Whereas high-dietary K+ intake-induced inhibition of NCC is important to facilitate ENaC-dependent renal K+ excretion during hyperkalemia (Ellison et al., 2015), because low NCC activity in the DCT should increase the Na+ delivery to the ASDN thereby enhancing ENaC-dependent renal K+ excretion. This evidence concerns the gene SLC12A3 and Hyperkalemia.