The notion that Clc-k1 and Clc-k2 function together in TAL and DCT up to the perinatal period likely explains why patients with classic Bartter syndrome with ClC-Kb mutation tend to have less-severe perinatal salt wasting than those with antenatal Bartter with NKCC2 or ROMK mutations. This evidence concerns the gene KCNJ1 and Bartter syndrome.