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      Treatment Options to Intensify Hemodialysis

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          Abstract

          At present, three methods are practiced to intensify hemodialysis (HD): 3 times weekly, 8-hour HD, short daily HD and slow daily nocturnal HD. Three times weekly 8-hour dialysis increase both the dialysis dose and time. The longest experiences are in Tassin. Five-year survival in Tassin was better in all age groups compared with the major registries – Japan, EDTA and US Medicare and more obvious for older age groups. The data of Tassin show that increasing the dialysis time provides better blood pressure control, need for no or less antihypertensive drugs, less intradialytic complications, better middle molecule and phosphate clearance, better nutritional status, less requirement for erythropoietin and increased survival. These data of Tassin could be mainly confirmed in our dialysis center. The main difference to Tassin was that in our center most of the patients still need few antihypertensive drugs. The reasons for the difference are that in Tassin the patients are on very low sodium diet (<5 g/day) and in Tassin extracellular volume (ECV) is reduced as far as possible independent of residual renal function. The concept of our center was to preserve residual renal function and accept slightly higher ECV and few antihypertensive drugs. Another concept to intensify HD is short daily HD (6 times/week for 90–180 min). This form of dialysis is offered as in-center and home HD with and without dialysis partner. All studies demonstrated significant improvement of nutritional status, quality of life, control of blood pressure, phosphate and anemia. Survival of AV fistula even with daily double punctures was excellent. The most extensive form of dialysis is slow daily nocturnal dialysis (6 times/week for 8–10 h). This form of dialysis provides excellent urea, phosphate clearance and fourfold increase of β<sub>2</sub>-microglobulin clearance. Patients discontinue phosphate binders and several patients need phosphate addition to dialysis. Blood pressure control is excellent, all patients are off antihypertensive drugs. Improvement of nutrition, anemia, blood pressure and quality of life is even more pronounced compared to short daily HD or 3 times weekly 8-hour HD. Nocturnal dialysis was able to improve sleep apnea. Nocturnal dialysis is offered only as home HD with and without dialysis partner. Any patient who could be trained for home HD was eligible. Presence of co-morbidities was not a contraindication.

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          Most cited references 5

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          Improvement of sleep apnea in patients with chronic renal failure who undergo nocturnal hemodialysis.

          Sleep apnea is common in patients with chronic renal failure and is not improved by either conventional hemodialysis or peritoneal dialysis. With nocturnal hemodialysis, patients undergo hemodialysis seven nights per week at home while sleeping. We hypothesized that nocturnal hemodialysis would correct sleep apnea in patients with chronic renal failure because of its greater effectiveness. Fourteen patients who were undergoing conventional hemodialysis for four hours on each of three days per week underwent overnight polysomnography. The patients were then switched to nocturnal hemodialysis for eight hours during each of six or seven nights a week. They underwent polysomnography again 6 to 15 months later on one night when they were undergoing nocturnal hemodialysis and on another night when they were not. The mean (+/-SD) serum creatinine concentration was significantly lower during the period when the patients were undergoing nocturnal hemodialysis than during the period when they were undergoing conventional hemodialysis (3.9+/-1.1 vs. 12.8+/-3.2 mg per deciliter [342+/-101 vs. 1131+/-287 micromol per liter], P<0.001). The conversion from conventional hemodialysis to nocturnal hemodialysis was associated with a reduction in the frequency of apnea and hypopnea from 25+/-25 to 8+/-8 episodes per hour of sleep (P=0.03). This reduction occurred predominantly in seven patients with sleep apnea, in whom the frequency of episodes fell from 46+/-19 to 9+/-9 per hour (P= 0.006), accompanied by increases in the minimal oxygen saturation (from 89.2+/-1.8 to 94.1+/-1.6 percent, P=0.005), transcutaneous partial pressure of carbon dioxide (from 38.5+/-4.3 to 48.3+/-4.9 mm Hg, P=0.006), and serum bicarbonate concentration (from 23.2+/-1.8 to 27.8+/-0.8 mmol per liter, P<0.001). During the period when these seven patients were undergoing nocturnal hemodialysis, the apnea-hypopnea index measured on nights when they were not undergoing nocturnal hemodialysis was greater than that on nights when they were undergoing nocturnal hemodialysis, but it still remained lower than it had been during the period when they were undergoing conventional hemodialysis (P=0.05). Nocturnal hemodialysis corrects sleep apnea associated with chronic renal failure.
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            Control of serum phosphate without any phosphate binders in patients treated with nocturnal hemodialysis.

