Sutherland Megan R, Black Mary Jane
Department of Anatomy and Developmental Biology and Monash Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Nat Rev Nephrol. 2023 Apr;19(4):218-228. doi: 10.1038/s41581-022-00668-8. Epub 2023 Jan 16.
In humans born at term, maximal nephron number is reached by the time nephrogenesis is completed - at approximately 36 weeks' gestation. The number of nephrons does not increase further and subsequently remains stable until loss occurs through ageing or disease. Nephron endowment is key to the functional capacity of the kidney and its resilience to disease; hence, any processes that impair kidney development in the developing fetus can have lifelong adverse consequences for renal health and, consequently, for quality and length of life. The timing of nephrogenesis underlies the vulnerability of developing human kidneys to adverse early life exposures. Indeed, exposure of the developing fetus to a suboptimal intrauterine environment during gestation - resulting in intrauterine growth restriction (IUGR) - and/or preterm birth can impede kidney development and lead to reduced nephron endowment. Furthermore, emerging research suggests that IUGR and/or preterm birth is associated with an elevated risk of chronic kidney disease in later life. The available data highlight the important role of early life development in the aetiology of kidney disease and emphasize the need to develop strategies to optimize nephron endowment in IUGR and preterm infants.
对于足月出生的人类，在肾发生完成时——大约在妊娠36周时——达到最大肾单位数量。肾单位数量不会进一步增加，随后保持稳定，直到因衰老或疾病而减少。肾单位数量是肾脏功能能力及其对疾病恢复力的关键；因此，任何损害发育中胎儿肾脏发育的过程都可能对肾脏健康产生终身不良后果，进而对生活质量和寿命产生影响。肾发生的时间决定了发育中的人类肾脏对早期不良生活暴露的易感性。事实上，发育中的胎儿在妊娠期暴露于次优的子宫内环境——导致子宫内生长受限（IUGR）——和/或早产会阻碍肾脏发育并导致肾单位数量减少。此外，新出现的研究表明，IUGR和/或早产与晚年患慢性肾病的风险升高有关。现有数据突出了早期生命发育在肾病病因中的重要作用，并强调需要制定策略来优化IUGR和早产婴儿的肾单位数量。
