The stimulation of postprandial K⁺ clearance involves aldosterone-independent and -dependent mechanisms. In this context, SGK1, an ubiquitously expressed kinase, is one of the primary aldosterone induced proteins in the aldosterone sensitive distal nephron (ASDN). Germline inactivation of SGK1 suggests that this kinase is fundamental for K⁺ excretion under conditions of K⁺ load, but the specific role of renal SGK1 remains elusive. To avoid compensatory mechanisms that may occur during nephrogenesis, we employed inducible, nephron-specific Sgk1^Pax8/LC1 mice to assess the role of renal-tubular SGK1 in K⁺ regulation. Under standard diet, these animals exhibited normal K⁺ handling. When challenged by a high K⁺ diet (HKD), they developed severe hyperkalemia, accompanied by a defect in K⁺ excretion. Molecular analysis revealed reduced NEDD4-2 phosphorylation and total expression. ENaC expression and α/ENaC proteolytic processing were also decreased in the mutant mice. Moreover, WNK1, which displayed in control mice punctuate staining in the DCT and diffuse distribution in the CNT/CCD, was diffused in the DCT and less expressed in the CNT/CD of Sgk^Pax8/LC1 mice. Besides, SPAK phosphorylation, and NCC phosphorylation/apical localization were reduced in the mutant. Consistent with the altered WNK1 expression, increased ROMK apical localization was observed. In conclusion, our data suggest that renal-tubular SGK1 is important in the regulation of K⁺ excretion via the control of NEDD4-2, WNK1 and ENaC.