596 Am i C/in Niar I990;52:596-60l . Printed in USA. © 1990 American Society for Clinical Nutrition Energy metabolism in acute and chronic renal failure3 Bruno Schneeweiss, Wolfgang Graninger, Felix Siockenhuber, Wilfred Drum!, Peter Ferenci, Sabine Eichinger, Georg Grimm, Anton N Laggner, and Kurt Lenz ABSTRACT Energy metabolism was measured by mdi- rect calorimetry in 86 patients with various forms of renal fail- ure and in 24 control subjects. In patients with acute renal fail- ure with sepsis, oxygen consumption, carbon dioxide produc- tion, and resting energy expenditure were increased (P < 0.05). In other groups with renal failure (acute renal failure without sepsis, chronic renal failure with conservative treatment or he- modialysis, and severe untreated azotemia) these indices were not different from those ofcontrol subjects. Urea nitrogen ap- pearance was decreased in patients with chronic renal failure undergoing conservative treatment, in those with severe un- treated azotemia, and in hemodialysis patients (P < 0.05). We conclude that renal failure has no influence on energy expendi- ture as long as septicemia is absent. Reduced urea nitrogen ap- pearance rates in chronic renal failure are due to a reduced en- ergy and protein intake. Wasting is a consequence of decreased food intake but not of hypermetabolism in chronic renal failure. Am J C/in Nutr 1990:52:596-601. KEY WORDS Energy metabolism, energy expenditure, energy intake, renal failure, malnutrition Introduction Energy metabolism is frequently altered in diseases involv- ing organs with important metabolic functions (1-6). New treatments based on a better understanding ofthese alterations may help to prevent weight loss and muscle wasting. Energy metabolism was studied in patients with renal failure by vari- ous authors, with conflicting results ( 1 , 7-19). Experimental studies suggested that both acute and chronic renal failure are associated with a hypometabolic state and hypothermia due to profound abnormalities in cell metabolism (7, 8, 20-24). Basal energy utilization was even more depressed than expected by a decrease in body temperature (1 1, 1 3). On the basis of these observations, it was assumed that renal failure in man might also be associated with a reduction in energy metabolism (7, 8, 10, 12). This assumption was supported by decreased respira- tory quotients in some patients with severe untreated uremia in end-stage renal failure ( 1 7). In contrast, in acute renal failure a hypermetabolic state was frequently observed (1 , 14-16), which is not necessarily the direct consequence of renal failure per se. Thus, the status ofenergy metabolism in renal failure is unclear. Furthermore, it is unknown whether possible changes in energy metabolism are directly related to renal failure itself. Therefore, in this study, energy expenditure and substrate oxi- dation rates of major fuels were measured in several well-de- fined groups of renal-failure patients by indirect calorimetry. Subjects and methods Subjects Studies were performed in the following groups of patients: 1) Patients with acute renal failure with septicemia (n = 18) whose clinical features are listed in Table L The diagnosis of sepsis was based on the following criteria: fever > 38.5 #{176}C, leu- cocytosis > 15 g/L with predominance of granulocytes, and two positive blood cultures, or at least one positive blood cul- ture plus isolation ofthe same organism from the focus of infec- tion. Drug therapy consisted of antibiotics, dopamine (3 zg. kg . min), and sucralfate. 2) Patients with acute renal failure without septicemia (n = I1 ). The diagnoses were acute glomerulonephritis in one, Goodpasture’s syndrome in one, drug-induced hemolysis in two, drug-induced interstitial nephritis in two, postischemic re- nal failure in three, and hypovolemia in two patients. Drug therapy before the study consisted of dopamine (3 gig. kg’. min) and sucralfate and cortisone in one patient. 3) Conservatively treated patients with chronic renal failure (defined as impaired renal function for 1y not requiring he- modialysis) (n = 1 7) as a result of chronic glomerulonephntis in four, chronic pyelonephritis in three, interstitial nephritis in nine, and nephrosclerosis in one patient. Drug therapy con- sisted ofantihypertensive drugs (clonidine, dihydralazine, and nifedipine) and allopurinol. 4) Patients with severe untreated azotemia (blood urea ni- trogen > 36 mmol/L) before initiation of hemodialysis (n = 1 5). The diagnoses were chronic glomerulonephritis in eight, chronic pyelonephritis in four, polycystic kidney disease in two, and hemolytic uremic syndrome in one patient. Drug therapy consisted of antihypertensive drugs (clonidine, dihy- dralazine, and nifedipine) and allopurinol. I From the First Department of Medicine and the First Department ofGastroenterology and Hepatology, University of Vienna. 2 Supported by Fonds zur F#{246}rderung der wissenschaftlichen Forschung (project P5209). 3 Address reprint requests to B Schneeweiss, First Department of Medicine, University of Vienna, Lazarettgasse 14, A-1090 Vienna, Austria. Receivediuly 19, 1989. Accepted for publication November 15, 1989. by guest on July 10, 2011 www.ajcn.org Downloaded from