Mineralocorticoids modify salt balance by both stimulating salt intake and inhibiting salt loss. Renal salt retention is accomplished by upregulation of reabsorption, an effect partially mediated by serum- and glucocorticoid-inducible kinase 1 (SGK1). The present study explored the contribution of SGK1 to the regulation of renal function, salt intake, and blood pressure during mineralocorticoid excess. DOCA/1% NaCl treatment increased blood pressure and creatinine clearance to a similar extent in SGK1-deficient sgk1^−/− and wild-type sgk1^+/+ mice but led to more pronounced increase of proteinuria in sgk1^+/+ mice (by 474 ± 89%) than in sgk1^−/− mice (by 154 ± 31%). DOCA/1% NaCl treatment led to significant increase of kidney weight (by 24%) and to hypokalemia (from 3.9 ± 0.1 to 2.7 ± 0.1 mmol/l) only in sgk1^+/+ mice. The treatment enhanced renal Na⁺ excretion significantly more in sgk1^+/+ mice (from 3 ± 1 to 134 ± 32 μmol·24 h⁻¹·g body wt⁻¹) than in sgk1^−/− mice (from 4 ± 1 to 49 ± 8 μmol·24 h⁻¹·g body wt⁻¹), pointing to SGK1-dependent stimulation of salt intake. With access to two drinking bottles containing 1% NaCl or water, DOCA treatment did not significantly affect water intake in either genotype but increased 1% NaCl intake in sgk1^+/+ mice (within 9 days from 3.5 ± 0.9 to 16.5 ± 2.4 ml/day) consistent with DOCA-induced salt appetite. This response was significantly attenuated in sgk1^−/− mice (from 2.6 ± 0.6 to 5.9 ± 0.9 ml/day). Thus SGK1 contributes to the stimulation of salt intake, kidney growth, proteinuria, and renal K⁺ excretion during mineralocorticoid excess.