Prematurity and perinatal stress, such as intrauterine growth restriction (IUGR) and chorioamnionitis, are pathological processes creating an impaired intrauterine environment. These intrauterine factors are associated with the development of proteinuria, hypertension, and chronic kidney disease (CKD) later in life. Initially, this was thought to be secondary to oligonephropathy, subsequent glomerular hypertrophy, and hyperfiltration, leading to glomerulosclerosis, a further decrease in nephron number, and finally CKD. Nowadays, there is increasing evidence that prematurity and perinatal stress affect not only nephron endowment but also the maturation of podocytes and vasculogenesis. IUGR is associated with podocyte damage and an aggravated course of nephrotic syndrome. Moreover, preterm birth and IUGR are known to cause upregulation of the postnatal renin-angiotensin system, resulting in hypertension. Chorioamnionitis causes damage to the glomeruli, thereby predisposing to the development of glomerulosclerosis. This review aims to summarize current knowledge on the influence of prematurity, IUGR, and chorioamnionitis on the development of different glomerular structures. After summarizing human and experimental data on low nephron number in general, a specific focus on the current understanding of podocyte and glomerular capillary formation in relation to prematurity and different causes of perinatal stress is presented.

早产和围产期压力，如宫内生长受限 (IUGR) 和绒毛膜羊膜炎，是造成宫内环境受损的病理过程。这些宫内因素与以后出现蛋白尿、高血压和慢性肾病 (CKD) 相关。最初，这被认为是继发于少肾病、随后的肾小球肥大和过度滤过，导致肾小球硬化、肾单位数量进一步减少，最终导致 CKD。如今，越来越多的证据表明早产和围产期压力不仅影响肾单位禀赋，而且影响足细胞的成熟和血管生成。IUGR 与足细胞损伤和肾病综合征的加重进程有关。而且，众所周知，早产和 IUGR 会导致出生后肾素 - 血管紧张素系统的上调，从而导致高血压。绒毛膜羊膜炎会对肾小球造成损害，从而导致肾小球硬化的发展。本综述旨在总结目前关于早产、IUGR 和绒毛膜羊膜炎对不同肾小球结构发育的影响的知识。在总结了一般低肾单位数的人类和实验数据后，特别关注当前对足细胞和肾小球毛细血管形成与早产和围产期应激的不同原因的理解。本综述旨在总结目前关于早产、IUGR 和绒毛膜羊膜炎对不同肾小球结构发育的影响的知识。在总结了一般低肾单位数的人类和实验数据后，特别关注当前对足细胞和肾小球毛细血管形成与早产和围产期应激的不同原因的理解。本综述旨在总结目前关于早产、IUGR 和绒毛膜羊膜炎对不同肾小球结构发育的影响的知识。在总结了一般低肾单位数的人类和实验数据后，特别关注当前对足细胞和肾小球毛细血管形成与早产和围产期应激的不同原因的理解。