Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 The developmental origins of health and disease: an overview
- 2 The ‘developmental origins’ hypothesis: epidemiology
- 3 The conceptual basis for the developmental origins of health and disease
- 4 The periconceptional and embryonic period
- 5 Epigenetic mechanisms
- 6 A mitochondrial component of developmental programming
- 7 Role of exposure to environmental chemicals in developmental origins of health and disease
- 8 Maternal nutrition and fetal growth and development
- 9 Placental mechanisms and developmental origins of health and disease
- 10 Control of fetal metabolism: relevance to developmental origins of health and disease
- 11 Lipid metabolism: relevance to developmental origins of health and disease
- 12 Prenatal hypoxia: relevance to developmental origins of health and disease
- 13 The fetal hypothalamic–pituitary–adrenal axis: relevance to developmental origins of health and disease
- 14 Perinatal influences on the endocrine and metabolic axes during childhood
- 15 Patterns of growth: relevance to developmental origins of health and disease
- 16 The developmental environment and the endocrine pancreas
- 17 The developmental environment and insulin resistance
- 18 The developmental environment and the development of obesity
- 19 The developmental environment and its role in the metabolic syndrome
- 20 Programming the cardiovascular system
- 21 The role of vascular dysfunction in developmental origins of health and disease: evidence from human and animal studies
- 22 The developmental environment and atherogenesis
- 23 The developmental environment, renal function and disease
- 24 The developmental environment: effect on fluid and electrolyte homeostasis
- 25 The developmental environment: effects on lung structure and function
- 26 Developmental origins of asthma and related allergic disorders
- 27 The developmental environment: influences on subsequent cognitive function and behaviour
- 28 The developmental environment and the origins of neurological disorders
- 29 The developmental environment: clinical perspectives on effects on the musculoskeletal system
- 30 The developmental environment: experimental perspectives on skeletal development
- 31 The developmental environment and the early origins of cancer
- 32 The developmental environment: implications for ageing and life span
- 33 Developmental origins of health and disease: implications for primary intervention for cardiovascular and metabolic disease
- 34 Developmental origins of health and disease: public-health perspectives
- 35 Developmental origins of health and disease: implications for developing countries
- 36 Developmental origins of health and disease: ethical and social considerations
- 37 Past obstacles and future promise
- Index
- References
23 - The developmental environment, renal function and disease
Published online by Cambridge University Press: 08 August 2009
Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 The developmental origins of health and disease: an overview
- 2 The ‘developmental origins’ hypothesis: epidemiology
- 3 The conceptual basis for the developmental origins of health and disease
- 4 The periconceptional and embryonic period
- 5 Epigenetic mechanisms
- 6 A mitochondrial component of developmental programming
- 7 Role of exposure to environmental chemicals in developmental origins of health and disease
- 8 Maternal nutrition and fetal growth and development
- 9 Placental mechanisms and developmental origins of health and disease
- 10 Control of fetal metabolism: relevance to developmental origins of health and disease
- 11 Lipid metabolism: relevance to developmental origins of health and disease
- 12 Prenatal hypoxia: relevance to developmental origins of health and disease
