University of Cologne, Faculty of Medicine, University Hospital Cologne, Department of Pediatric and Adolescent Medicine, Germany; University of Cologne, Faculty of Medicine, University Hospital Cologne, Center for Molecular Medicine Cologne (CMMC), Germany.
University of Cologne, Faculty of Medicine, University Hospital Cologne, Translational Experimental Pediatrics - Experimental Pulmonology, Department of Pediatric and Adolescent Medicine, Germany; University of Cologne, Faculty of Medicine, University Hospital Cologne, Center for Molecular Medicine Cologne (CMMC), Germany.
Semin Fetal Neonatal Med. 2022 Feb;27(1):101245. doi: 10.1016/j.siny.2021.101245. Epub 2021 May 8.
Adverse perinatal circumstances can cause acute kidney injury (AKI) and contribute to chronic kidney disease (CKD). Accumulating evidence indicate that a wide spectrum of perinatal conditions interferes with normal kidney development and ultimately leads to aberrant kidney structure and function later in life. The present review addresses the lack of mechanistic knowledge with regard to perinatal origins of CKD and provides a comprehensive overview of pre- and peri-natal insults, including genetic predisposition, suboptimal nutritional supply, obesity and maternal metabolic disorders as well as placental insufficiency leading to intrauterine growth restriction (IUGR), prematurity, infections, inflammatory processes, and the need for life-saving treatments (e.g. oxygen supplementation, mechanical ventilation, medications) in neonates. Finally, we discuss future preventive, therapeutic, and regenerative directions. In summary, this review highlights the perinatal vulnerability of the kidney and the early origins of increased susceptibility toward AKI and CKD during postnatal life. Promotion of kidney health and prevention of disease require the understanding of perinatal injury in order to optimize perinatal micro- and macro-environments and enable normal kidney development.
围产期不良情况可导致急性肾损伤 (AKI),并促成慢性肾脏病 (CKD)。越来越多的证据表明,广泛的围产期情况会干扰正常的肾脏发育,并最终导致生命后期肾脏结构和功能异常。本综述针对围产期 CKD 的发病机制知识的缺乏,并提供了围产期和围生期损伤的全面概述,包括遗传易感性、营养供应不足、肥胖和母体代谢紊乱以及胎盘功能不全导致的宫内生长受限 (IUGR)、早产、感染、炎症过程,以及新生儿需要救生治疗(例如氧补充、机械通气、药物)。最后,我们讨论了未来的预防、治疗和再生方向。总之,本综述强调了肾脏在围产期的脆弱性,以及在生命后期对 AKI 和 CKD 的易感性增加的早期起源。促进肾脏健康和预防疾病需要了解围产期损伤,以优化围产期微环境和大环境,并使正常的肾脏发育成为可能。