Fetal programming increases susceptibility to renal injury induced by ischemia‐reperfusion in IUGR offspring

Renal injury due to ischemia‐reperfusion (I‐R) is the major cause of acute renal failure. Whether susceptibility to renal injury from I‐R can be programmed during fetal life is unknown. Our laboratory has developed a unique rat model of placental insufficiency that results in intrauterine growth restriction (IUGR) and development of hypertension in IUGR rats. We hypothesized that IUGR will also lead to greater susceptibility to renal injury following I‐R. Physiological parameters were determined 1 week after mild renal ischemia (15 min); early histological renal changes were assessed in a subset of rats after 30 min of reperfusion. Mean arterial pressure (MAP), renal vascular resistance (RVR), and histological markers of renal damage were increased; glomerular filtration rate (GFR) and renal blood flow (RBF) were decreased following I‐R in IUGR compared to control (Table). Therefore, these findings suggest that influences during fetal life can program an increased susceptibility to renal injury suggesting IUGR individuals may be an ‘at risk’ population for renal disease.