- 13 The fetal hypothalamic–pituitary–adrenal axis: relevance to developmental origins of health and disease
- 14 Perinatal influences on the endocrine and metabolic axes during childhood
- 15 Patterns of growth: relevance to developmental origins of health and disease
- 16 The developmental environment and the endocrine pancreas
- 17 The developmental environment and insulin resistance
- 18 The developmental environment and the development of obesity
- 19 The developmental environment and its role in the metabolic syndrome
- 20 Programming the cardiovascular system
- 21 The role of vascular dysfunction in developmental origins of health and disease: evidence from human and animal studies
- 22 The developmental environment and atherogenesis
- 23 The developmental environment, renal function and disease
- 24 The developmental environment: effect on fluid and electrolyte homeostasis
- 25 The developmental environment: effects on lung structure and function
- 26 Developmental origins of asthma and related allergic disorders
- 27 The developmental environment: influences on subsequent cognitive function and behaviour
- 28 The developmental environment and the origins of neurological disorders
- 29 The developmental environment: clinical perspectives on effects on the musculoskeletal system
- 30 The developmental environment: experimental perspectives on skeletal development
- 31 The developmental environment and the early origins of cancer
- 32 The developmental environment: implications for ageing and life span
- 33 Developmental origins of health and disease: implications for primary intervention for cardiovascular and metabolic disease
- 34 Developmental origins of health and disease: public-health perspectives
- 35 Developmental origins of health and disease: implications for developing countries
- 36 Developmental origins of health and disease: ethical and social considerations
- 37 Past obstacles and future promise
- Index
- References
Summary
Introduction
Chronic renal disease is a major health problem in many societies. In some populations, including the Australian Aborigine, the Pima Indians of the USA, and certain populations of African-Americans, diseased kidneys due to chronic hypertension progress into end-stage renal disease, with a particularly high incidence (Hoy et al. 1999, Kett and Bertram 2004). The American Kidney Foundation estimates that as many as 20 million Americans, or approximately 10% of adults in the population, have some form of renal disease. Not only is it the ninth leading cause of death in Americans, but treatment for patients with chronic renal failure is amongst the most expensive for any chronic disease. The causes of kidney disease are numerous, including inherited and congenital renal defects, but by far the greatest risk factors are diabetes and hypertension. Similar to other adult-onset diseases, such as hypertension and diabetes mellitus, lifestyle factors such as a high-fat/high-salt diet, smoking and lack of exercise can contribute significantly to the development of renal disease. Epidemiological and experimental evidence is accumulating to suggest that, as with hypertension and diabetes, the susceptibility of an individual to develop renal disease may be increased if that person has been exposed to a poor or suboptimal intrauterine environment. If a substantive link can be proven between abnormal kidney development and the later development of hypertension and renal disease, then measures can be recommended which could decrease significantly the incidence of adult hypertension.
- Type
- Chapter
- Information
- Developmental Origins of Health and Disease , pp. 310 - 322Publisher: Cambridge University PressPrint publication year: 2006
References
