Leucocyte Sodium Transport in Uraemia

1975 ◽  
Vol 49 (3) ◽  
pp. 213-216 ◽  
Author(s):  
R. P. S. Edmondson ◽  
P. J. Hilton ◽  
N. F. Jones ◽  
J. Patrick ◽  
R. D. Thomas
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Rate Constant ◽  
Sodium Transport ◽  
Sodium Efflux ◽  
Control Subjects ◽  
Active Moiety ◽  
Total Sodium

1. In sixteen patients with severe chronic renal failure the rate constant for total sodium efflux from leucocytes was significantly reduced compared with that in thirty control subjects. This difference lay chiefly in the glycoside-sensitive (‘active’) moiety of sodium efflux. 2. In sixteen patients receiving regular haemodialysis, the rate constant for total sodium efflux from the leucocyte was significantly greater than in the undialysed uraemic patients though still subnormal. 3. In individual patients, an increase in sodium efflux could be detected as early as 1 week after regular haemodialysis was started. 4. These results are compatible with the existence of a dialysable molecule in uraemic plasma affecting leucocyte sodium transport.

Relations between Sodium Transport and Sodium Concentration in Human Erythrocytes in Health and Disease

1981 ◽  
Vol 60 (5) ◽  
pp. 555-564 ◽  
Author(s):  
M. Cumberbatch ◽  
D. B. Morgan
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Membrane Permeability ◽  
Sodium Transport ◽  
Healthy Subjects ◽  
Total Activity ◽  
Sodium Content ◽  
Sodium Efflux ◽  
Sodium Pumps ◽  
Erythrocyte Sodium

1. We have examined the inter-relationships between erythrocyte sodium content and sodium transport in a group of healthy subjects and in groups of patients with disorders known to change the sodium content of erythrocytes. 2. In the healthy subjects the sodium content of erythrocytes was inversely related to both the permeability of the erythrocyte membrane to sodium (as measured by the unidirectional, ouabain-sensitive, sodium efflux) and the total activity of the sodium pumps (as measured by the rate constant of ouabain-sensitive sodium efflux). There was a correlation between the total activity of the sodium pumps and the membrane permeability to sodium. 3. Changes in the erythrocyte sodium content were due to a decrease in the activity of the sodium pumps (as in hypokalaemia and digoxin treatment), or a decrease in the permeability of the erythrocyte membrane to sodium (as in chronic renal failure) or a reduction of both the membrane permeability and the number of sodium pumps (as in hyperthyroidism or elderly patients). 4. One interpretation of the results in the healthy subjects is that there are two components of sodium influx; one associated with the sodium pumps in what we have called ‘membrane-units’ and the other determined by the ground permeability of the membrane. 5. On the basis of this model we suggest that in the geriatric and hyperthyroid patients there is a reduction in the number of ‘membrane-units’, that in hypokalaemia and during digoxin treatment there is inhibition of the sodium-pump component of the ‘membrane-units’ and that in chronic renal failure there is a decrease in the permeability of the membrane to sodium.

Effects of Haemodialysis and Continuous Ambulatory Peritoneal Dialysis on Abnormalities of Ion Transport in vivo in Patients with Chronic Renal Failure

1993 ◽  
Vol 85 (6) ◽  
pp. 725-731 ◽  
Author(s):  
Christopher J. Brearley ◽  
Jeffrey K. Aronson ◽  
Nicholas A. Boon ◽  
Anthony E. G. Raine
Keyword(s):  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Chronic Renal Failure ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Rate Constant ◽  
Cation Transport ◽  
Rubidium Uptake ◽  
Control Subjects ◽  
Pump Activity