            We compared the efficacy and the long-term effects of nocturnal hemodialysis (NHD) versus conventional hemodialysis (CHD) in controlling serum phosphate levels in patients with end-stage renal disease (ESRD). Patients underwent thrice weekly CHD and were subsequently switched to NHD six nights weekly. In the "acute" study serum and dialysate phosphate were measured during and after dialysis, and the total dialysate was collected to calculate mass solute removal. Although pre-dialysis (1.7 +/- 0.6 vs. 1.5 +/- 0.8 mM) serum phosphate levels were similar in CHD and NHD, respectively, post-dialysis levels were slightly lower with CHD (0.7 +/- 0.2 vs. 0.8 +/- 0.2 mM, P < 0.05). The measured phosphate removed per session of CHD or NHD was comparable, 25.3 +/- 7.5 versus 26.9 +/- 9.8 mumol/session, respectively. On the other hand, the cumulative weekly phosphate removal was significantly higher with NHD as compared to CHD, 75.8 +/- 22.5 versus 161.6 +/- 59.0 mumol/week (P < 0.01). In the "chronic" study serum phosphate levels were measured monthly for five months on CHD and for five months after the patients were switched to NHD. Dietary phosphate intake and the dosage of phosphate binders were tabulated. Serum phosphate levels fell during NHD: 2.1 +/- 0.5 mM at the beginning of the study and 1.3 +/- 0.2 mM five months after being switched to NHD (P < 0.001). At the same time dietary phosphate intake increased by 50%. By the fourth month of NHD therapy none of the patients was taking any phosphate binders. In conclusion, NHD is more effective in controlling serum phosphate levels than CHD, allowing patients to discontinue their phosphate binders completely and to ingest a more liberal diet.
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              Behavior of non-protein-bound and protein-bound uremic solutes during daily hemodialysis.

              In the last few years, renewed interest in daily short hemodialysis (DHD; six 2-hour sessions per week) has become apparent as a consequence of the better clinical outcome of patients treated by this schedule. Uremic syndrome is characterized by the retention of a large number of toxins with different molecular masses and chemical properties. Some toxins are water soluble and non-protein bound, whereas others are partially lipophilic and protein bound. There is increased evidence that protein-bound toxins are responsible for the biochemical and functional alterations present in uremic syndrome, and the kinetics of urea is not applicable to these substances for their removal. The aim of this study is to investigate whether DHD is accompanied by increased removal of non-protein-bound and protein-bound toxins and a decrease in their prehemodialysis (pre-HD) serum levels. We studied 14 patients with end-stage renal disease treated by standard HD (SHD; three 4-hour sessions per week) for at least 6 months and randomly assigned them to a two-period crossover study (SHD to DHD and DHD to SHD). Patients maintained the same dialyzer, dialysate, and Kt/V during the entire study. At the end of 6 months of SHD and 6 months of DHD, we evaluated hemoglobin levels, hematocrits, recombinant human erythropoietin doses, and pre-HD and post-HD concentrations of serum urea, creatinine, uric acid, and the following protein-bound toxins: 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid, p-cresol, indole-3-acetic acid, indoxyl sulfate, and hippuric acid. Values for hemoglobin, hematocrit, and recombinant human erythropoietin dose did not change during the two study periods. Pre-HD concentrations of creatinine, urea, and uric acid decreased on DHD (creatinine, from 8.7 +/- 1.9 to 7.8 +/- 1.6 mg/dL; P < 0.05; urea, from 149.4 +/- 28.8 to 132.7 +/- 40 mg/dL; P = 0.05; uric acid, from 9.14 +/- 1.49 to 8.16 +/- 1.98 mg/dL; P = 0.06). Concerning protein-bound toxins, lower pre-HD levels during DHD were reported for indole-3-acetic acid (SHD, 0.16 +/- 0.04 mg/dL; DHD, 0.13 +/- 0.03 mg/dL; P = 0.01), indoxyl sulfate (SHD, 3.35 +/- 1.68 mg/dL; DHD, 2.85 +/- 1.08 mg/dL; P = 0.02), and p-cresol at the borderline of significance (SHD, 0.96 +/- 0.59 mg/dL; DHD, 0.78 +/- 0.33 mg/dL; P = 0.07). Such non-protein-bound compounds as uric acid, creatinine, and urea were removed significantly better by DHD, and pre-HD serum levels were reduced. Furthermore, pre-HD concentrations of some protein-bound solutes, such as indole-3-acetic acid, indoxyl sulfate, and p-cresol, also were lower during DHD. Copyright 2002 by the National Kidney Foundation, Inc.
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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                978-3-8055-7600-0
                978-3-318-00991-0
                1420-4096
                1423-0143
                2003
                2003
                05 June 2003
                : 26
                : 2
                : 90-95
                Affiliations
                Department of Nephrology, St. Elisabeth Hospital, Straubing, Germany
                Article
                70989 Kidney Blood Press Res 2003;26:90–95
                10.1159/000070989
                12771532
                © 2003 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 2, References: 28, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/70989
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