(2003). An update on ‘progression promoters’ in renal diseases. J. Natl. Med. Assoc., 95, 30–42.Google ScholarPubMed
, , , and (1999). Adverse effects of hyperglycemia on kidney development in rats: in vivo and in vitro studies. Diabetes, 48, 2240–5.CrossRefGoogle ScholarPubMed
, , , and (2001). Altered nephrogenesis due to maternal diabetes is associated with increased expression of IGF-II/mannose-6-phosphate receptor in the fetal kidney. Diabetes, 50, 1069–75.CrossRefGoogle ScholarPubMed
(2002). Growth and death in the developing mammalian kidney: signals, receptors and conversations. Bioessays, 24, 72–82.CrossRefGoogle ScholarPubMed
, , et al. (2001). Vitamin A controls epithelial/mesenchymal interactions through Ret expression. Nat. Genet., 27, 74–8.CrossRefGoogle ScholarPubMed
and (2004). Ontogeny of renal sodium transport. Semin. Perinatol., 28, 91–6.CrossRefGoogle ScholarPubMed
, , , and (2001). The maternal diet during pregnancy programs altered expression of the glucocorticoid receptor and type 2 11beta-hydroxysteroid dehydrogenase: potential molecular mechanisms underlying the programming of hypertension in utero. Endocrinology, 142, 2841–53.CrossRefGoogle ScholarPubMed
, , and (2000). Quantitative analysis of the developing rat kidney: absolute and relative volumes and growth curves. Anat. Rec., 258, 128–35.3.0.CO;2-P>CrossRefGoogle ScholarPubMed
, , et al. (2003). Long-term regulation of ENaC expression in kidney by angiotensin II. Hypertension, 41, 1143–50.CrossRefGoogle ScholarPubMed
and (1997). Nephron mass as a risk factor for progression of renal disease. Kidney Int. Suppl., 63, S124–7.Google ScholarPubMed
, , , and (1999). Expression of the beta2-subunit and apical localization of Na+−K+−ATPase in metanephric kidney. Am. J. Physiol., 277, F391–403.Google ScholarPubMed
, , et al. (1999). Ovine aquaporin-2: cDNA cloning, ontogeny and control of renal gene expression. Pediatr. Nephrol., 13, 379–90.CrossRefGoogle ScholarPubMed
and (2001). The infant of the diabetic mother: the critical developmental windows. Early Pregnancy, 5, 57–8.Google ScholarPubMed
, , et al. (1998). Prenatal dexamethasone causes oligonephronia, sodium retention, and higher blood pressure in the offspring. Pediatr. Res., 44, 317–22.CrossRefGoogle ScholarPubMed
(2004). A mechanistic perspective on the specificity and extent of COX-2 inhibition in pregnancy. Drug. Saf., 27, 421–6.CrossRefGoogle ScholarPubMed
, , et al. (2002). Longitudinal study of serum placental GH in 455 normal pregnancies: correlation to gestational age, fetal gender, and weight. J. Clin. Endocrinol. Metab., 87, 2734–9.CrossRefGoogle Scholar
(2004). Perinatal obstructive nephropathy. Semin. Perinatol., 28, 124–31.CrossRefGoogle ScholarPubMed
(2003) Micronutrients and reproductive health issues: an international perspective. J. Nutr., 133, 1969– 73S.CrossRefGoogle Scholar
, and (2003). Renal development in high-glucose ambience and diabetic embryopathy. Semin. Nephrol., 23, 583–92.CrossRefGoogle ScholarPubMed
and (2004). Maternal asthma as a model for examining fetal sex-specific effects on maternal physiology and placental mechanisms that regulate human fetal growth. Placenta, 25 (Suppl. A), S45–52.CrossRefGoogle ScholarPubMed
, , , , and (1995). The effects of anaemia on heart, placenta and body weight, and blood pressure in fetal and neonatal rats. J. Physiol., 488, 515–19.CrossRefGoogle ScholarPubMed
, , , and (2003). Nephron number, renal function, and arterial pressure in aged GDNF heterozygous mice. Hypertension, 41, 335–40.CrossRefGoogle ScholarPubMed
and (1966). A morphologic study of the mesonephros of the human embryo. J. Ultrastruct. Res., 16, 399–427.CrossRefGoogle ScholarPubMed
, , , , and (1996). Expression of aquaporins-1 and -2 during nephrogenesis and in autosomal dominant polycystic kidney disease. Am. J. Physiol., 271, F169–83.Google ScholarPubMed