1. We have studied Na+/K+ pump activity in vivo in three groups of subjects: patients with chronic renal failure not receiving maintenance dialysis, patients being treated by either haemodialysis or continuous ambulatory peritoneal dialysis, and matched control subjects. 2. To do this we have measured the changes in plasma and intraerythrocytic rubidium concentrations after an oral load of rubidium chloride, having previously shown that changes in the disposition of rubidium measured in this way reflect changes in the activity of the Na+/K+ pump in vivo. 3. Erythrocyte rubidium uptake was significantly reduced both in ten patients with chronic renal failure not receiving maintenance dialysis and in 12 patients being treated by haemodialysis, when compared with 31 healthy control subjects. In contrast, erythrocyte rubidium uptake was not altered in 13 patients treated by continuous ambulatory peritoneal dialysis. There was also a significantly reduced rate constant for erythrocyte rubidium uptake in patients with undialysed chronic renal failure (0.66 h−1) and in those treated by haemodialysis (0.78 h−1), whereas in patients treated by continuous ambulatory peritoneal dialysis the rate constant for erythrocyte rubidium uptake was not significantly different from control values (1.36h−1 and 1.41 h−1, respectively). 4. These findings are consistent with a reversal of the inhibition of erythrocyte Na+/K+ pump activity in vivo found in chronic renal failure by continuous ambulatory peritoneal dialysis, but not by haemodialysis. This difference may be due to the failure of haemodialysis to clear a circulating inhibitor of Na+, K+-ATPase or to the rapid re-accumulation of such an inhibitor after haemodialysis. Alternatively, it could be due to a dialysable inhibitor of potassium efflux, with a secondary reduction in the activity of the Na+/K+ pump. 5. Neither continuous ambulatory peritoneal dialysis nor haemodialysis reversed the abnormal disposition of rubidium in the plasma found in undialysed patients. This suggests that the putative inhibitor which accumulates in chronic renal failure does not affect cation transport in all tissues of the body, and that abnormalities of cation transport in chronic renal failure may be due to more than one mechanism.

Abnormal Sodium Transport in Leucocytes from Patients with Essential Hypertension and the Effect of Treatment

1974 ◽  
Vol 48 (s2) ◽  
pp. 169s-170s ◽  
Author(s):  
R. D. Thomas ◽  
R. P. S. Edmondson ◽  
P. J. Hilton ◽  
N. F. Jones
Keyword(s):  
Essential Hypertension ◽  
Rate Constant ◽  
Sodium Transport ◽  
Sodium Efflux ◽  
Accelerated Hypertension ◽  
Effect Of Treatment ◽  
Sodium Metabolism ◽  
Water Contents

1. In seventeen patients with untreated essential hypertension the sodium and water contents of leucocytes were significantly increased, whereas the rate constant for ouabain-sensitive sodium efflux was significantly reduced. 2. These abnormalities were not found in fourteen other patients with well-controlled hypertension. 3. Preliminary observations in accelerated hypertension suggest a different pattern of abnormality in leucocyte sodium metabolism.

scholarly journals Decrease of serum paraoxonase activity in chronic renal failure.

1998 ◽  
Vol 9 (11) ◽  
pp. 2082-2088
Author(s):  
T F Dantoine ◽  
J Debord ◽  
J P Charmes ◽  
L Merle ◽  
P Marquet ◽  
...  
Keyword(s):  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Chronic Renal Failure ◽  
Chronic Hemodialysis ◽  
Phenyl Acetate ◽  
Paraoxonase Activity ◽  
Control Subjects ◽  
Transplant Patients ◽  
End Stage ◽  
Serum Paraoxonase

