According to in vitro experiments, SGK and PKB/Akt isoforms stimulate ion channels and transporters critical for epithelial electrolyte transport. The kinases are activated by phosphoinositide dependent kinase PDK1 which may thus play an important role in intestinal and renal electrolyte transport. The present study has been performed to explore the role of PDK1 in electrolyte metabolism. As mice completely lacking functional PDK1 are not viable, hypomorphic mice expressing 10–25% of PDK1 (pdk1^hm) were compared to their wild type littermates (pdk1^wt). Body weight was significantly smaller in pdk1^hm than in pdk1^wt. Despite lower body weight of pdk1^hm mice absolute food and water intake were similar in pdk1^hm and pdk1^wt. Thus, food and water intake per gram body weight were larger in pdk1^hm than in pdk1^wt mice. Fecal dry weight and fecal excretion of Na⁺, K⁺, Ca²⁺ and phosphate (P_i) were again similar in pdk1^hm than pdk1^wt despite the smaller weight of pdk1^hm mice. Plasma Na⁺, K⁺, Ca²⁺ and phosphate concentrations were virtually identical in pdk1^hm than pdk1^wt. Moreover, glomerular filtration rate was similar in pdk1^hm than pdk1^wt mice. However, the fractional excretion of Na⁺ at low salt diet, the fractional excretion of K⁺ at standard diet and the fractional excretion of Ca²⁺ and P_i at both, standard and low salt diet were significantly larger in pdk1hm than in pdk1wt mice. The observations disclose subtle derangement of electrolyte and mineral metabolism in PDK1 deficient mice.