The aim of this study was to evaluate the changed expression of NCC, phosphorylated NCC (p-NCC), upstream DCT such as Na+-hydrogen exchanger 3 (NHE3), NKCC2, downstream DCT such as ENaCβ, pendrin, as well as K+-secreting channels such as ROMK and Maxi-K from uEVs and representative kidney tissues in patients with GS. This evidence concerns the gene SLC9A3 and Gerstmann syndrome.