Paraoxonase is an esterase that hydrolyzes organophosphate compounds. The enzyme is associated with HDL and could protect LDL against peroxidation, which suggests a possible involvement of paraoxonase in the antiatherogenic properties of HDL. Paraoxonase activity has been shown to be low in patients with myocardial infarction, diabetes mellitus, or familial hypercholesterolemia. Because cardiovascular disease is the main cause of death in chronic renal failure, serum paraoxonase activity was measured by spectrophotometry using three synthetic substrates (phenyl acetate, paraoxon, and 4-nitrophenyl acetate) in 305 patients with kidney disease, including 47 patients with non-end-stage chronic renal failure, 104 patients treated with hemodialysis, 22 patients treated with peritoneal dialysis, and 132 renal transplant patients. Patients were compared with two groups of aged-matched control subjects (total number = 195). Especially with 4-nitrophenyl acetate, paraoxonase activity was lower in patients with some degree of renal insufficiency (chronic renal failure [P < 0.05], chronic hemodialysis [P < 10(-4)], chronic peritoneal dialysis [P < 10(-4)]) than in control subjects. In transplant patients, paraoxonase activity was not found to be different from that in control subjects. The decrease of paraoxonase activity and thus the reduction of its antiatherogenic properties in renal failure could be an essential factor of premature vascular aging, especially when dialysis is used. Renal transplantation seems to restore paraoxonase activity.

A comparison of endogenous digoxin-like immunoreactivity and sodium transport inhibitory activity in umbilical arterial and venous serum

1988 ◽  
Vol 75 (6) ◽  
pp. 577-579 ◽  
Author(s):  
J. F. Morris ◽  
L. Poston ◽  
C. D. Wolfe ◽  
P. J. Hilton
Keyword(s):  
Umbilical Cord ◽  
Rate Constant ◽  
Sodium Transport ◽  
Inhibitory Activity ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Cord Serum ◽  
Paired Samples ◽  
Efflux Rate Constant

1. Endogenous digoxin-like immunoreactivity (EDLI) was measured by radioimmunoassay for digoxin in 13 paired samples of arterial and venous umbilical cord serum. EDLI was present in vein and artery, but was higher in the venous samples (P < 0.025). 2. The venous cord serum inhibited the ouabain-sensitive sodium efflux rate constant of a normal mixed leucocyte population when compared with the effect of arterial cord serum (P < 0.005). 3. It is suggested that the placenta may be involved in the production or metabolism of neonatal EDLI and of the inhibitor of sodium transport.

A Passive Sodium Transport Inhibitory Factor (Inhibitin) Released from Leukaemic Promyelocytes in Culture

1984 ◽  
Vol 66 (3) ◽  
pp. 365-368
Author(s):  
Kevin Morgan ◽  
M. Afzal Mir
Keyword(s):  
Rate Constant ◽  
Sodium Transport ◽  
Culture Media ◽  
Inhibitory Effect ◽  
Inhibitory Factor ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Stable Factor ◽  
Heat Stable ◽  
Efflux Rate Constant

1. Previous studies have shown that myeloid leukaemic blast cells contain a heat stable factor which inhibits bidirectional sodium transport in normal erythrocytes. This study was undertaken to establish whether leukaemic promyelocytes in culture secrete this factor. 2. Two cell-lines of leukaemic promyelocytes (HL-60 and JR) were grown and culture media from both reduced significantly the ouabain-insensitive sodium efflux rate constant, whereas conditioned culture medium (incubated like the cells in culture) had no inhibitory effect. 3. Promyelocyte extract reduced significantly (P < 0.01) the total sodium efflux rate constant from 0.393 ± 0.030 (sd) to 0.311 ± 0.060, and ouabain-insensitive efflux rate constant from 0.131 ± 0.008 to 0.079 ± 0.009 (P<0.001). 4. The inhibitory factor was heat stable (80°C for 30 min) and it inhibited sodium efflux through a pathway which was not inhibited by ouabain or frusemide. 5. These studies suggest that leukaemic promyelocytes secrete the previously identified passive sodium transport inhibitory factor.

