Both systolic and diastolic blood PRESSURE (BP) increase during the first month of life. LOW birth-weight infants have a LOWer mean BP than do term infants, but by 10 weeks of life this differences becomes negligible. BP increases more rapidly in preterm infants than term infants, especially in neonates with higher weight gain. Gestational age, birth weight, postnatal age and gender are considered the predictive factors of BP. But, some recent studies showed no significant difference in BP based on birth weight or length of the kidney. An inverse correlation has been reported between BP measurement and birth weight. Systolic BP is modestly higher in premature, VLBW, and LOW birth weight infants by school age and young adult life. Increased systolic and diastolic BP have been documented in extremely prematures at corrected age of 2.5 years. Human nephrogenesis continues through the 3rd trimester of pregnancy, and during the 36th week of gestation. Premature delivery interruptes renal development resulting to LOW nephron number at birth, small kidney, increased single nephron GFR, hyperfiltration, augmentation of glomerulosclerosis, subsequent hypertension and cardio vascular or chronic kidney disease later in life. Proposed mechanisms of hypertension include increased sympathetic activity, increased arterial stiffness and vascular resistance, attenuation of kidney development, accelerated postnatal growth in weight and length, alteration of angiotensin activity, proliferation of juxtaglomerular cells, and increased salt sensitivity. In a recent report, BP of small for gestational term infants was compatible with healthy controls. Therefore, monitoring of BP and proteinuria is recommended in LOW birth weight preterm infant before and after NICU discharge, and in children less than three years of age.