KRT32 and chronic kidney disease: Because of the strong expression of HKA2 in the distal colon, as well as the remarkable fecal K+ loss phenotype of HKA2-deficient mice44, we drew the hypothesis that the absence of the HKA2 could be beneficial in the context of end-stage renal disease by facilitating the elimination of K+ in the feces and limiting the development of hyperkalemia.