Abstract
Hemolysis is an important contributing cause of anemia in uremic patients. Uremia causes several erythrocyte abnormalities such as increased mechanical fragility1, increased autohemolysis2, and shortened erythrocyte survival1,2. These abnormalities may be due to a decrease in erythrocyte deformability, which is measured by filtrability as an index of cell rigidity. Several workers demonstrated that erythrocyte deformability is decreased in uremic patients3,4. Erythrocyte deformability is reduced by a rise in intracellular Na content, which may be due in part to a decline in the ATPase activity of the erythrocyte membrane. However, the relationship of erythrocyte deformability to uremic toxins has not been clarified. Giovannetti reported that guanidino compounds, especially methylguanidine (MG), caused hemolysis both in vivo and in vitro 5,6. Depressed Na-K ATPase activity of uremic erythrocytes was demonstrated by Cole7.
Keywords
ATPase Activity Erythrocyte Membrane Standard Medium Uremic Patient Uremic ToxinPreview
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Reference
- 1.J. F. Desforges and J. P. Dawson, The anemia of renal failure, Arch. Intern. Med., 101: 326 (1958).CrossRefGoogle Scholar
- 2.S. Giovannetti, P. Giagnoni and P. L. Balestri, Red cell survival in chronic uremia: its relationship with the spontaneous in vitro autohemolysis and with the degree of anamia, Experientia, 22: 739 (1966).CrossRefGoogle Scholar
- 3.S. Forman, M. Bischel and P. Hochstein, Erythrocyte deformability in uremic hemodialyzed patients, Ann. Intern. Med., 79: 841 (1973).PubMedGoogle Scholar
- 4.A. Rosenmund, U. Binswanger and P. W. Straub, Oxidative injury to erythrocytes, cell rigidity, and splenic hemolysis in hemodialyzed uremic patients, Ann. Intern. Med., 82: 460 (1975).PubMedGoogle Scholar
- 5.S. Giovannetti, M. Biagini, P. L. Balestri, R. Navelesi, P. Giagnoni, A. de Mattetis, P. Ferro-Milone and C. Perfetti, Uremia like syndrome in dogs chronically intoxicated with methylguanidine and creatinine, Clin. Sci., 36: 445 (1969).PubMedGoogle Scholar
- 6.S. Giovannetti, L. Cioni, P. L. Balestri and M. Biagini, Evidence that guanidine and some related compounds cause hemolysis in chronic uremia, Clin. Sci., 34: 141 (1968).PubMedGoogle Scholar
- 7.C. H. Cole, Decreased ouabain-sensitive adenosine triphosphatase activity in the erythrocyte membrane of patients with chronic renal disease, Clin. Sci., 45: 775 (1973).Google Scholar
- 8.S. Ichida, C. H. Kuo and T. Matsuda, Effects of La, Nn and ruthenuim red on Mg.Ca-ATPase activity and ATP-dependent Ca-binding of synaptic plasma membrane, Japan. J. Pharmacol., 26: 39 (1976).Google Scholar
- 9.H. Lowry, N. H. Rosebrough, A. L. Farr and R. J. Randall, Protein measurement with the folin phenol reagent, J. Biol. Chem., 193: 265 (1951).PubMedGoogle Scholar
- 10.T. Kikuchi, Y. Orita, A. Ando, H. Mikami, M. Fujii, A. Okada, and H. Abe, Liquid-chromatographic determination of guanidino compounds in plasma and erythrocyte of normal persons and uremic patients, Clin. Chem., 27: 1899 (1981).PubMedGoogle Scholar
- 11.M. A. Lichtman, D. R. Miller and R. I. Weed, Energy metabolism in uremic red cells: relationship of red cell adenosine triphosphate concentration to extracellular phosphate, Trans. Ass. Amer. Phycns., 82: 331 (1969).Google Scholar
- 12.C. H. Wallas, Metabolic studies on the erythrocyte from patients with chronic renal disease on hemolysis, Brit. J. Haematol., 27: 145 (1974).CrossRefGoogle Scholar
- 13.M. Matsumoto and A. Mori, Effects of guanidino compounds on rabbits brain microsomal Na-K ATPase activity, J. Neurochem., 27: 635 (1976).PubMedCrossRefGoogle Scholar
- 14.E. K. M. Smith and L. G. Welt, The red blood cell as a model for the study of uremic toxins, Arch. Intern. Med., 126: 827 (1970).CrossRefGoogle Scholar