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

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          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.

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          The clinical importance of nephron mass.

          Michael B Brenner, V Luyckx (2010)
          Abundant evidence supports the association between low birth weight (LBW) and renal dysfunction in humans. Anatomic measurements of infants, children, and adults show significant inverse correlation between LBW and nephron number. Nephron numbers are also lower in individuals with hypertension compared with normotension among white and Australian Aboriginal populations. The relationship between nephron number and hypertension among black individuals is still unclear, although the high incidence of LBW predicts low nephron number in this population as well. LBW, a surrogate for low nephron number, also associates with increasing BP from childhood to adulthood and increasing risk for chronic kidney disease in later life. Because nephron numbers can be counted only postmortem, surrogate markers such as birth weight, prematurity, adult height, reduced renal size, and glomerulomegaly are potentially useful for risk stratification, for example, during living-donor assessment. Because early postnatal growth also affects subsequent risk for higher BP or reduced renal function, postnatal nutrition, a potentially modifiable factor, in addition to intrauterine effects, has significant influence on long-term cardiovascular and renal health.
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            Nephron number, hypertension, renal disease, and renal failure.

            W Hoy, John Bertram, Michael D Hughson … (2005)
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              Maternal protein restriction suppresses the newborn renin-angiotensin system and programs adult hypertension in rats.

              Daisajou Woods, J Nyengaard, F Ingelfinger … (2001)
              Restriction of maternal protein intake during rat pregnancy produces offspring that are hypertensive in adulthood, but the mechanisms are not well understood. Our purpose was to determine whether this adult hypertension could be programmed during development by suppression of the fetal/newborn renin-angiotensin system (RAS) and a consequent reduction in nephron number. Pregnant rats were fed a normal protein (19%, NP) or low-protein (8.5%, LP) diet throughout gestation. Birth weight was reduced by 13% (p < 0.0005), and the kidney/body weight ratio was reduced in LP pups. Renal renin mRNA levels were significantly reduced in newborn LP pups; renal renin concentration and renin immunostaining were suppressed. Renal tissue angiotensin II levels were also suppressed in newborn LP (0.079 +/- 0.002 ng/mg, LP versus 0.146 +/- 0.016 ng/mg, NP, p < 0.01). Mean arterial pressure in conscious, chronically instrumented adult offspring (21 wk) was higher in LP (135 +/- 1 mm Hg, LP versus 126 +/- 1 mm Hg, NP, p < 0.00007), and GFR normalized to kidney weight was reduced in LP (p < 0.04). The number of glomeruli per kidney was lower in adult LP offspring (21,567 +/- 1,694, LP versus 28,917 +/- 2,342, NP, p < 0.03), and individual glomerular volume was higher (1.81 +/- 0.16 10(6) microm(3), LP versus 1.11 +/- 0.10 10(6) microm(3), NP, p < 0.005); the total volume of all glomeruli per kidney was not significantly different. Thus, perinatal protein restriction in the rat suppresses the newborn intrarenal RAS and leads to a reduced number of glomeruli, glomerular enlargement, and hypertension in the adult.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Nephrol
                Journal ID (iso-abbrev): Int J Nephrol
                Journal ID (publisher-id): IJN
                Title: International Journal of Nephrology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-214X
                ISSN (Electronic): 2090-2158
                Publication date (Print): 2012
                Publication date (Electronic): 17 June 2012
                Volume: 2012
                Electronic Location Identifier: 608025
                Affiliations
                1Division of Nephrology, School of Medicine, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil
                2Department of Physiology, School of Medicine, Federal University of São Paulo, 04023-062 São Paulo, SP, Brazil
                3Department of Molecular Cardiology, Cleveland Clinic, Cleveland, OH 44195, USA
                Author notes
                *Maria C. P. Franco: mdcfranco@ 123456nefro.epm.br

                Academic Editor: Umberto Simeoni

                Article
                DOI: 10.1155/2012/608025
                PMC ID: 3385608
                PubMed ID: 22778952
                SO-VID: 70f326d8-892a-4414-bed0-8af9bbb0bd83
                Copyright © Copyright © 2012 Maria C. P. Franco et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 March 2012
                Date revision received : 18 April 2012
                Date accepted : 2 May 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Nephrology
                Data availability:
                ScienceOpen disciplines: Nephrology

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