The mTOR pathway orchestrates cellular homeostasis. The rapamycin-sensitive mTOR complex (mTORC1) in the kidney has been widely studied; however, mTORC2 function in renal tubules is poorly characterized. Here, we generated mice lacking mTORC2 in the distal tubule (Rictor^fl/fl Ksp-Cre mice), which were viable and had no obvious phenotype, except for a 2.5-fold increase in plasma aldosterone. Challenged with a low-Na⁺ diet, these mice adequately reduced Na⁺ excretion; however, Rictor^fl/fl Ksp-Cre mice rapidly developed hyperkalemia on a high-K⁺ diet, despite a 10-fold increase in serum aldosterone levels, implying that mTORC2 regulates kaliuresis. Phosphorylation of serum- and glucocorticoid-inducible kinase 1 (SGK1) and PKC-α was absent in Rictor^fl/fl Ksp-Cre mice, indicating a functional block in K⁺ secretion activation via ROMK channels. Indeed, patch-clamp experiments on split-open tubular segments from the transition zone of the late connecting tubule and early cortical collecting duct demonstrated that Ba²⁺-sensitive apical K⁺ currents were barely detectable in the majority of Rictor^fl/fl Ksp-Cre mice. Conversely, epithelial sodium channel (ENaC) activity was largely preserved, suggesting that the reduced ability to maintain K⁺ homeostasis is the result of impaired apical K⁺ conductance and not a reduced electrical driving force for K⁺ secretion. Thus, these data unravel a vital and nonredundant role of mTORC2 for distal tubular K⁺ handling.