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Journal Article
Review
Preterm Birth: Long Term Cardiovascular and Renal Consequences.
BACKGROUND: Cardiovascular and chronic kidney diseases are a part of noncommunicable chronic diseases, the leading causes of premature death worldwide. They are recognized as having early origins through altered developmental programming, due to adverse environmental conditions during development. Preterm birth is such an adverse factor. Rates of preterm birth increased in the last decades, however, with the improvement in perinatal and neonatal care, a growing number of preterm born subjects has now entered adulthood. Clinical and experimental evidence suggests that preterm birth is associated with impaired or arrested structural or functional development of key organs/systems making preterm infants vulnerable to cardiovascular and chronic renal diseases at adulthood. This review analyzes the evidence of such cardiovascular and renal changes, the role of perinatal and neonatal factors such as antenatal steroids and potential pathogenic mechanisms, including developmental programming and epigenetic alterations.
CONCLUSION: Preterm born subjects are exposed to a significantly increased risk for altered cardiovascular and renal functions at young adulthood. Adequate, specific follow-up measures remain to be determined. While antenatal steroids have considerably improved preterm birth outcomes, repeated therapy should be considered with caution, as antenatal steroids induce long-term cardiovascular and metabolic alterations in animals' models and their involvement in the accelerated cellular senescence observed in human studies cannot be excluded.
CONCLUSION: Preterm born subjects are exposed to a significantly increased risk for altered cardiovascular and renal functions at young adulthood. Adequate, specific follow-up measures remain to be determined. While antenatal steroids have considerably improved preterm birth outcomes, repeated therapy should be considered with caution, as antenatal steroids induce long-term cardiovascular and metabolic alterations in animals' models and their involvement in the accelerated cellular senescence observed in human studies cannot be excluded.
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