Glucocorticoid (GC) hormones have well characterised roles in the development of several fetal organs, however, specific developmental roles of GCs in the fetal kidney are relatively unknown. We have explored both the expression and localisation of the glucocorticoid receptor (GR) transcription factor within developing fetal kidney during organogenesis and the effect of eliminating GR expression in GR-null mice. We show that loss of the GR has a profound effect on the renal transcriptome with 454 genes differentially expressed in the GR-null mouse kidney with most genes significantly downregulated (305) than upregulated (99) relative to wild-type controls, including the primary cilia-associated gene Centrosomal protein 290 (Cep290) with a fold change of -3.6. mRNA levels of five cilia-associated genes; Ccp110, Cep97, Cep290, Kif3a and Rpgr were significantly downregulated in GR-null mice with a fold change of -2.17, -1.79, -2.94, -1.82 and -1.87 respectively. We found that primary cilia length is decreased in kidney proximal tubule cells in GR-null mice (5.01 + 0.11, µm + SEM) compared with wild type controls (6.20 + 0.15, µm + SEM) and adopted abnormal structures. We also demonstrate that dexamethasone treatment of mouse collecting duct cells (IMCD3) increased the length of primary cilia compared to non-steroid treated controls (vehicle 2.46 + 0.03, µm + SEM vs dexamethasone 2.89 + 0.04 µm + SEM). Taken together these results demonstrate that GC signalling via the GR has functional effects on primary cilia biogenesis and are required for normal kidney structural development in vivo.