26
views
0
recommends
+1 Recommend
2 collections
    0
    shares

      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

      Submit here before July 31, 2024

      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found

      Dietary Acid Load and Incident Chronic Kidney Disease: Results from the ARIC Study

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background: Higher dietary acid load can result in metabolic acidosis and is associated with faster kidney disease progression in patients with chronic kidney disease (CKD). However, the relationship between dietary acid load and incident CKD has not been evaluated. Methods: We conducted prospective analyses of the Atherosclerosis Risk in Communities study participants without CKD at baseline (1987-1989, n = 15,055). Dietary acid load was estimated using the equation for potential renal acid load by Remer and Manz, incorporating dietary intake data from a food frequency questionnaire. Incident CKD was assessed from baseline through 2010 and defined as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m 2 accompanied by 25% eGFR decline, CKD-related hospitalization or death or end-stage renal disease identified by linkage to the US Renal Data System registry. Results: In the overall study population, 55% were female, 26% were African-American and mean age at baseline was 54 years. During a median follow-up of 21 years, there were 2,351 (15.6%) incident CKD cases. After adjusting for demographics (age, sex, race-center), established risk factors (diabetes status, hypertension status, overweight/obese status, smoking status, education level, physical activity), caloric intake and baseline eGFR, higher dietary acid load were associated with higher risk of incident CKD (hazard ratio [HR] for quartile 4 vs. 1: 1.13, 95% CI 1.01-1.28, p for trend = 0.02; HR per interquartile range increase: 1.06, 95% CI 1.00-1.11, p = 0.04). Conclusion: Dietary acid load is associated with incident CKD in a population-based sample. These data suggest a potential avenue for CKD risk reduction through diet.

          Related collections

          Most cited references13

          • Record: found
          • Abstract: found
          • Article: not found

          A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate.

          Current guidelines recommend Na(+)-based alkali for CKD with metabolic acidosis and plasma total CO2 (PTCO2) < 22 mM. Because diets in industrialized societies are typically acid-producing, we compared base-producing fruits and vegetables with oral NaHCO3 (HCO3) regarding the primary outcome of follow-up estimated GFR (eGFR) and secondary outcomes of improved metabolic acidosis and reduced urine indices of kidney injury. Individuals with stage 4 (eGFR, 15-29 ml/min per 1.73 m(2)) CKD due to hypertensive nephropathy, had a PTCO2 level < 22 mM, and were receiving angiotensin-converting enzyme inhibition were randomly assigned to 1 year of daily oral NaHCO3 at 1.0 mEq/kg per day (n=35) or fruits and vegetables dosed to reduce dietary acid by half (n=36). Plasma cystatin C-calculated eGFR did not differ at baseline and 1 year between groups. One-year PTCO2 was higher than baseline in the HCO3 group (21.2±1.3 versus 19.5±1.5 mM; P<0.01) and the fruits and vegetables group (19.9±1.7 versus 19.3±1.9 mM; P<0.01), consistent with improved metabolic acidosis, and was higher in the HCO3 than the fruits and vegetable group (P<0.001). One-year urine indices of kidney injury were lower than baseline in both groups. Plasma [K(+)] did not increase in either group. One year of fruits and vegetables or NaHCO3 in individuals with stage 4 CKD yielded eGFR that was not different, was associated with higher-than-baseline PTCO2, and was associated with lower-than-baseline urine indices of kidney injury. The data indicate that fruits and vegetables improve metabolic acidosis and reduce kidney injury in stage 4 CKD without producing hyperkalemia.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Bias in dietary-report instruments and its implications for nutritional epidemiology.

