Basal energy Expenditure (BEE) represents the energy consumption of an individual at complete rest. Rising basal energy Expenditure in maintenance hemodialysis (MHD) patients necessitates increased energy replenishment, esp. in anorexic patients in order to increase serum amino acid concentration and reduce high incidence of wasting syndrome and malnutrition1.Therefore, the determination of BEE is critical to establishing energy recommendations and maintaining nutritional balance in patients receiving hemodialysis (HD) 2. Using blood temperature monitor in HD, low temperature dialysis (dialysate temperature < 37C) and isothermal HD can maintain hemodynamic stability, which requires active cooling. The amount of this negative energy transfer is directly proportional to the amount of blood volume loss induced by ultrafiltration3.
In addition to signaling human appetite control from adipose tissue4 with leptin and gut hormone, BEE, in proportion to basal energy requirements also provide a feedback signal of driving habitual food intake and human appetite control. BEE is also useful for individualizing dialytic prescriptions for these patients 5.
Consequences of advanced chronic kidney disease are principal contributors to elevated BEE in patients on HD. It seems reasonable to speculate that the increase in BEE is attributable to protein catabolism caused by the inflammation and uremia. Uremic conditions cause proteolysis and lean body mass depletion owing to the inactivation of alanine aminotransferase and glycogenolysis because of decreased phosphofructokinase and pyruvate kinase activities in patients on HD 6. Besides ,renal failure may be related to increased energy metabolism due to metabolic acidosis, secondary hyperparathyroidism, insulin resistance 7, and microinflammation, with elevated C-reactive protein and cytokine levels 8, despite the role of the kidney as an essential metabolically active organ 9.HD patients with moderate to severe hyperparathyroidism also exhibit lean body mass depletion and increased BEE 10,11.Hyperparathyroidism causes skeletal myopathy. PTH not only causes abnormalities of skeletal muscle of bioenergetics, but also cause muscle proteolysis. Animal study showed the mechanism of increased BEE in hyperparathyroidism that PTH facilitate entering of excess calcium into the cells, precipitation as calcium phosphate compounds, and reducing the concentration of inorganic phosphorus, and then reducing high energy compound, such as ATP10,11.
Common comorbidities, such as diabetes, heart failure, and chronic inflammation, in advanced chronic kidney disease also contribute to elevated BEE in patients on HD. The development of type 2 diabetes, occurring early in the transition from normal glucose tolerance to impaired glucose tolerance is accompanied not only by an increase in BEE but also a decrease in insulin induced thermogenesis, which associated with progressive metabolic abnormalities independent of body size and body composition12. Besides well known risk factors for diabetic retinopathy, such as duration of diabetes, long standing hyperglycemia, subclinical inflammation, increased oxidative stress and hypercholesterolemia, a community-based cross-sectional study involving 1,184 participants with Type 2 diabetic retinopathy, a most specific microvascular complication of diabetes found that visceral fat, subcutaneous fat, body fat and increased basal energy expenditures were also the novel risk factors for diabetic retinopathy. The mechanism involves excessive gluconeogenesis and catabolism, leading to increased rates of energy expenditure. Sustained increased basal energy expenditure can manifest as sustained unintended weight loss13.Skeletal muscle catabolism has been observed in HD patients with poorly controlled diabetes with retinopathy and nephropathy owing to a combined effect of uremic factors and insulin resistance 14 and lean body mass depletion and elevated BEE 12,13.
The frequent occurrence of systemic microinflammation and various catabolic conditions in patients with chronic kidney disease may directly affect BEE. If CKD patients are in a state of subclinical inflammation, they are at risk for malnutrition. Not only increased BEE but also other related responses to inflammation contribute to the linkage of inflammation and malnutrition, which include increased oxygen consumption, increased systemic total protein turnover and peripheral amino acid mobilization, enhanced lipolysis and fat utilization, and increased concentrations of catecholamines, glucagon, and cortisol7. In addition, suppression of appetite may also be implicated. In some ESRD patients, peripheral blood mononuclear cells (PBMCs) overproduce pro-inflammatory IL-6 cytokines which induces protein catabolism, lipolysis, insulin resistance, and suppression of appetite and pathophysiologic ally link inflammation and malnutrition15.Following weight loss in obese patient in weight control center, the cellularity model predicts decline of BEE more effectively than the body fat model16
An overhydrated status in patients undergoing HD may increase BEE because of increased myocardial demand, increased activation of the sympathetic system, increased serum levels of tumor necrotic factors, and increased metabolism of the respiratory muscles 17.
One study identified several persistent pathophysiological alterations related to dialytic procedures, some even lasting up to 2 hours after HD, such as hypovolemia 18, dialytic loss of amino acids and protein catabolism 19,20, activation of complement system due to bio-incompatibility of dialysis membranes 21,22, and changes in hormonal levels, with significant increase in BEE after HD 23. To date, few studies have incorporated body composition, anthropometric data, diabetes mellitus (DM) status, and demographic data in predicting bioelectrical impedance analysis (BIA)–determined BEE in patients receiving HD. Therefore, in this study, we compared BIA-derived BEEs and BEEs calculated using the Harris–Benedict equation in patients undergoing HD, and we identified the determinants of BEE.