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DOCA\/1% NaCl treatment increased blood pressure and creatinine clearance to a similar extent in SGK1-deficient sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>and wild-type sgk1<jats:sup>+\/+<\/jats:sup>mice but led to more pronounced increase of proteinuria in sgk1<jats:sup>+\/+<\/jats:sup>mice (by 474 \u00b1 89%) than in sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>mice (by 154 \u00b1 31%). DOCA\/1% NaCl treatment led to significant increase of kidney weight (by 24%) and to hypokalemia (from 3.9 \u00b1 0.1 to 2.7 \u00b1 0.1 mmol\/l) only in sgk1<jats:sup>+\/+<\/jats:sup>mice. The treatment enhanced renal Na<jats:sup>+<\/jats:sup>excretion significantly more in sgk1<jats:sup>+\/+<\/jats:sup>mice (from 3 \u00b1 1 to 134 \u00b1 32 \u03bcmol\u00b724 h<jats:sup>\u22121<\/jats:sup>\u00b7g body wt<jats:sup>\u22121<\/jats:sup>) than in sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>mice (from 4 \u00b1 1 to 49 \u00b1 8 \u03bcmol\u00b724 h<jats:sup>\u22121<\/jats:sup>\u00b7g body wt<jats:sup>\u22121<\/jats:sup>), 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<jats:sup>+\/+<\/jats:sup>mice (within 9 days from 3.5 \u00b1 0.9 to 16.5 \u00b1 2.4 ml\/day) consistent with DOCA-induced salt appetite. This response was significantly attenuated in sgk1<jats:sup>\u2212\/\u2212<\/jats:sup>mice (from 2.6 \u00b1 0.6 to 5.9 \u00b1 0.9 ml\/day). 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