Red Blood Cell Sodium Transport and Phosphate Release in Uremia R.S. Swaminathan R.S. Swaminathan, Department of Chemical Pathology, The Chinese University of Hong Kong, Hong Kong Dear Sir, In a recent article, Walter and Becht [Nephron 34: 35–41, 1983] observed that red blood cell sodium transport and ouabain-sensitive phosphate release was diminished in uremics. I would like to make two comments about this article: (1) It is not universal to find a decreased red cellsodium transport in uremics. In a recent article [4], weobserved that erythrocyte sodium content was diminishedin 15 uremic patients and this was associated with adecreased ouabain-sensitive efflux rate of sodium, a normal ouabainsensitive efflux rate constant of sodium, anormal Na+, K+-ATPase activity and reduced number ofouabain-binding sites. On closer analysis of the data, itwas observed that in a small group of uremic patientswith low erythrocyte sodium, the ouabain-sensitive efflux rate constant of sodium was increased and in anothergroup of patients with a more severe degree of uremia theouabainsensitive efflux rate constant, efflux rateNa+, K+-ATPase activity and ouabain-binding capacitywere all reduced. We interpreted these findings as suggestive of a series of changes during the development ofrenal failure. During the progression of chronic renalfailure, there is initially an increase in the activity ofsodium pumps due to a ‘stimulator’ or absence of’inhibitor’. With further deterioration in renal function, activityof sodium pumps as well as membrane permeabilitydecrease. A low erythrocyte sodium content has beenobserved previously in chronic renal failure [1,2, 5]. (2) Walter and Becht measured ouabain-sensitivephosphate release and found it to be related to rateconstant of ouabain-sensitive sodium efflux. The phosphate release was used as an index of Na+, K+-ATPaseactivity in intact red cells. We agree that measurement ofNa+, K+-ATPase activity ofhemolysates, ghosts or membrane is not indicative of the activity in intact cells. Assuggested by Walter and Becht the phosphate release isnot entirely satisfactory as there may be variable reutilization of phosphate released. We have used a different approach to this problem by studying the disappearance of glucose. In a recent study of 25 healthy subjects, it was observed that the rate constant of sodium efflux and ouabain-binding sites were significantly related to ouabainsensitive glucose consumption (r = 0.433 p < 0.05, and r = 0.5575 p < O.01 respectively [Richardson and Swaminathan, unpubl. results]). The correlation co-efficient, although significant, was not high as between Na+, K+-ATPase of red cell ghosts and ouabain-binding sites (r = 0.94) [3]. Possible reasons are (a) the glucose consumption method is not sensitive enough, and (b) a small number of observations with a narrow range of sodium pump activity (range for rate constant 0.201–0.432 and for ouabain-binding sites 187–404). Further studies with more precise techniques are in progress to verify these possibilities. References
[1]
M. Cumberbatch,et al.
Erythrocyte sodium transport in chronic renal failure.
,
1982,
Clinical science.
[2]
G. Schmalzing,et al.
Red cell ouabain binding sites, Na+K+-ATPase, and intracellular Na+ as individual characteristics.
,
1981,
Life sciences.
[3]
M. Cumberbatch,et al.
Relations between sodium transport and sodium concentration in human erythrocytes in health and disease.
,
1981,
Clinical science.
[4]
F. Zannad,et al.
Digoxin in the elderly and in renal failure. Contribution of erythrocyte 86-rubidium uptake tests.
,
1981,
European journal of cardiology.
[5]
A. Keynan,et al.
Red blood cell content of water, sodium and potassium in body fluid disturbances.
,
1967,
Israel journal of medical sciences.