Prenatal programming of kidney disease

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.