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516parents of LBW infants need to learn proper dietary habits to prevent obesity and insulin resistance in the future. Guidance from the American Academy of Pediatrics recommends the following to avoid future obesity from infancy: (1) continued breast-feeding until 6 months of age; (2) no weaning before 4 months of age; (3) no fruit juices or juice containing fructose or sucrose; (4) supine position when awake to increase activity; and (5) no smoking by the mother34). The same kind of nutri-tional management is required in children and young adults born LBW.2. Short stature due to SGAIt is known that children born with SGA who do not have a catch-up by the age of 2 years will have short stature throughout childhood, which is called small-for-gestational-age short stature. A study of the natural history of 3,650 children with SGA reported that the percentage of cases with a height standard deviation score (SDS) below -2 SD at each age was 13.7% at age 2 years, 8.3% at age 5 years, and 7.9% at age 18 years35). Height growth is not expected after age 5 years35). The efficacy and safety of growth hormone (GH) therapy for chil-dren with SGA-induced short stature have been examined36, 37). In Japan, GH treatment is available within the insurance system for children with SGA-induced short stature who are 3 years of age or older, have a height SDS of less than -2.5, and are experiencing a decreased rate of height gain.3. Monitoring for the Future Development of CKD and HypertensionHow to follow-up on LWB infants, which now account for about 9% of all births, is an important issue. Infants born with FGR and those with kidney dysfunction or late-onset circulatory collapse on admission to neonatal intensive care units are at high risk of developing CKD38). Forty-five years have passed since the screening of renal diseases by school urinalysis started in Japan. Recently, some reports showed that glomerulosclerosis (FSGS) patients born with FGR were diagnosed as a result of regular screening tests at their school39, 40, 41). It is also known that tubular dysfunction commonly occurs in ELBW survivors42). It is difficult to detect trace amounts of protein in urine with the qualita-tive test (test paper method) used in the routine non-carriers26). In a study evaluating the severity of NAFLD in children, SGA was found to be a factor contributing to severity, as well as PNPLA3 variants27). Both over-nutrition and under-nutri-tion during the fetal period are considered to be high risk factors for developing NAFLD.4. Chronic Kidney Disease and HypertensionThe development of the human kidney begins around 5 weeks of gestation when the ampulla at the tip of the collecting duct repeatedly branches and elongates, forming a nephron consisting of a glomerulus and a Bowman’s capsule28). Nephron formation is completed by 34-36 weeks of gesta-tion, after which no new nephron formation occurs 28. For infants born at less than 36 weeks of gesta-tion, postnatal nephron formation is suppressed and terminates at about 10-40 days of age29). In fact, birth weight and length of gestation are predictors of the nephron number in adulthood. Thus, smaller birth weight and shorter gestational period are associated with a lower number of neph-rons in the individual30). Based on these studies, Brenner et al. proposed the hyperfiltration theory31). In infants with a low number of nephrons, the pres-sure on the remaining glomeruli is increased, and over-filtration occurs with each nephron. Over-fil-tration increases intraglomerular pressure and causes compensatory glomerular hypertrophy, leading eventually to nephrosclerosis31).A meta-analysis reported that preterm infants had an average systolic blood pressure 4.2 mmHg higher and diastolic blood pressure 2.6 mmHg higher in adulthood compared with full-term infants32). Glucocorticoid overexposure decreases the expression of DNA methyltransferase in the paraventricular nucleus (PVN), one of the blood pressure centers in the fetal brain14, 33). This increases the expression of the PVN target gene angiotensin II receptor type 1 (Agtr1a), which causes salt-sen-sitive hypertension14). Thus, the mechanism of hypertension in FGR/SGA children is hypothesized to be secondary to renal dysfunction or due to central epigenetic changes caused by the placental environment.Clinical Management of LBW Infants1. Nutritional supportIt is difficult to rectify the thrifty phenotype once it has been acquired after birth. Therefore, the