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Malnutrition has been reported to occur in up to 50% of patients with acute and chronic renal failure [69, 70]. It is implicated as the main cause of mortality in chronic dialysis patients [54, 71-77]. In this population where the annual mortality rate is 20% to 25%, atherosclerotic heart disease is thought to be the major cause of morbidity and mortality [76]. Because there is a strong association between hypoalbuminemia and cardiovascular disease, both malnutrition and inflammation have been implicated as the main factors in the high mortality of these patients [78]. The presence of PEM and inflammation are common and usually concurrent in dialysis patients to the extent where some investigators have termed the relationship the malnutrition-inflammation complex syndrome (MICS) [79]. There is overlap between patients with malnutrition and patients with inflammation. Both show evidence of depressed negative acute phase reactants such as serum albumin and transferrin, and increased inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6). These serum marker abnormalities are common in dialysis patients; CRP and IL-6 in particular have shown superior outcome predictabilities when compared with serum albumin [80]. Although chronic hemodialysis patients already have elevated levels of CRP in comparison to healthy adults, Ikizler et al. showed that CRP levels and reactance values of BIA were independent predictors of hospitalization in this population. In this small prospective study, serum albumin and other visceral proteins were not predictive of hospitalization and were thought to be mainly influenced by inflammation [76]. This has led some investigators to ask whether malnutrition alone is a risk factor for morbidity and mortality or only in its association with inflammation. In fact, low serum protein levels may primarily indicate inflammation and not malnutrition.

Over time, malnutrition and inflammation lead to weight loss in the dialysis patient, which can be explained by three main factors, low nutrient intake, the underlying disease, and the dialysis procedure.

A progressive decrease in dietary intake is frequently observed in patients with progression of kidney failure. Gastroparesis, taste disturbances, and diet restrictions in the "renal diet" are likely contributors. Anorexia plays a major role in PEM and is independently associated with mortality [81]. As these patients are unable to meet their energy requirements, loss of weight and muscle mass ensue. Kopple found poor intake and muscle mass to be independently associated with increased 1-year mortality [82]. In addition, protein and nutrient losses occur daily with patients on different forms of dialysis. Ikizler et al. describe a progressive decline in dietary protein intake in patients with a decreasing GFR [83].

Though nutritional status at the onset of dialysis is a good predictor of short- and long-term survival [84], the most effective method of managing malnutrition in these patients is still unclear. Improving nutritional status remains difficult in ESRD patients because of the associated anorexia. Nutritional support methods like oral supplementation, enteral feeding, and appetite stimulants can improve nutrient intake; however, there needs to be close follow-up with the patient. Enteral and parenteral nutrition are suggested after failure of oral supplementation. The addition of specialized amino acids like a-ketoglutarate and ornithine, glutamine, and arginine to hemodialysis has been shown to improve protein balance. Although recombinant human growth hormone (rhGH) administration produces short-term benefits in nitrogen balance, lean body mass and serum albumin levels in hemodialysis patients, it remains unclear whether GH administration reduces morbidity and mortality [85]. Furthermore, despite low serum and muscle levels of insulin-like growth factors (e.g., IGF-1), there is no evidence to suggest any outcome benefits of its administration in ESRD patients [84, 86]. Although evidence shows that nutritional support in various forms can improve nutritional indices in dialysis patients, it does not improve outcomes [54]. In reality, the clinical trials designed to answer these questions have not been adequately designed. The few studies on intradialytic parenteral nutrition (IDPN), i.e., intravenous supplementation of mixtures of glucose, amino acids, and/or lipids during the hemodialysis session, have been inconsistent in improving survival [69, 87-89].

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