The Kidney from Prenatal to Adult Life: Perinatal Programming and Reduction of Number of Nephrons during Development

Abstract

Modified embryonic-fetal development resulting in low birth weight may lead to a reduced nephron endowment, hypertension and renal diseases in adulthood. Regarding the involvement of genetic factors, several environmental conditions may also contribute towards reducing the number of nephrons in the fetus and infant, subsequently constituting a health burden in later life. To date no methods of investigation for the early detection of a reduced nephron reserve are available. However, more structured studies should be implemented to investigate the role of angiotensin-converting enzyme inhibitors in managing proteinurias and glomerulosclerosis in children with renal conditions characterized by reduce nephron number and glomerular hypertrophic changes. In view of the current lack of specific methods of investigation and management, close monitoring of children and young adults at risk of reduced renal reserve should be carried out to enhance the early detection of potential changes in renal function.

Ambulatory blood pressure monitoring and renal functions in term small-for-gestational age children

“…Although the Values are given as the mean ± SD B2MG, Beta-2 microglobulin; NAG, β-N-acetyl-D-glucosaminidase; GFR, glomerular filtration rate pathogenesis is still unclear, it has been proposed that fetal growth retardation may be associated with impaired nephronogenesis, resulting in fewer nephrons and an increased chance of renal disease later in life. Glomerular hyperfiltration resulting from a reduced number of nephrons could lead to systemic hypertension, glomerular sclerosis and progressive deterioration of renal function [22]. Nephrogenesis is a complex process that requires many factors.…”

Chronic Kidney Disease: A Life Course Health Development Perspective

“…Key considerations for prevention include developing ways to motivate young girls and women to adopt nutritional supplementation in the preconception period when there are clear benefits for doing so. There is increasing evidence (human and animal studies) that even modest levels of vitamin A deficiency can reduce nephron number in developing fetuses (Puddu et al 2009). These simple and easily treated risks should not be overlooked.…”

“…In infancy/childhood, the most overt cause of CKD and end-stage renal disease is birth defects or congenital anomalies of the kidney and urinary tract that result in inadequate renal mass to provide internal physiologic homeostasis for the provision of growth and development (NAPRTCS 2011;Chen et al 2012;Bagby 2015;Puddu et al 2009;Chiang et al 2010;Hsu et al 2014;Greenbaum et al 2011;Horbar et al 2012;Hack et al 2002;Stelloh et al 2012;Gilbert et al 1990;Lelievre-Pegorier et al 1998;Sutherland et al 2012a;Ortiz et al 2001;Brenner and Anderson 1987;Reidy and Kaskel 2007;Fogo 2007;Lopez-Hernandez and Lopez-Novoa 2012;Gubhaju et al 2009;Sutherland et al 2012b;White et al 2009;Bacchetta et al 2009;KeijzerVeen et al 2010;Rademacher and Sinaiko 2009;Salgado et al 2009; Centers for Disease Control and Prevention (CDC) 2007; Hodgin et al 2009a;Harambat et al 2012;Warady and Chadha 2007;Tabel et al 2010;Sanna-Cherchi et al 2009). The long-term consequences of prematurity on renal mass are more subtle but, as mentioned above, are becoming increasingly clear.…”

Personalized Neonatal Medicine

“…Consequently, a mismatch between pre-and postnatal nutrient environments may induce an altered cardiovascular, renal, pulmonary, and metabolic function in the adult age. Approaches such as individualized fortification of human milk may be very useful in this setting with long-term beneficial effects and should be considered in Neonatal Intensive Care Units and (NICUs) [22][23][24].…”