title: Perinatal programming of renal function.
abstract: OBJECTIVE
  Perinatal programming of renal function reflects the epigenetic alteration of genetically determined development by environmental factors. These include intrauterine malnutrition, pre and postnatal overnutrition, glucocorticoids, and certain toxins such as smoking. This review aims to summarize the most important findings.
  
  
  RESULTS
  Human studies may show an increased susceptibility toward the general prevalence of renal failure in already small for gestational age children and adolescents. In particular, glomerular diseases present with a more severe clinical course. Partially related, partially independently, arterial hypertension is found in this at-risk group. The findings can mostly be confirmed in animal models. Both intrauterine nutrient deprived and overfed rodents show a tendency toward developing glomerulosclerosis and other renal disorders. Animal studies attempt to imitate clinical conditions, however, there are difficulties in transferring the findings to the human setting. The reduction of nephron number, especially in intrauterine growth-restricted humans and animals, is one mechanism of perinatal programming in the kidneys. In addition, vascular and endocrine alterations are prevalent. The molecular changes behind these mechanisms include epigenetic changes such as DNA-methylation, microRNAs, and histone modifications.
  
  
  CONCLUSIONS
  Future research will have to establish clinical studies with clear and well defined inclusion criteria which also reflect prenatal life. The use of transgenic animal models might help to obtain a deeper insight into the underlying mechanisms.
authors.affiliation: Department of Pediatrics, University of Cologne, Cologne, Germany.
authors.forename: Jörg
authors.initials: J
authors.lastname: Dötsch
authors.forename: Miguel
authors.initials: M
authors.lastname: Alejandre-Alcazar
authors.forename: Ruth
authors.initials: R
authors.lastname: Janoschek
authors.forename: Eva
authors.initials: E
authors.lastname: Nüsken
authors.forename: Lutz T
authors.initials: LT
authors.lastname: Weber
authors.forename: Kai D
authors.initials: KD
authors.lastname: Nüsken
mesh_terms: D035843:Biomedical Research / Q000639:trends; D047108:Embryonic Development / Q000235:genetics / Q000502:physiology; D044127:Epigenesis, Genetic; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000196:embryology* / Q000502:physiology; D007674:Kidney Diseases / Q000196:embryology* / Q000235:genetics; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000235:genetics