**4.1.2 Chorioamnionitis**

Chorioamnionitis (a bacterial infection of the chorion and amnion) is a common antecedent of preterm birth (Romero et al., 2006; Goldenberg et al., 2008), especially in births prior to 30 weeks of gestation (Lahra and Jeffery, 2004); it is often complicated by IUGR. Chorioamnionitis may manifest as either a clinical or subclinical condition. When severe, it can ultimately give rise to the fetal inflammatory response syndrome which is characterised by funisitis, fetal vasculitis and an increase in of pro-inflammatory cytokines in fetal blood and amniotic fluid (Romero et al., 1998; Romero et al., 2003; Gotsch et al., 2007). It is likely that the fetal systemic inflammatory response will lead to renal inflammation in chorioamnionitis-exposed infants; conceivably if present *in utero* this will have deleterious effects on nephrogenesis, and if present at the time of delivery, it will adversely impact on renal function. In this regard, we have recent evidence in fetal sheep to demonstrate that exposure to chorioamnionitis late in gestation does adversely affect nephrogenesis, leading to a 23% and 18% reduction in nephron endowment in singleton and twin-exposed fetuses, respectively (Galinsky et al., 2011). It is important to note that we did not observe any morphological abnormalities in the glomeruli of these fetal kidneys. However, it is conceivable, that if renal inflammation is present at the time of birth, that this will further compromise postnatal nephrogenesis and renal function in the neonate. Following the hemodynamic transition at birth, it may be then that glomerular morphological abnormalities develop in these already compromised kidneys. Importantly in this regard, a multiple logistic regression analysis of 2508 preterm neonates, treated with indomethacin, showed a significant correlation between intrauterine inflammation and prevalence of renal and electrolyte abnormalities (Itabashi et al., 2003), thus suggesting that intrauterine inflammation in concert with postnatal indomethacin treatment can lead to renal dysfunction. Certainly our results support the idea that prematurity, when complicated with chorioamnionitis, is likely to exacerbate postnatal renal dysfunction and further studies are required to determine whether renal inflammation at the time of birth is associated with the formation of abnormal glomeruli in the neonatal period.