, , et al. (2003). Prevalence and risk factors for gestational diabetes assessed by universal screening. Diabetes Res. Clin. Pract., 62, 131–7.CrossRefGoogle ScholarPubMed
, , et al. (2003). Intrauterine undernutrition: renal and vascular origin of hypertension. Cardiovasc. Res., 60, 228–34.CrossRefGoogle Scholar
, , et al. (2001). Impaired cardiac functional reserve and left ventricular hypertrophy in adult sheep after prenatal dexamethasone exposure. Circ. Res., 89, 623–9.CrossRefGoogle ScholarPubMed
, , , and (2002a). Programming effects of short prenatal exposure to dexamethasone in sheep. Hypertension, 40, 729–34.CrossRefGoogle Scholar
, , et al. (2002b). Programming effects of short prenatal exposure to cortisol. FASEB J., 16, 1017–26.CrossRefGoogle Scholar
, , and (2002c). Programmed hypertension: kidney, brain or both?Trends Endocrinol. Metab., 13, 403–8.CrossRefGoogle Scholar
, , and (2002). Compensatory renal growth after unilateral nephrectomy in the ovine fetus. J. Am. Soc. Nephrol., 13, 406–10.Google ScholarPubMed
, , et al. (2003). Spatiotemporal distribution of insulin-like growth factor receptors during nephrogenesis in fetuses from normal and diabetic rats. Cell Tissue Res., 314, 367–79.CrossRefGoogle Scholar
, , , , and (2003). Micronutrients and fetal growth. J. Nutr., 133, 1747–56S.CrossRefGoogle ScholarPubMed
(2002). Normal and abnormal development of the kidney: a clinician's interpretation of current knowledge. J. Urol., 167, 2339–51.CrossRefGoogle ScholarPubMed
(2002). The role of the placenta in fetal programming: a review. Placenta, 23 (Suppl. A), S20–7.CrossRefGoogle ScholarPubMed
, , , and (2003). High urine volume and low urine osmolality are risk factors for faster progression of renal disease. Am. J. Kidney Dis., 41, 962–71.CrossRefGoogle ScholarPubMed
, , et al. (2003). National Kidney Foundation's Kidney Disease Outcomes Quality Initiative clinical practice guidelines for chronic kidney disease in children and adolescents: evaluation, classification, and stratification. Pediatrics, 111, 1416–21.CrossRefGoogle ScholarPubMed
and (2003). Molecular determinants of sodium and water balance during early human development. Semin. Neonatol., 8, 291–9.CrossRefGoogle ScholarPubMed
, , et al. (1999). Stemming the tide: reducing cardiovascular disease and renal failure in Australian Aborigines. Aust. NZ J. Med., 29, 480–3.CrossRefGoogle ScholarPubMed
, , , and (2003). Glomerular number and size in autopsy kidneys: the relationship to birth weight. Kidney Int., 63, 2113–22.CrossRefGoogle ScholarPubMed
, , , and (2003). Birth weight: a risk factor for progression in diabetic nephropathy?J. Intern. Med., 253, 343–50.CrossRefGoogle ScholarPubMed
and (2004). Nephron endowment and blood pressure: what do we really know?Curr. Hypertens. Rep., 6, 133–9.CrossRefGoogle ScholarPubMed
, , and (2000). Increased blood pressure but normal renal function in adult women born preterm. Pediatr. Nephrol., 15, 215–20.CrossRefGoogle ScholarPubMed
, and (2003). Renal tubule sodium transporter abundance profiling in rat kidney: response to aldosterone and variations in NaCl intake. Ann. NY Acad. Sci., 986, 562–9.CrossRefGoogle ScholarPubMed
, , , and (2000). Low birth weights contribute to high rates of early-onset chronic renal failure in the southeastern United States. Arch. Intern. Med., 160, 1472–6.CrossRefGoogle ScholarPubMed
, and (1999). Fetal exposure to a maternal low protein diet impairs nephrogenesis and promotes hypertension in the rat. Life Sci., 64, 965–74.CrossRefGoogle ScholarPubMed
, and (2003a). Nutritional programming of blood pressure and renal morphology. Arch. Physiol. Biochem., 111, 8–16.CrossRefGoogle Scholar
