Pathogenesis of perinatal programming.
OBJECTIVE
In recent years, there has been an increase in research designed to delineate the underlying causes of perinatal programming. Starting with epidemiological observations that birth weight was inversely associated with cardiovascular disease, a variety of studies both in humans and in experimental models have begun to demonstrate how the perinatal milieu can subtly alter vasculogenesis and nephrogenesis. Additionally, rates of prenatal and postnatal growth each appear to contribute to future vascular, renal and metabolic function. The purpose of this review is to discuss recent reports that have begun to elucidate factors that initiate perinatal programming as it affects renal disease and cardiovascular disease in later life.


RESULTS
Nephrogenesis per se is affected by changes in maternal nutrition and health, and recent data more specifically linking these changes with renal function and hypertension are presented. Additionally, renal functional changes in later life may be influenced by changes in renal tubular transporters noted early when maternal nutrition is compromised. Various hormonal systems affected by maternal nutrition in utero may effect subsequent changes in renal function via subtle alterations in renal function and structure initiated during nephrogenesis.


CONCLUSIONS
Current research is beginning to clarify certain aspects of perinatal programming and indicates that broad educational programmes might ultimately lessen both perinatal risks and long-term outcomes by encouraging therapeutic interventions in at-risk persons.
Ingelfinger
Julie R
JR
Pediatric Nephrology Unit, Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts 02114, USA. Jingelfinger@partners.org
D000818:Animals; D002318:Cardiovascular Diseases / Q000196:embryology; D002319:Cardiovascular System / Q000196:embryology* / Q000503:physiopathology; D005314:Embryonic and Fetal Development / Q000502:physiology*; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000502:physiology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000196:embryology; D007668:Kidney / Q000196:embryology* / Q000503:physiopathology; D007674:Kidney Diseases / Q000196:embryology; D009399:Nephrons / Q000196:embryology / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000196:embryology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats