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      Sarcopenia: A Major Challenge in Elderly Patients with End-Stage Renal Disease

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      Journal of Aging Research
      Hindawi Publishing Corporation

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          Abstract

          Sarcopenia is a condition of multifaceted etiology arising in many elderly people. In patients with chronic kidney, the loss of muscle mass is much more intensive and the first signs of sarcopenia are observed in younger patients than it is expected. It is associated with the whole-body protein-energy deficiency called protein-energy wasting (PEW). It seems to be one of the major factors limiting patient's autonomy as well as decreasing the quality of life. If it cannot be treated with the simple methods requiring some knowledge and devotion, we will fail to save patients who die due to cardiovascular disease and infection, despite proper conduction of renal replacement therapy. Many factors influencing the risk of sarcopenia development have been evaluated in number of studies. Many studies also were conducted to assess the efficacy of different therapeutic strategies (diet, physical activity, hormones). Nevertheless, there is still no consensus on treatment the patients with PEW. Therefore, in the paper we present the reasons and pathophysiology of sarcopenia as an important element of protein energy wasting (PEW) in elderly patients suffering from chronic kidney disease. We also analyze possible options for treatment according to up-to-date knowledge.

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          Most cited references137

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          Malnutrition-inflammation complex syndrome in dialysis patients: causes and consequences.

          Protein-energy malnutrition (PEM) and inflammation are common and usually concurrent in maintenance dialysis patients. Many factors that appear to lead to these 2 conditions overlap, as do assessment tools and such criteria for detecting them as hypoalbuminemia. Both these conditions are related to poor dialysis outcome. Low appetite and a hypercatabolic state are among common features. PEM in dialysis patients has been suggested to be secondary to inflammation; however, the evidence is not conclusive, and an equicausal status or even opposite causal direction is possible. Hence, malnutrition-inflammation complex syndrome (MICS) is an appropriate term. Possible causes of MICS include comorbid illnesses, oxidative and carbonyl stress, nutrient loss through dialysis, anorexia and low nutrient intake, uremic toxins, decreased clearance of inflammatory cytokines, volume overload, and dialysis-related factors. MICS is believed to be the main cause of erythropoietin hyporesponsiveness, high rate of cardiovascular atherosclerotic disease, decreased quality of life, and increased mortality and hospitalization in dialysis patients. Because MICS leads to a low body mass index, hypocholesterolemia, hypocreatininemia, and hypohomocysteinemia, a "reverse epidemiology" of cardiovascular risks can occur in dialysis patients. Therefore, obesity, hypercholesterolemia, and increased blood levels of creatinine and homocysteine appear to be protective and paradoxically associated with a better outcome. There is no consensus about how to determine the degree of severity of MICS or how to manage it. Several diagnostic tools and treatment modalities are discussed. Successful management of MICS may ameliorate the cardiovascular epidemic and poor outcome in dialysis patients. Clinical trials focusing on MICS and its possible causes and consequences are urgently required to improve poor clinical outcome in dialysis patients.
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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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              A role for brown adipose tissue in diet-induced thermogenesis.

              Measurement of energy balance during voluntary overeating in rats unequivocally establishes the quantitative importance of diet-induced thermogenesis in energy balance. Like cold-induced thermogenesis, this form of heat production involves changes in the activity of the sympathetic nervous system and brown adipose tissue which suggest that this tissue may determine metabolic efficiency and resistance to obesity.
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                Author and article information

                Journal
                J Aging Res
                J Aging Res
                JAR
                Journal of Aging Research
                Hindawi Publishing Corporation
                2090-2204
                2090-2212
                2012
                28 March 2012
                : 2012
                : 754739
                Affiliations
                Department of Nephrology, Transplantation and Internal Medicine, Pomeranian Medical University, 70-111 Szczecin, Poland
                Author notes

                Academic Editor: Stéphane Michel Schneider

                Article
                10.1155/2012/754739
                3321443
                22536505
                56668c22-9de6-4c2a-bb05-211a972aa807
                Copyright © 2012 M. Domański and K. Ciechanowski.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 1 August 2011
                : 22 November 2011
                : 30 December 2011
                Categories
                Review Article

                Molecular medicine
                Molecular medicine

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