Figure 1: Schematic representation of the proposed impact of adverse intrauterine environment on developmental programming of hypertension and chronic kidney disease (CKD). Maternally mediated environmental modulation of renal gene expression in the offspring leads to developmentally induced deviations from the optimal nephron number. A relative deficiency in the number of nephrons is thought to create an increased risk of CKD, hypertension, and cardiovascular morbidity in later life. Epigenetic modifications not only change target gene expression and program the phenotype of the developing fetus, but also account for transgenerational inheritance of programmed phenotype via permanent epigenetic imprinting. UB: ureteric bud and M: metanephric mesenchyme.