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      Erythrocyte Sodium Transport in Dialyzed Uremic Patients

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          To investigate the status of the Na + concentration and ionic fluxes in red cells of human subjects with dialyzed chronic uremia, the authors measured the Na +-K + pump activity as well as Na +-K + cotransport (CoT), Na +-Li + countertransport (CTT) and Na + passive permeability in erythrocytes from 37 normal subjects and 23 chronic uremic patiens receiving maintenance hemodialysis. The mean intracellular Na + concentration [Na +]i value in the pre-dialytic group was significantly lower than that in control subjects (p<.0001), but tended to recover to the normal value of [Na +]i in the post-dialytic group. The mean intracellular K + concentration value in the post-dialytic group was significantly higher than that of the control group (p<.001), but not significantly different from that of the pre-dialytic group. It was found that the Na +-K + pump activity of erythrocytes in the pre- and post-dialytic groups markedly decreased over that of the normal control group with statistical significance (p<.0001, respectively). The Na +-K + pump activity in the post-dialytic group, however, tended to recover, but not significantly. The rate constant for ouabain-sensitive Na + efflux in the post-dialytic group was significantly decreased over that of the normal controls (p<.05). The authors observed a significant decrease of the Na + CoT value (p<.001 respectively) and rate constant for Na + CoT (p<.05, respectively) in the patients with pre- and post-dialytic uremia vs. that of normal subjects. Also, the authors observed a marked decrease of the Na +-Li + CTT value in the patients in the pre- and post-dialytic groups than that of the control subjects (p<.05, respectively). Passive Na + permeability in the patients with pre-dialytic uremia was decreased markedly compared to the normal subjects (p<10 −5), but its value in the post-dialytic group tended to recover to the normal value. In conclusion, our studies demonstrate that another possible mechanism of inhibition of the Na +-K + pump in pre- dialytic uremia might then be a secondary adaptive response of the cell to maintain normal intracellular ion concentration and transmembrane ion gradients in the face of the reduced [Na +]i due to decreased passive Na + permeability.

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          Resting skeletal muscle membrane potential as an index of uremic toxicity. A proposed new method to assess adequacy of hemodialysis.

          Electrochemical disturbances of skeletal muscle cells in untreated uremia are characterized by an increase in the intracellular sodium and chloride content, a decrease in intracellular potassium, and a low resting membrane potential. In this study, we have reexamined the foregoing and, in addition, have examined the effects of hemodialysis. Three groups of patients were studied. In the first group of 22 uncomplicated uremic patients, whose creatinine clearance (Ccr) ranged from 2 to 12 cm(3)/min per 1.73 m(2), resting transmembrane potential difference (Em) of skeletal muscle cells was measured. In each of the nine patients whose Ccr ranged between 6.3 and 12 cm(3)/min, the Em was normal (i.e., -90.8+/-0.9 mV, mean+/-SEM). However, as Ccr dropped below 6.3 cm/min, the Em became progressively reduced and assumed a linear relationship with the Ccr. In the second study, nine individuals with end-stage renal disease, whose mean Ccr was 4.3 cm(3)/min, underwent measurement of Em and intracellular electrolyte concentration before and after 7 wk of hemodialysis. Before dialysis, the Em was -78.5+/-2.1 mV, intracellular sodium and chloride were elevated, and the intracellular potassium was reduced. After 7 wk of hemodialysis the Em rose to -87.8+/-1.3 mV, and the intracellular sodium, chloride, and potassium became normal. In the third study, seven patients who were stable on 6-h thrice-weekly dialysis were studied before and after reduction of dialysis to 6 h twice weekly. In those individuals whose Em remained normal after 6 wk, dialysis time was reduced further. On thrice-weekly dialysis the Em was -91.2+/-1.0 mV. With reduced dialysis, the Em fell to -80.1+/-0.8 mV (P < 0.001). In each case, the Em became abnormal before significant signs or symptoms of uremia were noted. These findings demonstrate that end-stage renal disease is associated with serious electrochemical changes in the muscle cell which are reversed by hemodialysis and recur when dialysis time is reduced. Thus, serial observations of muscle Em may be a potentially powerful tool to assess adequacy of dialysis therapy.
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            Mechanism of alteration of sodium potassium pump of erythrocytes from patients with chronic renal failure.

             J. Cheng,  T. Kahn,  D M Kaji (1984)
            We examined intracellular electrolytes, K influx, and [3H]ouabain-binding capacity of erythrocytes from 32 normal subjects and 45 patients with end-stage renal failure on dialysis, including 16 with high intracellular Na (mean 17.3 +/- 3.9 mmol/liter cell water). The [3H]ouabain-binding capacity of erythrocytes with high cell Na was markedly reduced as compared with that of erythrocytes from normal subjects (274 +/- 52 vs. 455 +/- 59 sites/cell, P less than 0.001). The mean serum creatinine was higher in the uremic group with high cell Na. There was a significant linear correlation between intracellular Na and [3H]ouabain-binding in both normal and uremic subjects. Cross-incubation of normal cells with uremic plasma for 24 h failed to reduce [3H]ouabain-binding capacity of normal cells. In spite of a substantial increase in cell Na, K pump influx was not higher in uremic erythrocytes with high cell Na. When intracellular Na was altered with nystatin (cell Na equal to 120 mmol/liter cell water in both groups), K pump influx was proportional to the number of Na-K pump sites so that the ion turnover rate per pump site was similar in the two groups. Uremic plasma failed to depress K pump influx of normal erythrocytes. The passive net influx of Na in uremic cells with high intracellular Na was not different from that observed in erythrocytes from normal subjects. When erythrocytes were separated by age on Percoll density gradients, the number of Na-K pump sites of the youngest uremic cells was significantly lower than that of the youngest normal cells, suggesting that decreased synthesis of Na-K pump sites, rather than accelerated loss of Na-K pump sites during aging, was responsible for the decrease in [3H]ouabain-binding capacity of erythrocytes from uremic subjects. Taken together, these findings suggest that a decrease in the number of Na-K pump sites plays a major role in the abnormality of Na-K pump of erythrocytes from patients with chronic renal failure.
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              An endogenous digoxin-like substance in patients with renal impairment.

              Digoxin concentrations were measured in serum samples from 102 patients with renal impairment who were receiving digoxin therapy. Many patients had values that differed widely on several currently available immunoassays, with differences as great as 2.9 ng/mL. In contrast, patients with normal renal function who were receiving digoxin had few discrepant results, with the largest difference being 0.5 ng/mL. We also assayed serum samples from 54 patients with renal impairment not on digoxin therapy and found that more than 60% of these digoxin-free patients had false-positive digoxin values on most assays. Our data suggest that a substance with digoxin-like immunoactivity is present in many patients with renal insufficiency. This substance may seriously compromise the accuracy and interpretation of digoxin concentration measurements.

                Author and article information

                Korean J Intern Med
                Korean J. Intern. Med
                The Korean Journal of Internal Medicine
                Korean Association of Internal Medicine
                January 1989
                : 4
                : 1
                : 9-17
                Department of Internal Medicine, Catholic University Medical College, Seoul, Korea
                Green Cross Bioscience Reference Laboratory
                Author notes
                Address reprint requests: Young-Suk Yoon, M.D., Department of Internal Medicine, Catholic University, Medical College, 505 Banpo-dong Seocho-ku, Seoul, Korea

                A preliminary report of this work was presented at the 38th annual meeting of the Korea Internal Medicine in Seoul, Korea, October, 1986. This work was supported in part by the Catholic Medical Center, clinical research funds.

                Copyright © 1989 The Korean Association of Internal Medicine

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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