In healthy newborn babies, nephrogenesis proceeds unnoticed until birth. With start of the perinatal period, morphogenetic activity in the renal outer cortex consisting of an inner maturation zone and an outer nephrogenic zone is downregulated by unknown signals. One of the results is that the entire nephrogenic zone as well as the contained progenitor cells and niches disintegrate. In contrast, a too early inactivation of the nephrogenic zone takes place in the kidneys of preterm and low birth weight babies. Although they are born in a period of active nephrogenesis, pathological findings show that they evolve to a high incidence oligonephropathy. However, very few data exist about cell biological changes that are evoked by harming, further most of causing molecules, exact cell targets, and related molecular pathways are not identified. Although impairment of nephrogenesis was the subject of research in animal species, there is only limited information available pertaining to the pathological traces in the nephrogenic zone of the human fetal kidney. In this situation, the lack of basic morphological data is particularly aggravating. Surprisingly, there are not even ultrastructural investigations available. Since concrete information is lacking also in relevant textbooks, the current contribution likes to present key features of the nephrogenic zone in the fetal human kidney. Simultaneously, it is a call to explore systematically a hardly known area.
Keywords: Fetal human kidney; Impaired nephrogenesis; Low birth weight babies; Nephrogenic zone; Niche; Preterm infants; Renal capsule.