Renal tubular sodium handling was investigated prospectively in 48 normotensive subjects, 53 untreated hypertensive patients, and 13 patients with white coat hypertension using endogenous trace lithium as a marker of proximal sodium reabsorption. A 12-hour daytime ambulatory blood pressure recording was performed in all patients to confirm the diagnosis of hypertension. Patients were included in the white coat hypertension group if their office blood pressure was above 160/90 mm Hg but the mean value of their 12-hour ambulatory recording was lower than 140/90 mm Hg. All participants were studied on their normal diet and ate salt freely. Fractional excretions of sodium (FENa), lithium (FELi), and potassium (FEK) were measured simultaneously before blood pressure recording. FENa was significantly higher in hypertensive patients (0.84 +/- 0.05%, P < .05) than in normotensive control subjects (0.60 +/- 0.06%), and FELi was comparable in the two groups (15.4 +/- 0.65% in hypertensive patients and 17.0 +/- 0.9% in control subjects). However, the relation between FENa and FELi was significantly different in normotensive subjects and hypertensive patients (P < .001), so that for a given increase in FENa a smaller increase in FELi was observed in hypertensive patients. In addition, the ratios of urinary lithium to sodium and urinary potassium to sodium were significantly reduced in hypertensive patients, suggesting an increased proximal reabsorption of sodium. Similar alterations in renal tubular sodium handling were observed in patients with white coat hypertension. These results suggest that an increased sodium reabsorption in the proximal tubule may contribute to the maintenance of hypertension and that white coat hypertension might represent a prehypertensive state.