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      Malnutrition, Inflammation, Atherosclerosis Syndrome (MIA) and Diet Recommendations among End-Stage Renal Disease Patients Treated with Maintenance Hemodialysis

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          Abstract

          Malnutrition-inflammation-atherosclerosis syndrome is one of the causes of increased mortality in chronic kidney disease (CKD). The aim of the study was to assess the inflammation and nutritional status of patients in end-stage kidney disease treated with maintenance hemodialysis. The study included a group of 98 hemodialyzed patients with stage 5 CKD (38 women and 60 men). Albumin, prealbumin (PRE), and C-reactive protein (CRP) were measured in serum samples collected before mid-week dialysis. Fruit and vegetables frequency intakes were assessed with a questionnaire. CRP was above the reference limit of 5 mg/L in 53% of patients. Moreover, the Glasgow Prognostic Score (GPS) indicated the co-occurrence of inflammation and protein calorie malnutrition in 11% of patients, and the presence of either inflammation or malnutrition in 25%. The questionnaire revealed that hemodialyzed patients frequently exclude fruit and vegetables from their diets. Nearly 43% of the interviewed patients declared frequently eating vegetables, and 35% declared frequently eating fruit, a few times per week or less. The most frequently selected fruit and vegetables had a low antioxidant capacity. The strict dietary restrictions in CKD are difficult to fulfill, and if strictly followed, may lead to protein-calorie malnutrition.

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          Zinc in Infection and Inflammation

          Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps (NET) formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors of differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B (NF-κB), a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.
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            Uremic toxins originating from colonic microbial metabolism.

            Numerous molecules, which are either excreted or metabolized by the kidney, accumulate in patients with chronic kidney disease (CKD). These uremic retention molecules (URMs), contributing to the syndrome of uremia, may be classified according to their site of origin, that is, endogenous metabolism, microbial metabolism, or exogenous intake. It is increasingly recognized that bacterial metabolites, such as phenols, indoles, and amines, may contribute to uremic toxicity. In vitro studies have implicated bacterial URMs in CKD progression, cardiovascular disease, and bone and mineral disorders. Furthermore, several observational studies have demonstrated a link between serum levels of bacterial URMs and clinical outcomes. Bacterial metabolism may therefore be an important therapeutic target in CKD. There is evidence that besides reduced renal clearance, increased colonic generation and absorption explain the high levels of bacterial URMs in CKD. Factors promoting URM generation and absorption include an increased ratio of dietary protein to carbohydrate due to insufficient intake of fiber and/or reduced intestinal protein assimilation, as well as prolonged colonic transit time. Two main strategies exist to reduce bacterial URM levels: interventions that modulate intestinal bacterial growth (e.g., probiotics, prebiotics, dietary modification) and adsorbent therapies that bind bacterial URMs in the intestines to reduce their absorption (e.g., AST-120, sevelamer). The efficacy and clinical benefit of these strategies are currently an active area of interest.
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              Metabolic Acidosis of CKD: An Update.

              The kidney has the principal role in the maintenance of acid-base balance. Therefore, a decrease in renal ammonium excretion and a positive acid balance often leading to a reduction in serum bicarbonate concentration are observed in the course of chronic kidney disease (CKD). The decrease in serum bicarbonate concentration is usually absent until glomerular filtration rate decreases to  24 mEq/L might be associated with worsening of cardiovascular disease adds complexity to treatment decisions. Further study of the mechanisms through which metabolic acidosis contributes to the progression of CKD, as well as the pathways involved in mediating the benefits and complications of base therapy, is warranted.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                11 January 2018
                January 2018
                : 10
                : 1
                : 69
                Affiliations
                [1 ]Faculty of Medicine, Dietetics, Jagiellonian University Medical College, Anny St. 12, 31-008 Kraków, Poland; malgorzatamaraj@ 123456gmail.com
                [2 ]Department of Diagnostics, Jagiellonian University Medical College, Kopernika 15A St., 31-501 Kraków, Poland; mbkusnie@ 123456cyf-kr.edu.pl (B.K.-C.); k.gawlik@ 123456uj.edu.pl (K.G.); dorota.pawlica@ 123456uj.edu.pl (D.P.-G.)
                [3 ]Department of Medical Diagnostics, Faculty of Pharmacy, Jagiellonian University Medical College, Medyczna 9 St., 30-688 Kraków, Poland; paulina.dumnicka@ 123456uj.edu.pl
                [4 ]Dialysis Therapy Centre, St’ Queen Jadwiga Clinical District Hospital No. 2, Lwowska St. 60, 35-301 Rzeszów, Poland; agala.edu@ 123456gmail.com
                [5 ]Faculty of Medicine, University of Rzeszów, Kopisto Ave. 2a, 35-310 Rzeszów, Poland
                [6 ]Diagnostic Department, University Hospital in Krakow, Kopernika 15B St., 31-501 Kraków, Poland; azabek@ 123456su.krakow.pl (A.Z.-A.); mbmazur@ 123456cyf-kr.edu.pl (M.M.-L.)
                [7 ]Department of Physiology, Jagiellonian University Medical College, Grzegórzecka 16 St., 31-531 Kraków, Poland
                [8 ]Department of Nephrology, Jagiellonian University Medical College, Kopernika 15C, 31-501 Kraków, Poland; marek.kuzniewski@ 123456uj.edu.pl
                Author notes
                [* ]Correspondence: piotr.ceranowicz@ 123456uj.edu.pl ; Tel.: +48-12-619-9630
                Author information
                https://orcid.org/0000-0001-6617-0852
                https://orcid.org/0000-0003-3478-0108
                Article
                nutrients-10-00069
                10.3390/nu10010069
                5793297
                29324682
                39bea3aa-be6e-4ce4-a199-f8b22a128f44
                © 2018 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/).

                History
                : 02 December 2017
                : 09 January 2018
                Categories
                Article

                Nutrition & Dietetics
                diet,chronic kidney disease,inflammation,hemodialysis
                Nutrition & Dietetics
                diet, chronic kidney disease, inflammation, hemodialysis

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