الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
In patients with CKD, as the GFR declines, numerous nutritional and metabolic disorders develop, and PEM develops as a sequence of loss of the kidney role in energy homeostasis and regulation of nutrients metabolism and the dietary requirements for many nutrients are altered. The possible causes of PEM include inadequate nutrients intake, increased loss of nutrients, increased net catabolism and chronic inflammation associating renal failure. Manifestations of PEM in patients with CKD include: decreased food intake, low body weight, decreased total body fat percent and skinfold thickness, decreased muscle mass and arm circumference, low growth rate in children, decreased total body nitrogen, increased levels of acute phase proteins and proinflammatory cytokines, decreased levels of albumin, prealbumin, transferrin, cholesterol and plasma amino acids. Classically dietary intake, biochemical measurements, and body composition, are used to assess the protein–energy nutritional status in CKD patients but composite scores as SGA of nutrition and MIS are also utilized. More technologically based nutritional measures that have been used in CKD patients include DEXA and BIA. However, no uniform approach has been agreed upon for rating the severity of malnutrition in CKD patients.