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Nephrol Dial Transplant (2001) 16 wSuppl 6x: 2122

Nutrition in patients with acute renal failure

S. Bozfakoglu

Division of Nephrology, Department of Internal Medicine, Medical School of Istanbul, University of Istanbul,
Istanbul, Turkey

Introduction retarded because of renal failure. Acidosis and release

of proteases from activated leukocytes can stimulate
Acute renal failure (ARF) is a common disease protein breakdown. Moreover, inflammatory medi-
affecting approximately 5% of all hospitalized patients ators such as tumor necrosis factor-a (TNF-a) and
and 1030% of the patients in intensive care units. The interleukins as well as renal replacement therapy
mortality rate is still very high (above 50%), despite by itself can mediate hypercatabolism. Additionally,
advances in the management of critically ill patients inadequate nutrition contributes to the loss of lean
and in the renal replacement therapies. Pre-existing or body mass in ARF w2,47x.
hospital-acquired malnutrition is an important factor
contributing to high mortality seen in patients with
ARF w14x. Nutritional support has, therefore, been Carbohydrate metabolism
accepted as an important part of the management of
ARF. ARF is frequently associated with hyperglycaemia
During the course of ARF, multiple metabolic mainly because of insulin resistance. Despite the clear-
changes occur. ARF affects both fluid, electrolyte, ance of insulin is decreased and plasma insulin concen-
acidbase balance and the metabolism of proteins, tration is elevated, maximal insulin-stimulated glucose
amino acids, carbohydrates, lipids and energy. The uptake by skeletal muscle is decreased by 50%. Hepatic
metabolic alterations in ARF patients are determined gluconeogenesis, mainly from conversion of amino
not only by acute loss of renal function, but also by acids released during protein catabolism occuring in
the type and intensity of renal replacement therapy. ARF, is increased and is insensitive to the negative
Furthermore, the underlying disease plays an import- feedback that is normally activated by glucose loading.
ant role in the development of metabolic changes The synthesis of glycogen within the muscles is also
w2,4,5x. deficient w2,4,5x.

Protein and amino acid metabolism Lipid metabolism

The hallmark of metabolic changes in ARF is protein In patients with ARF, triglyceride content of plasma
catabolism and negative nitrogen balance. The causes lipoproteins is elevated. Total cholesterol and in
of hypercatabolism are complex and manifold. The particular high-density lipoprotein cholesterol levels
major stimulus of protein catabolism in ARF is are decreased whereas low-density lipoprotein choles-
insulin resistance. The maximal insulin-stimulated pro- terol and very-low-density lipoprotein cholesterol are
tein synthesis is decreased and protein degradation is increased. The main cause of these abnormalities is the
increased. As a result, excessive release of amino acids impairment of lipolysis w4,5x.
from muscle occurs, and gluconeogenesis and urea-
genesis are increased due to hepatic uptake of these
amino acids from the circulation. On the other hand, Energy metabolism
synthesis of some amino acids in the kidney is
impaired, while catabolism of peptide hormones is
Energy expenditure remains unchanged and near-
normal in uncomplicated ARF such as monofactorial
ARF. In contrast, oxygen consumption and resting
Correspondence and offprint requests to: Semra Bozfakog lu,
University of Istanbul, Medical School of Istanbul, Department of energy expenditure increases by 30% and even
Internal Medicine, Division of Nephrology, 34390 Capa-Istanbul, more when sepsis or systemic inflammatory response
Turkey. syndrome is associated with ARF w2x.

# 2001 European Renal AssociationEuropean Dialysis and Transplant Association

22 S. Bozfakog

Metabolic effects of renal replacement Route of administration

Enteral nutrition should be the primary type of
Renal replacement therapies, especially extracorporeal nutritional support for patients with ARF, because
therapies (haemodialysis and continuous renal replace- even small amounts of nutrients can help to support
ment therapies (CRRT)) have significant metabolic intestinal functions. Unfortunately, it is impossible in
and nutritional consequences. Protein catabolism is many patients to meet all the requirements by the enteral
increased via substrate losses, activation of protein route alone and parenteral nutrition (supplementary
breakdown from release of leukocyte-derived pro- anduor temporarily) may become indispensable w5x.
teases, and release of cytokines such as TNF-a and
interleukins stimulated by bloodmembrane inter-
action during dialysis. Membranes used in haemo- Conclusion
filtration are more porous and small proteins are also
filtered. Moreover, many water soluble substances Nutritional support is of vital importance to maintain
such as vitamins and carnitine are lost during extra- lean body mass, stimulate immune and repair func-
corporeal therapies. Peritoneal dialysis as a renal tions, and decrease the mortality rate in the manage-
replacement therapy especially results in protein and ment of the patients with ARF. So, this support should
amino acids losses w2,46x. thus be established as early as possible during the
course of ARF, although some gastrointestinal side
effects of enteral nutrition and some technical, meta-
bolic, and infectious complications of parenteral
Nutrient requirements in patients with ARF nutrition can be observed.

If there is no associated hypercatabolic state, the intake

of protein or amino acid should be 1.0 gukg body References
weightuday. Hypercatabolic patients with ARF should
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