“Physiological” renal regenerating medicine in VLBW preterm infants: could a dream come true?

Abstract

An emerging hypothesis from the recent literature explain how specific adverse factors related with growth retardation as well as of low birth weight (LBW) might influence renal development during fetal life and then the insurgence of hypertension and renal disease in adulthood. In this article, after introducing a brief overview of human nephrogenesis, the most important factors influencing nephron number at birth will be reviewed, focusing on the "in utero" experiences that lead to an increased risk of developing hypertension and/or kidney disease in adult. Since nephrogenesis in preterm human newborns does not stop at birth, but it continues for 4-6 weeks postnatally, a better knowledge of the mechanisms able to accelerate nephrogenesis in the perinatal period, could represent a powerful tool in the hands of neonatologists. We suggest to define this approach to a possible therapy of a deficient nephrogenesis at birth "physiological renal regenerating medicine". Our goal in preterm infants, especially VLBW, could be to prolong the nephrogenesis not only for 6 weeks after birth but until 36 weeks of post conceptual age, allowing newborn kidneys to restore their nephron endowment, escaping susceptibility to hypertension and to renal disease later in life.

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

“…117,118 The identification of these potentially modifiable epigenetic factors raises the possibility that eventually strategies might be developed to extend a premature infant' s period of normal nephrogenesis to 36 weeks' postmenstrual age, allowing their kidneys to attain a normal nephron number despite their premature birth. 119,120 Nutrition…”

Cell Projections and Extracellular Matrix Cross the Interstitial Interface within the Renal Stem/Progenitor Cell Niche: Accidental, Structural or Functional Cues?

“…Either survival of stem/progenitor cells is limited [5,6] or an effective regeneration of parenchyma is missing due to environmental factors [7,8]. In consideration of these facts the question arises which cell biological mechanisms are preventing the restoration of renal parenchyma [9]. Since revealing data are missing until now, the panel of speculations is broad.…”

CD44 immunoreactivity in the developing human kidney: a marker of renal progenitor stem cells?

“…Further studies are needed, in order to better clarify the role of CD44-reactive multipotent cells in human kidney development, that might help to better understand the mechanisms at the basis of renal stem cell involvement in renal repair and regeneration 19 in childhood and adulthood kidney disease.…”