The effect of a chronic glucose osmotic diuresis on electrolyte homeostasis was evaluated in alloxan diabetic rats with urine volumes greater than 150 ml/day and glycosuria of 4 to 10 gm/day. Results were compared with control rats for periods up to 84 days. Sodium and potassium intake and urinary losses were significantly higher in diabetic animals throughout the study periods. Negative Na balance, however, persisted for only four days, and negative K balance for only 18 days. Blood volumes were elevated probably secondary to the osmotic effect of hyperglycemia (serum glucose greater than 600 mg %). Plasma renin activity decreased progressively, in part because of an early decrease in renin substrate at a time when renin concentration was normal. Despite hyperkalemia, mean plasma aldosterone was not increased compared with that in control rats, suggesting diabetic rats had relative hypoaldosteronism. Although three diabetic rats became hypertensive, no significant difference in mean blood pressure was observed between the groups. The results suggest that diabetic rats have losses of Na and K early in their diabetes, following which mechanisms to conserve Na and K are activated preventing further electrolyte depletion despite continuation of the osmotic diuresis. Decreased renin activity with inadequate stimulation of aldosterone would contribute to K conservation. Maintenance of Na balance must be explained by increased Na intake and other renal Na conserving mechanisms.