Conductivity pulses needed for Diascan® measurements: does it cause sodium burden?

and T-MARE regulatory sequences of HNF1β was evidenced. In conclusion, although mutations in RARE and TMARE regulatory sequences of HNF1β may nevertheless be implicated in some renal congenital disorders, we show here that mutations in these sequences are not a frequent cause of CAKUT. More experiments are required to assess the role of the RA-MAFB-HNF1β pathway in kidney development. Moreover, the molecular basis of these renal malformations is still poorly understood, and further works remain to be done to identify new CAKUT genes. Delineation of transcriptional networks involved in early human metanephros development may be a way to identify these new genes.