Abstract
Red-cell lithium–sodium countertransport is increased in patients with essential hypertension. It has been proposed that sodium–hydrogen ion exchange in the brush border of the renal proximal tubules is analogous to red-cell countertransport. To investigate the rate of sodium reabsorption by the proximal renal tubules in hypertension, we measured lithium clearance (a measure of proximal tubular reabsorption of sodium), as well as red-cell countertransport, in 14 patients with untreated essential hypertension and in 31 controls. As a group, the hypertensive patients had a higher average (±SEM) rate of red-cell countertransport (0.378±0.030 mmol of lithium per liter of cells per hour, P<0.01) and a lower renal fractional lithium clearance (13.96±0.69 percent, P<0.01) than normotensive subjects (0.317±0.015 mmol of lithium per liter of cells per hour and 17.75±0.81 percent, respectively). Within the normotensive group, subjects with hypertension in at least one first-degree relative had significantly lower fractional lithium clearances than subjects with no hypertensive relatives (15.37±0.84 percent vs. 19.06±1.07 percent, P<0.05). We conclude that hypertensive patients have heightened proximal tubular reabsorption of sodium and that red-cell countertransport is a marker of the renal abnormality. Enhanced proximal tubular sodium reabsorption may precede the development of essential hypertension. (N Engl J Med 1986; 314:198–201.)