Zohdi Vladislava, Sutherland Megan R, Lim Kyungjoon, Gubhaju Lina, Zimanyi Monika A, Black M Jane
Department of Anatomy and Developmental Biology, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, VIC 3800, Australia.
Int J Nephrol. 2012;2012:136942. doi: 10.1155/2012/136942. Epub 2012 Aug 27.
Epidemiological studies have clearly demonstrated a strong association between low birth weight and long-term renal disease. A potential mediator of this long-term risk is a reduction in nephron endowment in the low birth weight infant at the beginning of life. Importantly, nephrons are only formed early in life; during normal gestation, nephrogenesis is complete by about 32-36 weeks, with no new nephrons formed after this time during the lifetime of the individual. Hence, given that a loss of a critical number of nephrons is the hallmark of renal disease, an increased severity and acceleration of renal disease is likely when the number of nephrons is already reduced prior to disease onset. Low birth weight can result from intrauterine growth restriction (IUGR) or preterm birth; a high proportion of babies born prematurely also exhibit IUGR. In this paper, we describe how IUGR and preterm birth adversely impact on nephrogenesis and how a subsequent reduced nephron endowment at the beginning of life may lead to long-term risk of renal disease, but not necessarily hypertension.
流行病学研究已明确证实低出生体重与长期肾病之间存在密切关联。这种长期风险的一个潜在中介因素是低出生体重婴儿在生命开始时肾单位数量减少。重要的是，肾单位仅在生命早期形成；在正常妊娠期间，肾发生在大约32 - 36周时完成，个体一生中在此之后不会形成新的肾单位。因此，鉴于关键数量的肾单位丧失是肾病的标志，当在疾病发作前肾单位数量就已经减少时，肾病的严重程度增加和病情加速发展的可能性就很大。低出生体重可能由宫内生长受限（IUGR）或早产导致；很大比例的早产婴儿也表现出宫内生长受限。在本文中，我们描述了宫内生长受限和早产如何对肾发生产生不利影响，以及生命开始时随后肾单位数量减少如何可能导致肾病的长期风险，但不一定导致高血压。
