Abstract

Primary hypertension continues to be one of the main risk factors for cardiovascular disease worldwide. A stable intrauterine environment is critical for the future development and health of the fetus. The developing kidney has been found to be especially vulnerable during this time period, and epidemiological studies have demonstrated that an adverse in utero environment is associated with an increased risk of hypertension and chronic kidney disease. Macro- and micronutrient deficiencies as well as exposure to tobacco, alcohol, and certain medications during gestation have been shown to negatively impact nephrogenesis and reduce one’s nephron number. In 1988, Brenner et al. put forth the controversial hypothesis that a reduced nephron complement is a risk factor for hypertension and chronic kidney disease in adulthood. Since then numerous animal and human studies have confirmed this relationship demonstrating that there is an inverse association between blood pressure and nephron number. As our understanding of the developmental programming of hypertension and other non-communicable diseases improves, more effective preventive health measures can be developed in the future.

Highlights

  • Primary hypertension is one of the leading risk factors for morbidity and mortality in the world, and it has been designated as the primary risk factor for the global disease burden [1, 2]

  • There is an increasing body of literature demonstrating the relationship between nephron number and hypertension

  • These studies show that there is an inverse relationship between nephron endowment and hypertension. As this relationship is established, factors that contribute to determining nephron number are being elucidated

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Summary

Developmental Origins and Nephron Endowment in Hypertension

Primary hypertension continues to be one of the main risk factors for cardiovascular disease worldwide. The developing kidney has been found to be especially vulnerable during this time period, and epidemiological studies have demonstrated that an adverse in utero environment is associated with an increased risk of hypertension and chronic kidney disease. Macro- and micronutrient deficiencies as well as exposure to tobacco, alcohol, and certain medications during gestation have been shown to negatively impact nephrogenesis and reduce one’s nephron number. In 1988, Brenner et al put forth the controversial hypothesis that a reduced nephron complement is a risk factor for hypertension and chronic kidney disease in adulthood. As our understanding of the developmental programming of hypertension and other non-communicable diseases improves, more effective preventive health measures can be developed in the future

INTRODUCTION
NEPHRON ENDOWMENT
DETERMINANTS OF NEPHRON NUMBER
Birth Weight
Genetic Factors
DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE
Animal Studies
Low Birth Weight and Nephron Number in Humans
Impact of Ethnic and Racial Factors
Postnatal Influences on Nephron Number
Findings
CONCLUSION
Full Text
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