Impaired Nutritive Skeletal Muscle Blood Flow in Patients with Chronic Renal Failure

1990 ◽  
Vol 79 (3) ◽  
pp. 239-245 ◽  
Author(s):  
John R. Bradley ◽  
Janice R. Anderson ◽  
David B. Evans ◽  
Alan J. Cowley
Keyword(s):  
Skeletal Muscle ◽  
Renal Failure ◽  
Blood Flow ◽  
Chronic Renal Failure ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Control Subjects ◽  
Calf Blood Flow ◽  
Before And After ◽  
And Control

1. The possibility that abnormalities of skeletal muscle may limit the exercise tolerance of patients with chronic renal failure was investigated in patients undergoing regular haemodialysis. 2. Blood flow to the calf, a vascular bed consisting predominantly of skeletal muscle, was measured in six patients before and after exercise and compared with values obtained from 12 control subjects. 3. The patients were limited on exertion and had an abnormal response of calf blood flow to bicycle exercise. Resting calf blood flow was similar in patients and control subjects, but the mean increase in calf blood flow in response to submaximal exercise was 0.55 (sem 0.12) ml min−-1 100 ml−-1 in the patients and 1.43 (sem 0.17) ml min−-1 100 ml−-1 in the control subjects. The increase after symptom-limited maximal exercise was 1.50 (sem 0.80) ml min−-1 100 ml−-1 in the patients and 4.20 (sem 0.40) ml min−-1 100 ml−-1 in the control subjects. 4. Skeletal muscle biopsies from eight haemodialysis patients were studied by histochemistry and electron microscopy. 5. Oxidative enzyme activity was increased and there were large subsarcolemmal aggregates of structurally normal mitochondria. Necrotic capillaries were observed as empty basement membrane tubes containing fragments of degenerating endothelium. 6. The changes were compatible with a response to a chronic reduction in skeletal muscle blood flow.

Abnormal rhythmic oscillations of atrial natriuretic peptide and brain natriuretic peptide in chronic renal failure

2006 ◽  
Vol 110 (4) ◽  
pp. 491-501 ◽  
Author(s):  
Erling B. Pedersen ◽  
Egidijus Bacevicius ◽  
Jesper N. Bech ◽  
Karsten Solling ◽  
Henrik B. Pedersen
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Level ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Maximum Amplitude ◽  
Dialysis Patients ◽  
Control Subjects ◽  
Healthy Control ◽  
The Mean

Secretion of ANP (atrial natriuretic peptide) and BNP (brain natriuretic peptide) is pulsatile in healthy humans. However, the patterns of secretion of ANP and BNP have not been studied in chronic renal failure. The aim of the present study was to test the hypotheses that ANP and BNP are secreted in pulses in dialysis patients, and that pulsatile secretion is regulated by prostaglandins. Blood samples were drawn every 2 min through an intravenously inserted plastic needle over a period of 1–2 h in 13 dialysis patients and 13 healthy control subjects (Study 1), and in 15 healthy control subjects, who participated in a randomized placebo-controlled cross-over study after treatment with indomethacin and placebo (Study 2). Plasma concentrations of ANP and BNP were determined by RIAs, and the results were analysed for pulsatile behaviour by Fourier transformation. The results from Study 1 showed that the secretion of ANP and BNP was pulsatile in nine patients with chronic renal failure. The maximum amplitude was significantly higher in chronic renal failure compared with control subjects for both ANP and BNP (ANP, 4.3 compared with 0.7 pmol/l; BNP, 2.0 compared with 0.3 pmol/l; values are medians) and correlated positively with the mean plasma level of ANP (ρ=0.900, P=0.001; n=9) and BNP (ρ=0.983, P=0.000; n=9). The frequency was the same for patients and controls. The results from Study 2 demonstrated pulsatile secretion in all subjects, but both the amplitude and frequency were unaffected by indomethacin. The maximum amplitude correlated positively with the mean plasma level of ANP and BNP during both placebo and indomethacin treatment. It can be concluded that the secretion of ANP and BNP is pulsatile with abnormally high amplitude in chronic renal failure, that prostaglandins apparently are not involved in the secretion of these peptides in healthy subjects and that the high secretion rate in chronic renal failure results in higher ANP and BNP in plasma.

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