Prenatal programming of kidney diseaseVehaskari, V MattiCurrent Opinion in Pediatrics: April 2010 - Volume 22 - Issue 2 - p 176–182 doi: 10.1097/MOP.0b013e328336ebc9 Nephrology: Edited by Michel Baum Abstract Author Information Abstract Purpose of review: To introduce the concept of prenatal programming; to discuss the emerging evidence that adverse prenatal environment programs increased risk of chronic kidney disease in the offspring in later life; to review the mechanism involved; and to present potential intervention strategies. Recent findings: New observational studies in humans and studies in animal models have strengthened the association between low birth weight and chronic kidney disease in adulthood. The consequences of low birth weight are less obvious in children and young animals. A likely mechanism is that adverse intrauterine environment results in decreased final number of nephrons. The existing fewer glomeruli compensate by hyperfiltrating, which may accelerate the normal gradual age-related loss of nephrons throughout one's lifespan. Beginning life with a low nephron count may not cause morbidity during childhood because of the large functional reserve kidneys have, but as the count later falls below a critical level, chronic kidney disease may become manifest. Early life dietary factors may modify the risk. Summary: The charge for pediatricians is to identify children at risk, to counsel families to minimize any further renal risk factors such as smoking, obesity, and hypertension, and, in some cases together with a nephrologist, to institute pharmacologic therapy. Author Information Department of Pediatrics and the Research Institute for Children, Louisiana State University Health Sciences Center, 200 Henry Clay Avenue, New Orleans, Louisiana, USA Correspondence to V. Matti Vehaskari, MD, PhD, Department of Pediatrics and the Research Institute for Children, Louisiana State University Health Sciences Center, 200 Henry Clay Avenue, New Orleans, LA 70118, USA Tel: +1 504 896 9238; fax: +1 504 896 9240; e-mail: email@example.com © 2010 Lippincott Williams & Wilkins, Inc.