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      Association between Serum Uric Acid Levels, Nutritional and Antioxidant Status in Patients on Hemodialysis

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          Abstract

          Purpose: To determine the relationship between uric acid (UA) and nutritional and antioxidant status in hemodialysis (HD) patients, given that hyperuricemia could be an indicator of good nutritional status possibly because of the antioxidant properties of UA. Methods: Cross-sectional study with 93 patients on HD. Hyperuricemia was considered as UA ≥6.0 mg/dL in females and ≥7.0 mg/dL in males. Nutritional variables were registered. Blood samples were taken before the dialysis session to determine oxidative damage as plasma malondialdehyde (MDA) content, and antioxidant capacity measuring 2,2-diphenyl-piclrylhidrazil radical (DPPH ) scavenging activity and oxygen radical absorbance capacity (ORAC) value. Results: Patients with hyperuricemia had higher creatinine (11.9 vs. 10.5 mg/dL; p = 0.004), potassium (5.5 vs. 5.0 mg/dL; p = 0.014) levels; phase angle (5.8 vs. 4.9; p = 0.005), protein consumption (normalized protein nitrogen appearance, nPNA, 1.03 vs. 0.83; p = 0.013) than normouricemic patients. DPPH scavenging activity was higher in hyperuricemic subjects (1.139 vs. 1.049 mM Trolox equivalents; p = 0.007); likewise, hyperuricemic subjects had less oxidant damage measured by MDA (10.6 vs. 12.7 nmol/mL; p = 0.020). Subjects with normouricemia were at higher risk of having a reactance to height (Xc/H) ratio less than 35 (OR 2.79; 95% CI, 1.1–7.017, p = 0.028); nPNA < 1.0 (OR 3.78; 95% CI, 1.4–10.2, p = 0.007), diagnosis of cachexia (OR 2.95; 95% CI, 1156–7.518, p = 0.021), potassium levels <5 (OR 2.97; 95% CI, 1.136–7.772, p = 0.023) and PA < 5.5° (OR 3.38; 95% CI, 1.309–8.749, p = 0.012.) Conclusions: Patients with hyperuricemia had higher antioxidant capacity and better nutritional status. Purines and protein restrictions in HD patients with hyperuricemia need to be reviewed individually for each patient. More studies are needed to stablish a cut point of UA levels in renal population.

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          Global, regional, and national burden of chronic kidney disease, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017

          Summary Background Health system planning requires careful assessment of chronic kidney disease (CKD) epidemiology, but data for morbidity and mortality of this disease are scarce or non-existent in many countries. We estimated the global, regional, and national burden of CKD, as well as the burden of cardiovascular disease and gout attributable to impaired kidney function, for the Global Burden of Diseases, Injuries, and Risk Factors Study 2017. We use the term CKD to refer to the morbidity and mortality that can be directly attributed to all stages of CKD, and we use the term impaired kidney function to refer to the additional risk of CKD from cardiovascular disease and gout. Methods The main data sources we used were published literature, vital registration systems, end-stage kidney disease registries, and household surveys. Estimates of CKD burden were produced using a Cause of Death Ensemble model and a Bayesian meta-regression analytical tool, and included incidence, prevalence, years lived with disability, mortality, years of life lost, and disability-adjusted life-years (DALYs). A comparative risk assessment approach was used to estimate the proportion of cardiovascular diseases and gout burden attributable to impaired kidney function. Findings Globally, in 2017, 1·2 million (95% uncertainty interval [UI] 1·2 to 1·3) people died from CKD. The global all-age mortality rate from CKD increased 41·5% (95% UI 35·2 to 46·5) between 1990 and 2017, although there was no significant change in the age-standardised mortality rate (2·8%, −1·5 to 6·3). In 2017, 697·5 million (95% UI 649·2 to 752·0) cases of all-stage CKD were recorded, for a global prevalence of 9·1% (8·5 to 9·8). The global all-age prevalence of CKD increased 29·3% (95% UI 26·4 to 32·6) since 1990, whereas the age-standardised prevalence remained stable (1·2%, −1·1 to 3·5). CKD resulted in 35·8 million (95% UI 33·7 to 38·0) DALYs in 2017, with diabetic nephropathy accounting for almost a third of DALYs. Most of the burden of CKD was concentrated in the three lowest quintiles of Socio-demographic Index (SDI). In several regions, particularly Oceania, sub-Saharan Africa, and Latin America, the burden of CKD was much higher than expected for the level of development, whereas the disease burden in western, eastern, and central sub-Saharan Africa, east Asia, south Asia, central and eastern Europe, Australasia, and western Europe was lower than expected. 1·4 million (95% UI 1·2 to 1·6) cardiovascular disease-related deaths and 25·3 million (22·2 to 28·9) cardiovascular disease DALYs were attributable to impaired kidney function. Interpretation Kidney disease has a major effect on global health, both as a direct cause of global morbidity and mortality and as an important risk factor for cardiovascular disease. CKD is largely preventable and treatable and deserves greater attention in global health policy decision making, particularly in locations with low and middle SDI. Funding Bill & Melinda Gates Foundation.
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            A proposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease.

