Institute of Anatomy, University of Regensburg, Regensburg, Germany.
Ann Anat. 2021 Jul;236:151705. doi: 10.1016/j.aanat.2021.151705. Epub 2021 Feb 16.
Clinical experiences reveal that the kidneys of preterm and low birth weight infants are highly vulnerable. Noxae of various molecular composition can damage the outer renal cortex, resulting in an early termination of nephron formation. However, in contrast to what is known about the rodent kidney, with reference to the damage on the early stages of nephron anlage such as the comma-shaped body, renal vesicles, pretubular aggregate or nephrogenic niche, this information in the fetal human kidney is not available. The few documented pathological alterations in the fetal human kidney during late gestation are glomeruli with a dilated Bowman's space and a shrunken tuft, the reduction in width of the nephrogenic zone and the lack of here contained S-shaped bodies. The latter points out that the shaping, folding or expansion of the developing nephron must be disrupted. Since these specific aspects have been little investigated, the aim of the present microanatomical contribution is to highlight it.
Firstly, the individual stages of nephron anlage in the fetal human kidney during late gestation were documented by microscopic images. Then, as a stylistic tool for the pointing to specific sites of the running developmental process, a series of true to scale sketches were produced.
The generated sketches depict the spatial expansion of the transiently appearing stages of nephron anlage. These are restricted to the nephrogenic zone and are framed by the inner side of the renal capsule, the related collecting duct ampulla and a perforating radiate artery. Practical hints and a consequent nomenclature explain the developmental course and help us to identify the precise location of the proximal - distal poles, medial - lateral profiles, connecting points, adhesion sites or folds at the developing nephron on microscopic specimens.
The impairment of nephrogenesis in preterm and low birth weight babies is an unsolved biomedical issue. To contribute, by provided true to scale sketches, numerous practical hints and a consequent nomenclature typical features of nephron formation in the fetal human kidney at late gestation are demonstrated.
临床经验表明,早产儿和低出生体重儿的肾脏非常脆弱。各种分子组成的活性氧可以损伤外肾皮质,导致肾单位形成提前终止。然而,与已知的啮齿动物肾脏不同,对于肾单位原基的早期损伤,如逗号形胚体、肾小囊、肾小管集合或肾发生龛,这些信息在胎儿人类肾脏中并不存在。在妊娠晚期,胎儿人类肾脏中仅有少数有记载的病理性改变,包括扩张的Bowman 氏腔和缩小的肾小球丛、肾发生区变窄以及缺乏包含其中的 S 形小体。后一种情况表明,发育中的肾单位的塑造、折叠或扩张必然受到干扰。由于这些具体方面研究较少,本研究旨在强调这一点。
首先,通过显微镜图像记录妊娠晚期胎儿人类肾脏中肾单位原基的各个阶段。然后,作为指向特定发育过程的风格化工具,生成了一系列按比例绘制的真实草图。
生成的草图描绘了肾单位原基的短暂出现阶段的空间扩展。这些阶段仅限于肾发生区,由肾被膜的内侧、相关的集合管壶腹和穿透性放射状动脉所包围。实用提示和相应的命名法解释了发育过程,并帮助我们识别发育中的肾单位在显微镜标本上的近端-远端极、内侧-外侧轮廓、连接点、粘连部位或折叠的确切位置。
早产儿和低出生体重儿的肾发生受损是一个尚未解决的生物医学问题。本研究通过提供按比例绘制的真实草图、大量实用提示和相应的命名法,展示了妊娠晚期胎儿人类肾脏中肾单位形成的典型特征。