, and (2003b). Early gestation is a critical period in the nutritional programming of nephron number in the sheep. Pediatr. Res., 53 (Suppl.), 30A.Google Scholar
, , et al. (2003). Angiotensin II regulates 11beta-hydroxysteroid dehydrogenase type 2 via AT2 receptors. Kidney Int., 64, 970–7.CrossRefGoogle ScholarPubMed
, , et al. (1998). Mild vitamin A deficiency leads to inborn nephron deficit in the rat. Kidney Int., 54, 1455–62.CrossRefGoogle ScholarPubMed
, , , , and (2003). Effect of maternal iron restriction during pregnancy on renal morphology in the adult rat offspring. Br. J. Nutr., 90, 33–9.CrossRefGoogle ScholarPubMed
, , et al. (2001). Pathogenesis of twin–twin transfusion syndrome: the renin–angiotensin system hypothesis. Fetal Diagn. Ther., 16, 241–4.CrossRefGoogle ScholarPubMed
, , and (2002). Upregulation of renal BSC1 and TSC in prenatally programmed hypertension. Am. J. Physiol. Renal Physiol., 283, F202–6.CrossRefGoogle ScholarPubMed
(2004). Renal sodium handling for body fluid maintenance and blood pressure regulation. Yakugaku Zasshi, 124, 301–9.CrossRefGoogle ScholarPubMed
, , , and (1994). Intrauterine growth retardation leads to a permanent nephron deficit in the rat. Pediatr. Nephrol., 8, 175–80.CrossRefGoogle ScholarPubMed
, , and (2000). Maternal cocaine abuse and fetal renal arteries: a morphometric study. Pediatr. Nephrol., 14, 315–18.CrossRefGoogle ScholarPubMed
and (1999). Functional development of the meso- and metanephros. Pediatr. Nephrol., 13, 171–8.CrossRefGoogle ScholarPubMed
, , , and (2002a). Maternal glucocorticoid treatment programs alterations in the renin–angiotensin system of the ovine fetal kidney. Endocrinology, 143, 4455–63.CrossRefGoogle Scholar
, and (2002b). Fetal uninephrectomy leads to postnatal hypertension and compromised renal function. Hypertension, 39, 1071–6.CrossRefGoogle Scholar
, and (2003). Kidney development and the fetal programming of adult disease. Bioessays, 25, 212–20.CrossRefGoogle ScholarPubMed
(2003). Intrauterine determinants of diabetic kidney disease in disadvantaged populations. Kidney Int. Suppl., 83, S13–16.CrossRefGoogle Scholar
, and (1998). Intrauterine diabetes exposure and the risk of renal disease in diabetic Pima Indians. Diabetes, 47, 1489–93.CrossRefGoogle ScholarPubMed
, , and (2001). Effect of prenatal dexamethasone on rat renal development. Kidney Int., 59, 1663–9.CrossRefGoogle ScholarPubMed
, , , and (2003). Prenatal dexamethasone programs hypertension and renal injury in the rat. Hypertension, 41, 328–34.CrossRefGoogle ScholarPubMed
, , and (2001). Regional Brazilian diet-induced low birth weight is correlated with changes in renal hemodynamics and glomerular morphometry in adult age. Biol. Neonate, 80, 239–46.CrossRefGoogle ScholarPubMed
, , et al. (2004). Angiotensin receptor blockers in diabetic nephropathy: renal and cardiovascular end points. Semin. Nephrol., 24, 147–57.CrossRefGoogle ScholarPubMed
, , , , and (2003). Uteroplacental insufficiency increases apoptosis and alters p53 gene methylation in the full-term IUGR rat kidney. Am. J. Physiol. Regul. Integr. Comp. Physiol., 285, R962–70.CrossRefGoogle ScholarPubMed
, , and (2003). A double-blind randomized study of fetal side effects during and after the short-term maternal administration of indomethacin, sulindac, and nimesulide for the treatment of preterm labor. Am. J. Obstet. Gynecol., 188, 1046–51.CrossRefGoogle ScholarPubMed
, , , and (2003). Intrauterine growth restriction is accompanied by decreased renal volume in the human fetus. Am. J. Obstet. Gynecol., 188, 1320–5.CrossRefGoogle ScholarPubMed
, , et al. (2003). Effect of a diabetic environment in utero on predisposition to type 2 diabetes. Lancet, 361, 1861–5.CrossRefGoogle ScholarPubMed
