Influence of Birth Weight on the Renal Development and Kidney Diseases in Adulthood: Experimental and Clinical Evidence

Abstract

Several clinical and experimental studies support the hypothesis that foetal programming is an important determinant of nephropathy, hypertension, coronary heart disease, and type 2 diabetes during adulthood. In this paper, the renal repercussions of foetal programming are emphasised, and the physiopathological mechanisms are discussed. The programming of renal diseases is detailed based on the findings of kidney development and functional parameters.

Морфологічні особливості нирок плодів та новонароджених від матерів з підгострим інфекційно-запальним процесом у черевній порожнині, викликаним Escherichia coli (експериментальне дослідження)

“…В части публикаций отмечено, что у людей формирование нефронов завершается примерно на 32-34-й неделе гестации, и поэтому любой дефицит количества нефронов, возникающий при рождении, не может быть компенсирован путем усиленного нефрогенеза после рождения [15,16]. В то же время имеются публикации, где указано, что у недоношен-ных детей нефрогенез наблюдается до 40-го дня по-сле рождения [15,17].…”

Chronic Kidney Disease: A Life Course Health Development Perspective

“…In addition, increased glomerular apoptosis has been observed (Pham et al 2003). Studies of the mechanism by which intrauterine growth retardation may induce hypertension have suggested a role for the renin-angiotensin system, renal sympathetic activation, maternal glucocorticoid and fetal kidney 11beta-hydroxysteroid dehydrogenase type 2 activation, and increased sodium retention (Baserga et al 2010;Ojeda et al 2007;Grigore et al 2007;Langley-Evans 1997;Sanders et al 2005;Franco et al 2012). Several studies have indicated that altered gene expression may be the result of epigenetic regulation (Baserga et al 2010;Pham et al 2003;Woroniecki et al 2011).…”

“…While glomerular hypertrophy is thought to be maladaptive, there are conflicting data on the benefit of interventions designed to block renal hypertrophy, such as with mTOR inhibition (Vogelbacher et al 2007;Kurdian et al 2012;Fukuda et al 2012). While the ESCAPE trial (which included children with congenital anomalies of the kidney and urinary tract) showed strict blood pressure control in conjunction with ACE inhibition was beneficial, retrospective analyses were unable to identify a benefit from ACE inhibition in children with congenital anomalies of the kidney and urinary tract (Ardissino et al 2007;Neild 2009).…”

“…While the ESCAPE trial (which included children with congenital anomalies of the kidney and urinary tract) showed strict blood pressure control in conjunction with ACE inhibition was beneficial, retrospective analyses were unable to identify a benefit from ACE inhibition in children with congenital anomalies of the kidney and urinary tract (Ardissino et al 2007;Neild 2009). Interestingly, recent studies have suggested that an imbalance between podocyte and nephron growth can induce glomerulosclerosis (Fukuda et al 2012). Further studies are needed to better understand the developmental determinants of nephron and podocyte growth and whether imbalance of podocyte and glomerular growth contributes to glomerulosclerosis in genetic forms of focal glomerulosclerosis.…”

The functional state of the kidneys in newborns with intrauterine delay development

“…Задержка внутриутробного развития (ЗВУР) -это системное нарушение созревания и развития всех органов и систем ребенка, поэтому постнатально ЗВУР может проявиться недостаточностью функции любого органа или системы, в том числе почек у новорожденного ребенка [2].…”