            The recent research findings concerning syndromes of muscle wasting, malnutrition, and inflammation in individuals with chronic kidney disease (CKD) or acute kidney injury (AKI) have led to a need for new terminology. To address this need, the International Society of Renal Nutrition and Metabolism (ISRNM) convened an expert panel to review and develop standard terminologies and definitions related to wasting, cachexia, malnutrition, and inflammation in CKD and AKI. The ISRNM expert panel recommends the term 'protein-energy wasting' for loss of body protein mass and fuel reserves. 'Kidney disease wasting' refers to the occurrence of protein-energy wasting in CKD or AKI regardless of the cause. Cachexia is a severe form of protein-energy wasting that occurs infrequently in kidney disease. Protein-energy wasting is diagnosed if three characteristics are present (low serum levels of albumin, transthyretin, or cholesterol), reduced body mass (low or reduced body or fat mass or weight loss with reduced intake of protein and energy), and reduced muscle mass (muscle wasting or sarcopenia, reduced mid-arm muscle circumference). The kidney disease wasting is divided into two main categories of CKD- and AKI-associated protein-energy wasting. Measures of chronic inflammation or other developing tests can be useful clues for the existence of protein-energy wasting but do not define protein-energy wasting. Clinical staging and potential treatment strategies for protein-energy wasting are to be developed in the future.
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              High-throughput assay of oxygen radical absorbance capacity (ORAC) using a multichannel liquid handling system coupled with a microplate fluorescence reader in 96-well format.

              The oxygen radical absorbance capacity (ORAC) assay has been widely accepted as a standard tool to measure the antioxidant activity in the nutraceutical, pharmaceutical, and food industries. However, the ORAC assay has been criticized for a lack of accessibility due to the unavailability of the COBAS FARA II analyzer, an instrument discontinued by the manufacturer. In addition, the manual sample preparation is time-consuming and labor-intensive. The objective of this study was to develop a high-throughput instrument platform that can fully automate the ORAC assay procedure. The new instrument platform consists of a robotic eight-channel liquid handling system and a microplate fluorescence reader. By using the high-throughput platform, the efficiency of the assay is improved with at least a 10-fold increase in sample throughput over the current procedure. The mean of intra- and interday CVs was
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                27 August 2020
                September 2020
                : 12
                : 9
                Affiliations
                [1 ]Department of Nephrology and Mineral Metabolism, Instituto Nacional de Ciencias Médicas y Nutricion Salvador Zubirán, México City PC 14080, Mexico; etna.lucero@ 123456gmail.com (E.D.-Z.); analaura.9403@ 123456gmail.com (A.L.L.-S.); cristino.cruzr@ 123456incmnsz.mx (C.C.-R.)
                [2 ]Medicine Faculty, Universidad Nacional Autónoma de México, México City ZC 04510, Mexico
                [3 ]Chemistry Faculty, Universidad Nacional Autónoma de México, México City ZC 04510, Mexico; pedraza@ 123456unam.mx (J.P.-C.); omarnoelmedina@ 123456gmail.com (O.N.M.-C.)
                [4 ]Centro de Atención Renal, Estado de México ZC 53100, Mexico; francisco.bueno@ 123456hemocare.com.mx
                Author notes
                [* ]Correspondence: angeles.espinosac@ 123456incmnsz.mx ; Tel./Fax: +52-5655-0382
                Article
                nutrients-12-02600
                10.3390/nu12092600
                7551179
                32867018
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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