Abstract 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. References 1. Welt LG, Sach JR, McManus TJ: An ion transport defect in erythrocytes from uremic patients. Trans Assoc Amer Physicians 77:169-181, 1964. 2. Smith EKM: Studies of the Membrane Adenosinetriphosphatase of Human Red Cells in Health and Disease, thesis. University of London, 1968. 3. Beilin LJ, Knight GJ, Munro-Faure AD, et al: The sodium, potassium and water contents of red blood cells of healthy human adults. J Clin Invest 45:1817-1825,1966.Crossref 4. Sachs JR, Welt LG: The concentration dependence of active potassium transport in the human red blood cell. J Clin Invest 46:65-76, 1967.Crossref 5. Skou JC: The influence of some cations on an adenosinetriphosphatase from peripheral nerves. Biochem Biophys Acta 23:394-401,1957.Crossref 6. Smith EKM, Welt LG: The activation of human erythrocyte membrane adenosinetriphosphatase by low concentrations of sodium and potassium. Amer J Physiol , to be published. 7. Lichtman MA, Miller D, Freeman RB: Erythrocyte adenosinetriphosphate depletion during hypophosphatemia in a uremic subject. New Eng J Med 280:240-244,1968.Crossref 8. Villamil MF, Rettori MF, Kleeman CR: Sodium transport by red blood cells in uraemia. J Lab Clin Med 72:308-317,1968. 9. Cole CH, Balfe JW, Welt LG: Induction of a ouabain-sensitive ATPase defect by uremic plasma. Trans Assoc Amer Physicians 81:213-220,1968. 10. Dunn MJ: Alterations of red blood cell sodium transport during malarial infection. J Clin Invest 48:674-684, 1969.Crossref 11. Smith EKM, Samuel PD: Abnormalities in the sodium pump of erythrocytes from patients with hyperthyroidism. Clin Sci 38:49-61, 1970. 12. Giovanetti S, Balestri LP, Cioni L: Spontaneous in vitro autohemolysis of blood from chronic uremic patients. Clin Sci 29:407-416, 1966. 13. Giovanetti S, Cioni L, Balestri PL, et al: Evidence that guanidines and some related compounds cause haemolysis in chronic uraemia. Clin Sci 34:141-148, 1968. 14. Morgan JM, Morgan RE: Study of the effect of uremic metabolites on erythrocyte glycolysis. Metabolism 13:629-635, 1964.Crossref 15. Theil GB, et al: Red cell glutathione content and stability in renal insufficiency. J Lab Clin Med 58:736-742, 1961. 16. Jesenovic N, Fiser-Herman M: Comparison of the concentrations of glutathione and of iodine-reducing substances in human erythrocytes. Clin Chem Acta 14:293-299, 1966.Crossref 17. Kuroyanagi T, et al: The ADP and ATP levels and the phosphorylating activity of erythrocytes in patients with uremia associated with chronic renal failure. Tohoku J Exp Med 84:105-112, 1964.Crossref 18. Wilson DM, Schwartz FD: In vivo incorporation of iodopyracet into erythrocytes of healthy and azotemic patients. J Lab Clin Med 72:951-957, 1968.
Archives of Internal Medicine – American Medical Association
Published: Nov 1, 1970