            To evaluate measurement error structure in dietary assessment instruments and to investigate its implications for nutritional studies, using urinary nitrogen excretion as a reference biomarker for protein intake. The dietary assessment methods included different food-frequency questionnaires (FFQs) and such conventional dietary-report reference instruments as a series of 24-hour recalls, 4-day weighed food records or 7-day diaries. Six original pilot validation studies within the European Prospective Investigation of Cancer (EPIC), and two validation studies conducted by the British Medical Research Council (MRC) within the Norfolk cohort that later joined as a collaborative component cohort of EPIC. A sample of approximately 100 to 200 women and men, aged 35-74 years, from each of eight validation studies. In assessing protein intake, all conventional dietary-report reference methods violated the critical requirements for a valid reference instrument for evaluating, and adjusting for, dietary measurement error in an FFQ. They displayed systematic bias that depended partly on true intake and partly was person-specific, correlated with person-specific bias in the FFQ. Using the dietary-report methods as reference instruments produced substantial overestimation (up to 230%) of the FFQ correlation with true usual intake and serious underestimation (up to 240%) of the degree of attenuation of FFQ-based log relative risks. The impact of measurement error in dietary assessment instruments on the design, analysis and interpretation of nutritional studies may be much greater than has been previously estimated, at least regarding protein intake.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The role of renin-angiotensin-aldosterone system in the progression of chronic kidney disease.

              The renin-angiotensin-aldosterone system (RAAS) is a well known regulator of blood pressure (BP) and determinant of target-organ damage. It controls fluid and electrolyte balance through coordinated effects on the heart, blood vessels, and Kidneys. Angiotensin II (AII) is the main effector of the RAAS and exerts its vasoconstrictor effect predominantly on the postglomerular arterioles, thereby increasing the glomerular hydraulic pressure and the ultrafiltration of plasma proteins, effects that may contribute to the onset and progression of chronic renal damage. AII may also directly contribute to accelerate renal damage by sustaining cell growth, inflammation, and fibrosis. Interventions that inhibit the activity of the RAAS are renoprotective and may slow or even halt the progression of chronic nephropathies. ACE inhibitors and angiotensin II receptor antagonists can be used in combination to maximize RAAS inhibition and more effectively reduce proteinuria and GFR decline in diabetic and nondiabetic renal disease. Recent evidence suggests that add-on therapy with an aldosterone antagonist may further increase renoprotection, but may also enhance the risk hyperkalemia. Maximized RAAS inhibition, combined with intensified blood pressure control (and metabolic control in diabetics) and amelioration of dyslipidemia in a multimodal approach including lifestyle modifications (Remission Clinic), may achieve remission of proteinuria and renal function stabilization in a substantial proportion of patients with proteinuric renal disease. Ongoing studies will tell whether novel drugs inhibiting the RAAS, such as the renin inhibitors or the vasopeptidase inhibitors, may offer additional benefits to those who do not respond, or only partially respond, to this multimodal regimen.
                Bookmark

                Author and article information

                Journal
                AJN
                Am J Nephrol
                10.1159/issn.0250-8095
                American Journal of Nephrology
                Am J Nephrol
                S. Karger AG (Basel, Switzerland karger@ 123456karger.com http://www.karger.com )
                0250-8095
                1421-9670
                February 2016
                21 January 2016
                : 42
                : 6
                : 427-435
                Affiliations
                aWelch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University, bDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, cDivision of General Internal Medicine, Department of Medicine, Johns Hopkins School of Medicine, and dDivision of Nephrology, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Md., eDivision of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, Minn., and fDivision of Preventive Medicine, Department of Family Medicine and Public Health, University of California San Diego School of Medicine, San Diego, Calif., USA
                Article
                AJN2015042006427 PMC4733508 Am J Nephrol 2015;42:427-435
                10.1159/000443746
                PMC4733508
                26789417
                6055e6a3-12ff-4acc-82bb-249c87169ded
                © 2016 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 or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center. 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 September 2015
                : 10 December 2015
                Page count
                Figures: 2, Tables: 2, References: 42, Pages: 9
                Categories
                Original Report: Patient-Oriented, Translational Research

                Medicine,General social science
                Chronic kidney disease,Diet,Magnesium,Vegetable protein
                Medicine, General social science
                Chronic kidney disease, Diet, Magnesium, Vegetable protein

                Comments

                Comment on this article