Many potential risk factors or low birth weight (LBW)may negativelymodify the renal developmental program in utero, resulting in congenital oligonephropathy (< 0.3.106 nephrons per kidney). Impaired vasculatory development is another consequence of LBW. Low capillary density and endothelial dysfunction are present throughout the tissues. Renal functions ofLBW children are limited to early postnatally due to oligonephropathy and nephron structural and functional immaturity. Since the nephron compensatory hypertrophy, kidney functions in LBW children reach the physiological values by early childhood. In contrast, the late consequences of LBW are prognosticaly more serious. Higher incidence of hypertension and type 2 diabetes mellitus (LBW associated diseases) occurs within the population of LBW patients in early adulthood. The exact pathogenic mechanism of this association is not known. Genetic factors, risk factors ofLBW, oligonephropathy, endothelial dysfunction, low capillary density and adult risk factors probably play important roles. Associated diseased contribute to the subsequent decline in renal functions, microalbuminuria may serve as an early predictor of kidney damage. Consequently, the overall incidence of chronic renal failure among LBW children in the adulthood is higher comparing to those born in term.

        Key words: low birth weight, congenital oligonephropathy, endothelial dysfunction, associated diseases, microalbuminuria, chronic renal failure