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      Adequate hemodialysis improves anemia by enhancing glucose-6-phosphate dehydrogenase activity in patients with end-stage renal disease

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          Abstract

          Background

          We conducted this study to determine the erythrocyte glucose-6-phosphate dehydrogenase (G6PD) activity level in patients with end-stage renal disease (ESRD) on maintenance hemodialysis (HD) and to determine the effect of hemodialysis adequacy on G6PD activity levels and its impact on anemia.

          Methods

          Eighty-two patients (48 men and 34 women) receiving regular hemodialysis for ESRD through arteriovenous fistulae for at least one year prior to the start of the study were enrolled in this study. G6PD activity levels were measured in all patients and the average Kt/V was used as a parameter of HD adequacy. Patients were divided into two groups according to Kt/V values. Group 1 included 45 patients with Kt/V˃1.2 (adequate HD), and group 2 included 37 patients with Kt/V˃1.2 (inadequate HD). The average hemoglobin level and the weekly dose of an erythropoietin-stimulating agent, epoetin alpha (ESA), for each patient were calculated for one year.

          Results

          The mean (SD) erythrocyte G6PD activity for all patients on hemodialysis was 7.64 ± 1.85 U/g Hb. Patients who had received adequate hemodialysis had a significantly higher average erythrocyte G6PD (mean (SD) = 9.2 ± 0.7 U/g Hb) compared to patients who had inadequate hemodialysis (mean (SD) = 5.7 ± 0.7U/g Hb) ( P-value <0.005). The mean hemoglobin concentration was significantly higher in patients with adequate hemodialysis compared to those with inadequate hemodialysis.

          Conclusion

          Our study demonstrated the beneficial effect of adequate hemodialysis in correcting anemia by enhancing the erythrocyte G6PD activity in patients.

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          Most cited references22

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          The intensity of hemodialysis and the response to erythropoietin in patients with end-stage renal disease.

          Anemia (characterized by a hematocrit of 30 percent or lower) persists in 40 to 60 percent of patients treated for end-stage renal disease with maintenance hemodialysis, despite concomitant erythropoietin (epoetin) therapy. We tested the hypothesis that inadequate dialysis is a key reason for the insufficient response to erythropoietin in patients with end-stage renal disease who are receiving hemodialysis. We prospectively studied 135 randomly selected patients undergoing hemodialysis who had been receiving intravenous erythropoietin for at least four months. The adequacy of dialysis was assessed by measuring the percent reduction in the blood urea nitrogen concentration and the serum albumin concentration. The hematocrit was measured weekly for four weeks, transferrin saturation was measured, and coexisting illnesses were documented. To determine the effect of an increased level of dialysis on the hematocrit, the thrice-weekly schedule of dialysis was increased to raise the mean urea-reduction value from 60.7 to 72 percent for six weeks in 20 consecutive patients whose base-line urea-reduction value was less than 65 percent. The change in the hematocrit in these patients was compared with that observed in the next 20 patients who had an equivalent base-line urea-reduction value but whose level of dialysis was not altered. The mean hematocrit of the entire group was 29.2 +/- 4 percent, and the mean thrice-weekly dose of erythropoietin was 59 +/- 29 U per kilogram of body weight. The mean serum albumin concentration was 3.8 +/- 0.4 g per deciliter, the mean urea-reduction value was 62 +/- 4.8 percent, and the mean transferrin saturation was 20 +/- 9 percent. Multiple regression analysis revealed direct correlations between the hematocrit and the serum albumin concentration (P = 0.009) and between the hematocrit and the urea-reduction value (P = 0.012) after adjustment for other factors. A logistic-regression analysis indicated that an 11 percent increase in the urea-reduction value doubled the odds that a patient would have a hematocrit above 30 percent. After six weeks of increased intensity of dialysis in 20 patients with base-line urea-reduction values of less than 65 percent, the mean (+/- SE) hematocrit rose from 28.4 +/- 0.78 percent to 32.3 +/- 0.71 percent (P = 0.002); there was no significant change in a control group of 20 patients with equivalent base-line urea-reduction values in whom the dialysis level was not altered (28.2 +/- 0.84 percent to 26.3 +/- 0.85 percent; P = 0.175). In patients with end-stage renal disease, inadequate hemodialysis is associated with a suboptimal response to erythropoietin therapy. Increasing the intensity of dialysis in patients with anemia who are receiving inadequate dialysis results in a significant increase in the hematocrit.
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            Anemia in chronic kidney disease: causes, diagnosis, treatment.

            S Nurko (2006)
            Most patients with chronic kidney disease eventually become anemic. We should view the management of anemia in these patients as part of the overall management of the many clinically relevant manifestations of chronic kidney disease. Erythropoiesis-stimulating agents (ESAs) are safe and should be used, as treating anemia may forestall some of the target-organ damage of chronic kidney disease.
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              • Article: not found

              The anemia of chronic renal failure: pathophysiology and the effects of recombinant erythropoietin.

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                Author and article information

                Contributors
                ayeshmahmoud@hotmail.com
                ahnafb@yahoo.com
                elhamelamin12@hotmail.com
                yskhader@just.edu.jo
                kma1234@msn.com
                mohrabb@hotmail.com
                Journal
                BMC Nephrol
                BMC Nephrol
                BMC Nephrology
                BioMed Central (London )
                1471-2369
                26 September 2014
                26 September 2014
                2014
                : 15
                : 1
                : 155
                Affiliations
                [ ]Department of Internal Medicine, King Abdullah University Hospital, Faculty of Medicine, Jordan University of Science and Technology, P.O. Box 3030, Irbid, 22110 Jordan
                [ ]Saad specialist hospital, Al Khobar, Saudi Arabia
                [ ]Faculty of Medicine & Health Sciences, El Imam Elmahdi University, P.O. Box 209, Khartoum, 11588 Sudan
                [ ]Department of Public Health, Faculty of Medicine, Jordan University of Science and Technology, P.O. Box 3030, Irbid, 22110 Jordan
                Article
                844
                10.1186/1471-2369-15-155
                4181374
                25261071
                f5a9fc42-a919-4b5c-88ac-750e6344bd4b
                © Ayesh (Haj Yousef) et al.; licensee BioMed Central Ltd. 2014

                This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 27 May 2014
                : 23 September 2014
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2014

                Nephrology
                anemia,glucose-6-phosphate dehydrogenase,hemodialysis
                Nephrology
                anemia, glucose-6-phosphate dehydrogenase, hemodialysis

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