title: The role of maternal nutrition, metabolic function and the placenta in developmental programming of renal dysfunction.
abstract: The intrauterine environment is critical for the development of the foetus. Barker and colleagues were the first to identify that adverse perturbations during foetal development are associated with an increased risk of developing diseases in adulthood, including cardiorenal disease. Specifically for the kidney, perturbations in utero can lead to nephron deficits and renal dysfunction by a number of mechanisms. Altered programming of nephron number is associated with an increased risk of developing kidney disease via glomerular hypertrophy and reduced vasodilative capacity of the renal blood vessels; both of which would contribute to hypertension in adulthood, with males being more susceptible to disease outcomes. Additionally, alterations in the renin-angiotensin system (RAS) such as an upregulation or downregulation of specific receptors, depending on the nature of the insult, have also been implicated in the development of renal dysfunction. Sex-specific differences in the expression of the RAS during late gestation and in the early postnatal environment have also been identified. Extensive research has demonstrated that both uteroplacental insufficiency and maternal malnutrition alter renal development in utero. Equally, exposure to maternal diabetes and maternal obesity during development are also associated with an increased risk of developing renal disease, however, the mechanism behind this association is poorly understood. Therefore, identifying the link between an adverse intrauterine environment and the programmed kidney disease risk in adulthood may facilitate the development of strategies to alleviate the epidemics of cardiorenal disease worldwide, in addition to understanding why males are more susceptible to adult-onset cardiovascular diseases.
authors.affiliation: Department of Physiology, The University of Melbourne, Parkville, Vic., Australia.
authors.forename: V F I
authors.initials: VF
authors.lastname: Richter
authors.affiliation: Department of Physiology, The University of Melbourne, Parkville, Vic., Australia.
authors.forename: J F
authors.initials: JF
authors.lastname: Briffa
authors.affiliation: School of Biomedical Sciences, University of Queensland, St. Lucia, Qld, Australia.
authors.forename: K M
authors.initials: KM
authors.lastname: Moritz
authors.affiliation: Department of Physiology, The University of Melbourne, Parkville, Vic., Australia.
authors.forename: M E
authors.initials: ME
authors.lastname: Wlodek
authors.affiliation: Department of Physiology, The University of Melbourne, Parkville, Vic., Australia.
authors.forename: D H
authors.initials: DH
authors.lastname: Hryciw
mesh_terms: D000818:Animals; D005260:Female; D006801:Humans; D007668:Kidney / Q000196:embryology* / Q000378:metabolism / Q000503:physiopathology*; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity; D010920:Placenta / Q000503:physiopathology*; D010927:Placental Insufficiency; D011247:Pregnancy; D011248:Pregnancy Complications
keywords: gestational diabetes; intrauterine growth restriction; maternal malnutrition; maternal obesity; renal dysfunction; uteroplacental insufficiency