, and (2002) Iron deficiency and marginal vitamin A deficiency affect growth, hematological indices and the regulation of iron metabolism genes in rats. J. Nutr., 132, 3607–15.CrossRefGoogle ScholarPubMed
, , , and (2003). Adverse pregnancy outcomes associated with maternal enalapril antihypertensive treatment. Pharmacoepidemiol. Drug. Saf., 12, 633–46.CrossRefGoogle ScholarPubMed
(2003). Anaemia and micronutrient deficiencies. Br. Med. Bull., 67, 149–60.CrossRefGoogle ScholarPubMed
, , , and (2000). Normal kidney function and elevated natriuresis in young men born with low birth weight. Pediatr. Nephrol., 15, 96–100.Google ScholarPubMed
, and (2001). Prenatal programming of adult hypertension in the rat. Kidney Int., 59, 238–45.CrossRefGoogle ScholarPubMed
, , , , and (2004). Kidney angiotensin and angiotensin receptor expression in prenatally programmed hypertension. Am. J. Physiol. Renal. Physiol., 287, F262–7.CrossRefGoogle ScholarPubMed
(2002). Physiological importance of aquaporin water channels. Ann. Med., 34, 192–200.CrossRefGoogle ScholarPubMed
, , et al. (2002). Midkine is involved in kidney development and in its regulation by retinoids. J. Am. Soc. Nephrol., 13, 668–76.Google ScholarPubMed
(2004). Retinoids and receptor interacting protein 140 (RIP140) in gene regulation. Curr. Med. Chem., 11, 1527–32.CrossRefGoogle Scholar
, and (2002). Protein restriction in pregnancy is associated with increased apoptosis of mesenchymal cells at the start of rat metanephrogenesis. Kidney Int., 61, 1231–42.CrossRefGoogle ScholarPubMed
, , and (2001). Maternal undernutrition during early to midgestation programs tissue-specific alterations in the expression of the glucocorticoid receptor, 11beta-hydroxysteroid dehydrogenase isoforms, and type 1 angiotensin II receptor in neonatal sheep. Endocrinology, 142, 2854–64.CrossRefGoogle ScholarPubMed
, , and (2003). Sexually dimorphic effects of maternal alcohol intake and adrenalectomy on left ventricular hypertrophy in rat offspring. Am. J. Physiol. Endocrinol. Metab., 285, E31–9.CrossRefGoogle ScholarPubMed
, , , and (2004). Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care, 27, 1047–53.CrossRefGoogle ScholarPubMed
, , , , and (1998). Ovine AQP1: cDNA cloning, ontogeny, and control of renal gene expression. Pediatr. Nephrol., 12, 545–53.CrossRefGoogle ScholarPubMed
Wintour, E. M., Dodic, M., Johnston, H., Moritz, K. and Peers, A. (1999). Kidney and urinary tract. In Fetal Medicine: Basic Science and Clinical Practice (ed. and ). London: Churchill Livingstone, pp. 155–71.Google Scholar
, , , , and (2003). Reduced nephron number in adult sheep, hypertensive as a result of prenatal glucocorticoid treatment. J. Physiol., 549, 929–35.CrossRefGoogle ScholarPubMed
, and (2003). The risk of stillbirth in pregnancies before and after the onset of diabetes. Diabet. Med., 20, 703–7.CrossRefGoogle ScholarPubMed
(1999). Neonatal uninephrectomy causes hypertension in adult rats. Am. J. Physiol., 276, R974–8.Google ScholarPubMed
, , and (2001a). Maternal protein restriction suppresses the newborn renin–angiotensin system and programs adult hypertension in rats. Pediatr. Res., 49, 460–7.CrossRefGoogle Scholar
, and (2001b). Hypertension after neonatal uninephrectomy in rats precedes glomerular damage. Hypertension, 38, 337–42.CrossRefGoogle Scholar
, and (2004). Programming of adult blood pressure by maternal protein restriction: role of nephrogenesis. Kidney Int., 65, 1339–48.CrossRefGoogle ScholarPubMed
, , and (2003). Iron, lipocalin, and kidney epithelia. Am. J. Physiol. Renal Physiol., 285, F9–18.CrossRefGoogle ScholarPubMed
, and (2004.) Does a nephron deficit in rats predispose to salt-sensitive hypertension?Kidney Blood Press. Res., 27, 239–47.CrossRefGoogle ScholarPubMed
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