BackgroundThe developmental origin of health and disease concept identifies the brain, cardiovascular, liver, and kidney systems as targets of fetal adverse programming with adult consequences. As the limits of viability in premature infants have been pushed to lower gestational ages, the long-term impact of prematurity on kidneys still remains a significant burden during hospital stay and beyond.ObjectivesThe purpose of this study is to summarize available evidence, mechanisms, and short- and long-term renal consequences of prematurity and identify nephroprotective strategies and areas of uncertainty.ResultsKidney size and nephron number are known to be reduced in surviving premature infants due to disruption of organogenesis at a crucial developmental time point. Inflammation, hyperoxia, and antiangiogenic factors play a role in epigenetic conditioning with potential life-long consequences. Additional kidney injury from hypoperfusion and nephrotoxicity results in structural and functional changes over time which are often unnoticed. Nephropathy of prematurity and acute kidney injury confound glomerular and tubular maturation of preterm kidneys. Kidney protective strategies may ameliorate growth failure and suboptimal neurodevelopmental outcomes in the short term. In later life, subclinical chronic renal disease may progress, even in asymptomatic survivors.ConclusionAwareness of renal implications of therapeutic interventions and renal conservation efforts may lead to a variety of short and long-term benefits. Adequate monitoring and supplementation of microelement losses, gathering improved data on renal handling, and exploration of new avenues such as reliable markers of injury and new therapeutic strategies in contemporary populations, as well as long-term follow-up of renal function, is warranted.

中文翻译：

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早产的肾脏后果

背景健康和疾病概念的发展起源将大脑、心血管、肝脏和肾脏系统确定为具有成人后果的胎儿不良编程的目标。由于早产儿生存能力的极限已被推到更低的胎龄，早产对肾脏的长期影响仍然是住院期间及以后的重大负担。目的本研究的目的是总结可用的证据、机制和早产的短期和长期肾脏后果，并确定肾脏保护策略和不确定领域。结果已知由于器官发生在关键发育时间点被破坏，存活早产儿的肾脏大小和肾单位数量会减少。炎症、高氧、和抗血管生成因子在具有潜在终生后果的表观遗传调节中发挥作用。灌注不足和肾毒性导致的额外肾损伤会随着时间的推移导致结构和功能发生变化，而这些变化通常被忽视。早产儿肾病和急性肾损伤混淆早产肾的肾小球和肾小管成熟。肾脏保护策略可能会在短期内改善生长障碍和次优的神经发育结果。在以后的生活中，亚临床慢性肾病可能会进展，即使在无症状的幸存者中也是如此。结论意识到治疗干预和肾脏保护工作对肾脏的影响可能会带来各种短期和长期益处。充分监测和补充微量元素损失，收集有关肾脏处理的改进数据，