a confirmed risk factor for hypertension and chronic kidney disease.
Conclusions:
- The number of nephrons established during fetal development is critical for adult cardiovascular and kidney health.
- Understanding developmental programming offers pathways for preventing non-communicable diseases.
- Future preventive health strategies can target improving the intrauterine environment to enhance nephrogenesis.
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