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      Fluid Intake and Vasopressin: Connecting the Dots

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          In the last decade, cross-sectional and multiple cohort studies have associated total fluid intake or water intake with the risk for chronic kidney disease (CKD) and even the risk of developing hyperglycemia. Urine biomarkers have also been linked to the risk of CKD and lithiasis, and these biomarkers respond quickly to variations in fluid intake. High circulating copeptin levels, a surrogate marker of arginine vasopressin, have been associated with metabolic syndrome, renal dysfunction and increased risk for diabetes mellitus, cardiovascular disease and death. The aim of this paper was to explore how the various findings on water intake, hydration and health are interconnected, to highlight current gaps in our understanding and to propose a model that links water intake, homeostatic mechanisms to maintain water balance and health outcomes. Since plasma copeptin and vasopressin have been demonstrated to be sensitive to changes in water intake, inversely associated with 24-hour urine volume, and associated with urine biomarkers and fluid intake, vasopressin is proposed as the central player in this theoretical physiological model.

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          Most cited references 11

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          Fluid and nutrient intake and risk of chronic kidney disease.

          We evaluated the association between fluid and nutrient intake and chronic kidney disease (CKD). Two cross-sectional population-based studies. Validated nutrition food frequency questionnaires (FFQ) administered to people >50 years, identified in a door-to-door census of a well-defined suburban area. Based upon nutrition tables we calculated intakes of over 40 nutrients (factors) and total daily energy intake. Primary outcome was CKD. Fluid (total content of fluid and drinks assessed in the FFQ) and nutrient intake was stratified in quintiles and association with CKD analysed by logistic regression, expressed as unadjusted and adjusted odds ratios, with testing for linear trend. The proportion of participants who completed the FFQ and had glomerular filtration rate (GFR) measures was 2744/3654 (75.0%) for the first and 2476/3508 (70.6%) for the second survey. CKD was present in 12.4-23.5% men and 14.9-28.7% women (mean ages 66.4-65.4 years), respectively. Participants who had the highest quintile of fluid intake (3.2 L/day) had a significantly lower risk of CKD (odds ratio 0.5, 95%CI 0.32 to 0.77, P for trend = 0.003). These findings were consistent across both study periods, both equations to calculate GFR and both GFR thresholds. Higher intakes of fluid appear to protect against CKD. CKD may be preventable at a population level with low-cost increased fluid intake. © 2011 The Authors. Nephrology © 2011 Asian Pacific Society of Nephrology.
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            Is Open Access

            Hydration biomarkers in free-living adults with different levels of habitual fluid consumption

            Little is known about the impact of habitual fluid intake on physiology. Specifically, biomarkers of hydration status and body water regulation have not been adequately explored in adults who consume different fluid volumes in everyday conditions, without prolonged exercise or environmental exposure. The purpose of the present study was to compare adults with habitually different fluid intakes with respect to biomarkers implicated in the assessment of hydration status, the regulation of total body water and the risk of kidney pathologies. In the present cross-sectional study, seventy-one adults (thirty-two men, thirty-nine women, age 25–40 years) were classified according to daily fluid intake: thirty-nine low drinkers (LD; ≤ 1·2 litres/d) and thirty-two high drinkers (HD; 2–4 litres/d). During four consecutive days, urinary parameters (first morning urine (FMU) on day 1 and subsequent 24 h urine (24hU) collections), blood parameters, and food and beverage intake were assessed. ANOVA and non-parametric comparisons revealed significant differences between the LD and HD groups in 24hU volume (1·0 (se 0·1) v. 2·4 (se 0·1) litres), specific gravity (median 1·023 v. 1·010), osmolality (767 (se 27) v. 371 (se 33) mOsm/kg) and colour (3·1 (se 0·2) v. 1·8 (se 0·2)). Similarly, in the FMU, the LD group produced a smaller amount of more concentrated urine. Plasma cortisol, creatinine and arginine vasopressin concentrations were significantly higher among the LD. Plasma osmolality was similar between the groups, suggesting physiological adaptations to preserve plasma osmolality despite low fluid intake. The long-term impact of adaptations to preserve plasma osmolality must be examined, particularly in the context of renal health.
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              Disorders of body water homeostasis.

              Disorders of body fluids are among the most commonly encountered problems in the practice of clinical medicine. This is in large part because many different disease states can potentially disrupt the finely balanced mechanisms that control the intake and output of water and solute. It therefore behoves clinicians treating such patients to have a good understanding of the pathophysiology, the differential diagnosis and the management of these disorders. Because body water is the primary determinant of the osmolality of the extracellular fluid, disorders of body water homeostasis can be divided into hypo-osmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The classical hyperosmolar disorder is diabetes insipidus (DI), and the classical hypo-osmolar disorder is the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This chapter first reviews the regulatory mechanisms underlying water and sodium metabolism, the two major determinants of body fluid homeostasis. The major disorders of water metabolism causing hyperosmolality and hypo-osmolality, DI and SIADH, are then discussed in detail, including the pathogenesis, differential diagnosis and treatment of these disorders.

                Author and article information

                Ann Nutr Metab
                Annals of Nutrition and Metabolism
                Ann Nutr Metab
                S. Karger AG (Basel, Switzerland karger@ 123456karger.com http://www.karger.com )
                June 2016
                16 June 2016
                : 68
                : 2
                : 6-11
                Hydration and Health Department, Danone Research, Palaiseau, France
                ANM2016068S02006 Ann Nutr Metab 2016;68(suppl 2):6-11
                © 2016 The Author(s) Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND). Usage and distribution for commercial purposes as well as any distribution of modified material requires written permission. 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
                Figures: 2, References: 30, Pages: 6


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