QJM Advance Access published online on January 25, 2008
QJM, doi:10.1093/qjmed/hcm127
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Indicators of lean body mass catabolism: emphasis on the creatinine excretion rate
From the 1Department of Paediatrics, Hospital das Clínicas, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil, 2Department of Critical Care Medicine, The Hospital for Sick Children and Departments of Anaesthesia and Medicine, University of Toronto, Toronto, 3Division of Paediatric Nephrology, Stollery Children's Hospital, University of Alberta, Edmonton and 4Division of Nephrology, St Michael's Hospital, University of Toronto, Toronto, Canada
Address correspondence to Ana PCP Carlotti, MD, Department of Paediatrics, Hospital das Clínicas, Faculty of Medicine of Ribeirão, Preto, University of São Paulo, Av. dos Bandeirantes, 3900, 14049-900, Ribeirão Preto, SP, Brazil. email: carlotti{at}fmrp.usp.br
Received 18 June 2007 and in revised form 21 August 2007
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Abstract |
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Background: The major stress response to critical illness leads to a catabolic state and loss of lean body mass.
Aims: To test whether an increased rate of creatinine excretion might provide unique and timely information to monitor cell catabolism; to relate this information to balances of cell constituents (nitrogen, potassium, phosphate and magnesium); to evaluate the effectiveness of nutritional therapy to reverse this catabolic process.
Design: Prospective observational study.
Methods: Children with severe traumatic brain injury admitted to the paediatric critical care units of The Hospital for Sick Children, Toronto, Canada and Hospital das Clínicas, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Brazil were studied. Complete 24 h urine collections were obtained for measurement of creatinine excretion rate and daily balances of nitrogen, potassium, phosphate and magnesium.
Results: Seventeen patients were studied for 3–10 days. On Day 1, all had negative balances for protein and phosphate. Balances for these intracellular constituents became positive when protein intake was 
1 g/kg/day and energy intake was 50% of estimated energy expenditure (P < 0.0001). Creatinine excretion rate was positively correlated with the urea appearance rate (r = 0.60; P < 0.0001), and negatively with protein balance (r = -0.45; P < 0.0001). Sepsis developed in four patients; before its clinical detection, there were negative balances for all intracellular markers and an abrupt rise in the excretion of creatinine.
Conclusions: Negative balances of intracellular components and an increase in rate of creatinine excretion heralded the onset of catabolism.