<i>Background/Aims:</i> The serum- and glucocorticoid-inducible kinase SGK1 was originally cloned as a glucocorticoid-regulated gene and later as a transcriptional target for mineralocorticoids. SGK1 regulates channels and transporters including the renal Na⁺ channel ENaC. It contributes to mineralocorticoid regulation of renal Na⁺ excretion and salt appetite. The present study explored the contribution of SGK1 to effects of glucocorticoids on mineral and electrolyte metabolism. <i>Methods:</i> SGK1-knockout mice (<i>sgk1</i>^–/–) and their wild-type littermates (<i>sgk1</i>^+/+) were analyzed in metabolic cages with or without treatment for 14 days with dexamethasone (3 mg/kg b.w., i.p.). Blood pressure was determined by the tail-cuff method. <i>Results:</i> Prior to treatment fluid intake, urinary flow rate, urinary Na⁺, K⁺, phosphate and Cl^– excretion, plasma electrolyte and glucose concentrations as well as blood pressure were similar in <i>sgk1</i>^–/– and<i> sgk1</i>^+/+ mice. Dexamethasone did not significantly alter renal Na⁺, K⁺, Cl^– and Ca²⁺ excretion but decreased plasma Ca²⁺ and phosphate concentration in <i>sgk1</i>^+/+ mice. The effect on Ca²⁺ was significantly augmented and the effect on phosphate significantly blunted in <i>sgk1</i>^–/– mice. Dexamethasone significantly increased fasting blood glucose concentrations in both genotypes. Dexamethasone increased blood pressure in <i>sgk1</i>^+/+ mice, an effect significantly blunted in <i>sgk1</i>^–/– mice. <i>Conclusions:</i> The present observations disclose SGK1-sensitive glucocorticoid effects on calcium-phosphate metabolism and blood pressure.