Figure 1815

Glucose metabolism in acute renal failure (ARF): Stimulation of hepatic gluconeogenesis. A second feature of glucose metabolism (and at the same time the dominating mechanism of accelerated protein breakdown) in ARF is accelerated hepatic gluconeogenesis, mainly from conversion of amino acids released during protein catabolism. Hepatic extraction of amino acids, their conversion to glucose, and urea production are all increased in ARF (see Fig. 18-7) [12].

In healthy subjects, but also in patients with chronic renal failure, hepatic gluconeogenesis from amino acids is readily and completely suppressed by exogenous glucose infusion. In contrast, in ARF hepatic glucose formation can only be decreased, but not halted, by substrate supply. As can be seen from this experimental study, even during glucose infusion there is persistent gluconeogenesis from amino acids in acutely uremic dogs (•) as compared with controls dogs (o) whose livers switch from glucose release to glucose uptake [32].

These findings have important implications for nutrition support for patients with ARF: 1) It is impossible to achieve positive nitrogen balance; 2) Protein catabolism cannot be suppressed by providing conventional nutritional substrates alone. Thus, for future advances alternative means must be found to effectively suppress protein catab-olism and preserve lean body mass. (From Cianciaruso et al. [32]; with permission.)

Lipid metabolism

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