Carbohydrates and Lipids

Patients with acute renal failure (ARF) may present with a widely varying hormonal and metabolic status. The isolated acute loss of excretory renal function causes metabolic alterations that are similar to those encountered in chronic renal failure. More often, however, ARF is associated with conditions such as sepsis, trauma, and multiple-organ failure and is seen in about 36% of patients in the intensive care unit (ICU). These latter patients usually sustain profound hormonal dysfunction, which results in impairment of protein, carbohydrate, and lipid metabolisms.

The metabolic response to stress in critically ill patients is characterized by the increased production of stress mediators, such as counterregulatory hormones (catecholamines, cortisol, glucagon, growth hormone), cytokines (interleukin-1, interleukin-6, tumor necrosis factor-alpha), and other immune mediators (thromboxane A2, prostaglandins). These stress mediators upregulate, in critical illness, membrane expression of glucose transporters (GLUT), allowing glucose to enter cells with consequent intracellular glucose levels higher than extracellular levels leading to glucose overload in several tissues; they are responsible for insulin resistance, enhanced proteolysis, glycogenolysis, gluconeogenesis, and lipolysis and ultimately lead to negative nitrogen balance, hyperglycemia, and hypertriglyceridemia.