肾脏差异的胎儿起源。

Fetal origins of renal disparities.

机构信息

Duke Clinical Research Institute, Duke University, Durham, NC 27705, USA.

出版信息

Semin Nephrol. 2010 Jan;30(1):42-50. doi: 10.1016/j.semnephrol.2009.10.002.

DOI:10.1016/j.semnephrol.2009.10.002

PMID:20116647

Abstract

Epidemiologic studies of populations continue to emerge showing that early-life factors influence the risk of developing several chronic diseases of adulthood. Susceptibility to environmental factors is particularly problematic during renal development, which is not complete until 36 weeks of gestation. Environmental deprivation may lead to adaptations including early growth restriction, whereas late insults may alter the kidney during the final stages of development. Because disparities among those who are more likely to have low birth weight mirrors the disparities observed among those more likely to develop kidney-related disorders, fetal origins have been presumed to explain some of the observed disparities. Although current empiric evidence supports a link between fetal programming and childhood/adult kidney disease, affected pathways may vary by race.

摘要

人群的流行病学研究不断涌现，表明生命早期因素会影响成年后发生多种慢性疾病的风险。肾脏发育直到妊娠 36 周才完成，在此期间，对环境因素的易感性特别成问题。环境剥夺可能导致适应，包括早期生长受限，而晚期损伤可能在发育的最后阶段改变肾脏。由于那些更有可能出生体重低的人群之间的差异反映了那些更有可能发生与肾脏相关的疾病的人群之间的差异，因此人们推测胎儿起源可以解释一些观察到的差异。尽管目前的经验证据支持胎儿编程与儿童/成人肾脏疾病之间存在联系，但受影响的途径可能因种族而异。