Sodium transport abnormalities in uremia may be demonstrated in human erythrocytes by finding an increased intracellular sodium concentration. This is thought to be the result of an impaired sodium potassium pump associated with a defect in membrane adenosine triphosphatase (ATPase) which may serve as a link between the pump and its energy supply. The defect is reversed by effective treatment of uremia. Diminished activity of membrane ATPase can be induced in normal cells by incubation in plasma from patients with uremia whose erythrocytes have a high sodium concentration. Toxic substances known to accumulate in uremia do not inhibit the sodium pump or membrane ATPase in vitro. No single factor has yet been found which will induce the defect described, but the red blood cell is a useful model for further study of the metabolic defects induced by uremia.