Summary
Red cell ATP levels were measured in 65 patients with renal failure and in 50 controls using the firefly luciferin luciferase assay. The average ATP levels were increased in patients with renal failure (4.88 µmol/g Hb,p < 0.01) as compared to the controls (3.64 µmol/g Hb). A correlation was obtained between red cell ATP levels and inorganic serum phosphate (r=0.6186,p<0.001). ATP levels and correlation to inorganic serum phosphate were further analysed in respect to treatment of renal insufficiency by hemodialysis, peritoneal dialysis (CAPD), kidney transplantation or duration of renal disease. No significant differences were observed except that red cell ATP did not correlate with inorganic serum phosphate in patients treated by CAPD. The severity of renal disease as judged by clinical findings was not related to red cell ATP levels. The mechanisms leading to elevated red cell ATP levels in uremic subjects are not completely understood. A stimulated red cell glycolysis due to hyperphosphatemia, a reduced ATP hydrolysis due to inhibition of membrane bound Na/K ATPase and a younger red cell population in patients with renal insufficiency were put forward. There is some evidence that an altered adenosine metabolism is also involved.
Similar content being viewed by others
References
Becher HJ, Weise HJ, Volkermann U, Schollmeyer P (1980) Enhanced purine nucleotide synthesis in erythrocytes of uremic patients. Klin Wochenschr 58:1243–1250
Beutler E, Mathai K (1967) A comparison of normal red cell ATP levels as measured by the firefly system and the hexokinase system. Blood 30:311–320
Chillar RK, Desforges JF (1974) Red-cell organic phosphates in patients with chronic renal failure on maintenance haemodialysis. Br J Haematol 26:549–556
Guest GM, Rapoport S (1941) Organic acid-soluble phosphorus compounds of the blood. Physiol Rev 21:410
Hawkins CF, Kyd JM, Bagnara AS (1980) Adenosine metabolism in human erythrocytes: a study of some factors which affect the metabolic fate of adenosine in intact red cells in vitro. Arch Biochem Biophys 202:380–387
Hurt GA, Chanutin A (1964) Organic phosphate compounds of erythrocytes from individuals with uremia. J Lab Clin Med 64:675–684
Jahrmärker H (1964) Über den Adeninnucleotidgehalt der Erythrocyten bei Niereninsuffizienz. Klin Wochenschr 42:123–126
Jahrmärker H (1968) Beobachtungen bei der Phosphat-Aktivierung der Erythrocytenglykolyse. In: Deutsch E, Gerlach E, Moser K (eds) Metabolism and membrane permeability of erythrocytes and thrombocytes. Thieme, Stuttgart, pp 19–33
Kramer HJ, Gospodinov D, Krück F (1976) Functional and metabolic studies on red blood cell sodium transport in chronic uremia. Nephron 16:344–358
Lerner MH, Rubinstein D (1970) The role of adenosine and adenine as precursors for adenine nucleotide synthesis by fresh and preserved human erythrocytes. Biochim Biophys Acta 224:301–310
Lichtman MA, Miller DR (1970) Erythrocyte glycolysis, 2,3-diphosphoglycerate and adenosine triphosphate concentration in uremic subjects: relationship to extracellular phosphate concentration. J Lab Clin Med 76:267–279
Sawada K (1979) Studies on the adenine nucleotide metabolism in uremic erythrocytes. Nippon Jinze Gakhai Shi 11:1193–1205
Schneider W, Jutzler GA (1974) Implications of cyclic adenosine 3′,5′-monophosphate in chronic renal failure. N Engl J Med 291:155
Schneider W (1978) Zur Pathogenese der urämischen Thrombozytopenie. In: Marx R, Thies HA (eds) Niere, Blutgerinnung und Hämostase. Schattauer, Stuttgart New York, S 221–236
Wallas CH (1974) Metabolic studies on red cells from patients with chronic renal disease on haemodialysis. Br J Haematol 26:71–78
Warrendorf EM, Rubinstein D (1973) The elevation of adenosine triphosphate levels in human erythrocytes. Blood 42:637–647
Walt IG, Sachs JR, McManus TJ (1964) An ion transport defect in erythrocytes from uremic patients. Trans Assoc Am Phys 77:169–181
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Planker, M., Schnurr, E. & Schneider, W. Elevated ATP levels in the red cells of patients with renal failure. Klin Wochenschr 61, 709–713 (1983). https://doi.org/10.1007/BF01487617
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/BF01487617