Although the majority of preterm neonates now survive infancy, there is emerging epidemiological evidence to demonstrate that individuals born preterm exhibit an elevated risk for the development of hypertension and renal impairment later in life, thus supporting the developmental origins of health and disease hypothesis. The increased risk may potentially be attributed to a negative impact of preterm birth on nephron endowment. Indeed, at the time when most preterm neonates are delivered, nephrogenesis in the kidney is still ongoing with the majority of nephrons normally formed during the third trimester of pregnancy. A number of clinical studies have provided evidence of altered renal function during the neonatal period, but to date there have been limited studies describing the consequences of preterm birth on kidney structure. Importantly, studies in the preterm baboon have shown that nephrogenesis is clearly ongoing following preterm birth; however, the presence of abnormal glomeruli (up to 18% in some cases) is of concern. Similar glomerular abnormalities have been described in autopsied preterm infants. Prenatal and postnatal factors such as exposure to certain medications, hyperoxia and intrauterine and/or extrauterine growth restriction are likely to have a significant influence on nephrogenesis and final nephron endowment. Further studies are required to determine the factors contributing to renal maldevelopment and to identify potential interventional strategies to maximize nephron endowment at the start of life, thereby optimizing long-term renal health for preterm individuals.