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      Biocompatible Peritoneal Dialysis Solution Preserves Residual Renal Function

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          Abstract

          Background/Aims: The long-term effects of biocompatible peritoneal dialysis (PD) solution on residual renal function (RRF), inflammation, adipokines and metabolic acidosis are controversial. We evaluated the effects of biocompatible PD solution in continuous ambulatory PD (CAPD) patients for an additional 12-month period. Method: Among 91 incident patients who started CAPD with either biocompatible PD solution (Balance®, Fresenius; LS, n = 48) or conventional PD solution (CAPD/DPCA®, Fresenius; CS, n = 43), 63 patients, who were followed for 12 months, were enrolled and followed for an additional 12 months. Results: After 24 months of treatment, the glomerular filtration rate (GFR) of the LS group was twofold higher compared to the CS group (33.5 ± 30.7 vs. 16.3 ± 17.9 l/week/1.73 m<sup>2</sup>, respectively, p = 0.021). In a subgroup of patients with an initial GFR >2 ml/min/1.73 m<sup>2</sup>, the GFR of the LS group was significantly higher than the rate of the CS group after 24 months (43.7 ± 30.5 vs. 18.6 ± 19.0 l/week/1.73 m<sup>2</sup>, respectively, p = 0.042). Over a 24-month period, effluent cancer antigen-125 levels were significantly increased in the LS group compared to the CS group, while effluent interleukin-6 levels did not differ between the two groups. The serum tCO<sub>2</sub> levels were consistently higher in the LS group compared to the CS group. Conclusions: We found that the effect of LS on preserving RRF may be maintained over a 24-month treatment period in CAPD patients, and LS use may have other benefits, such as the correction of metabolic acidosis.

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          Most cited references29

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          Bicarbonate supplementation slows progression of CKD and improves nutritional status.

          Bicarbonate supplementation preserves renal function in experimental chronic kidney disease (CKD), but whether the same benefit occurs in humans is unknown. Here, we randomly assigned 134 adult patients with CKD (creatinine clearance [CrCl] 15 to 30 ml/min per 1.73 m(2)) and serum bicarbonate 16 to 20 mmol/L to either supplementation with oral sodium bicarbonate or standard care for 2 yr. The primary end points were rate of CrCl decline, the proportion of patients with rapid decline of CrCl (>3 ml/min per 1.73 m(2)/yr), and ESRD (CrCl <10 ml/min). Secondary end points were dietary protein intake, normalized protein nitrogen appearance, serum albumin, and mid-arm muscle circumference. Compared with the control group, decline in CrCl was slower with bicarbonate supplementation (5.93 versus 1.88 ml/min 1.73 m(2); P < 0.0001). Patients supplemented with bicarbonate were significantly less likely to experience rapid progression (9 versus 45%; relative risk 0.15; 95% confidence interval 0.06 to 0.40; P < 0.0001). Similarly, fewer patients supplemented with bicarbonate developed ESRD (6.5 versus 33%; relative risk 0.13; 95% confidence interval 0.04 to 0.40; P < 0.001). Nutritional parameters improved significantly with bicarbonate supplementation, which was well tolerated. This study demonstrates that bicarbonate supplementation slows the rate of progression of renal failure to ESRD and improves nutritional status among patients with CKD.
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            Daily oral sodium bicarbonate preserves glomerular filtration rate by slowing its decline in early hypertensive nephropathy.

            In most patients with hypertensive nephropathy and low glomerular filtration rate (GFR), the kidney function progressively declines despite the adequate control of the hypertension with angiotensin-converting enzyme inhibition. Previously we found that 2 years of oral sodium citrate slowed GFR decline in patients whose estimated GFR (eGFR) was very low (mean 33 ml/min). This treatment also slowed GFR decline in an animal model of surgically reduced nephron mass. Here, we tested if daily oral sodium bicarbonate slowed GFR decline in patients with hypertensive nephropathy with reduced but relatively preserved eGFR (mean 75 ml/min) in a 5-year, prospective, randomized, placebo-controlled, and blinded interventional study. Patients matched for age, ethnicity, albuminuria, and eGFR received daily placebo or equimolar sodium chloride or bicarbonate while maintaining antihypertensive regimens (including angiotensin-converting enzyme inhibition) aiming for their recommended blood pressure targets. After 5 years, the rate of eGFR decline, estimated using plasma cystatin C, was slower and eGFR was higher in patients given sodium bicarbonate than in those given placebo or sodium chloride. Thus, our study shows that in hypertensive nephropathy, daily sodium bicarbonate is an effective kidney protective adjunct to blood pressure control along with angiotensin-converting enzyme inhibition.
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              Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR.

              Metabolic acidosis often accompanies low glomerular filtration rate and induces secretion of endothelin, which in turn might mediate kidney injury. Here we tested whether treatment of metabolic acidosis in patients with low glomerular filtration rate reduced the progression of kidney disease. Fifty-nine patients with hypertensive nephropathy and metabolic acidosis had their blood pressure reduced with regimens that included angiotensin-converting enzyme inhibition. Thirty patients were then prescribed sodium citrate, and the remaining 29, unable or unwilling to take sodium citrate, served as controls. All were followed for 24 months with maintenance of their blood pressure reduction. Urine endothelin-1 excretion, a surrogate of kidney endothelin production, and N-acetyl-beta-D-glucosaminidase, a marker of kidney tubulointerstitial injury, were each significantly lower, while the rate of estimated glomerular filtration rate decline was significantly slower. The estimated glomerular filtration rate was statistically higher after 24 months of sodium citrate treatment compared to the control group. Hence it appears that sodium citrate is an effective kidney-protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition.
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                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                S. Karger AG
                0250-8095
                1421-9670
                2012
                October 2012
                22 September 2012
                : 36
                : 4
                : 305-316
                Affiliations
                aDepartment of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, bDepartment of Internal Medicine, Seoul National University College of Medicine, cTransplantation Research Institute, Seoul National University, Seoul, dDepartment of Internal Medicine and Kidney Research Institute, Hallym University College of Medicine, Chuncheon, and eDepartment of Internal Medicine, Gachon University of Medicine and Science, Incheon, Republic of Korea; fDepartment of Medicine, University of Hong Kong, Hong Kong, SAR, China
                Author notes
                *Sung Gyun Kim, MD, Department of Internal Medicine and Kidney Research Institute, Hallym University College of Medicine, 896 Pyeongchon-dong, Dongan-gu, Anyang 431-070 (Republic of Korea), E-Mail sgkim@hallym.ac.kr
                Article
                342523 Am J Nephrol 2012;36:305–316
                10.1159/000342523
                23007025
                a2ad9f26-e046-4f69-bd55-e21a00c69f81
                © 2012 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.

                History
                : 23 April 2012
                : 10 August 2012
                Page count
                Figures: 3, Tables: 3, Pages: 12
                Categories
                Original Report: Patient-Oriented, Translational Research

                Cardiovascular Medicine,Nephrology
                End-stage renal disease,Peritoneal dialysis,Glycation end products,Creatinine clearance

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