Nutritional Support and Hyper-Alimentation in Acute Renal Failure

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1 REVIEW ARTICLE JIACM 2002; 3(3): Nutritional Support and Hyper-Alimentation in Acute Renal Failure Sham Sunder*, Suman Lata** Metabolic and nutritional status of acute renal failure (ARF) varies markedly. Some patients are hyper-catabolic, while the others are acidaemic with marked increase in serum urea, potassium, and phosphates. In some, net protein degradation can be upto 200 to 250 gm/day, while in others there may be increased basal energy expenditure, viz., sepsis, poly-trauma, burns, multi-organ failure, rhabdomyolysis 1,2. The hyper-catabolic ARF is usually associated with these entities. The various biochemical alterations of hyper-catabolic ARF are enlisted in table I and the primary goals of nutritional support in these patients are currently directed towards : 1. To reduce negative protein balance, i.e., preserving lean mass To preserve or restore normal body composition by maintaining milieu interior. 3. To normalise altered chemical composition of plasma and tissue by preventing specific metabolic alterations To enhance renal recovery by limiting uraemic toxicity in ARF patients 3. These patients are metabolically stabilised either by oral or enteral nutrition and during recent years enteral nutrition has become the primary type of nutritional support. Only in few patients with hypercatabolic ARF parental nutrition will be necessary where oral or enteral nutrition is not possible. Use of continuous renal replacement therapy (RRT) as continuous veno-venous haemodialysis (CVVH) at bed-side in critically ill ARF patient can be of tremendous aid in nutritional therapy by two ways; firstly, by removing large amount of water, electrolytes, and metabolites each day and secondly, * Senior Nephrologist ** Senior Resident Department of Medicine, Dr. RML Hospital, New Delhi by safely administering large amount of aminoacids and other nutrients on per day basis. Inadequate nutrition may contribute to lean body mass and can potentiate the catabolic response of ARF not only by substrate losses but also by activation of protein breakdown, hence mortality. Table I : Biochemical alterations in hypercatabolic ARF 1,6. 1. Release of endotoxins, T.N.F., IL-I by underlying catabolic illness. 2. Increased concentration of counter-regulatory hormones, e.g., epinephrine, cortisone, and glucagon. 3. Acidaemia promotes catabolism of proteins and amino-acids. 4. Increased protein catabolism if energy intake is inadequate. 5. Nutritional loss during dialysis. Metabolic consequences and nutritional requirement in patients with acute renal failure, i.e., nutritional strategies. Acute renal failure not only affects water, electrolytes, and acid base metabolism but induces global change of the milieu interior with specific alteration in protein and aminoacid, carbohydrate, and lipid metabolism. 2 Metabolic alterations and consequences in them are basically due to acute loss of renal function, the underlying disease, and the type of renal replacement therapy 3. Energy requirement : Acutely ill patients are likely to have increased energy expenditure. Generally, the energy requirement for ARF patient is between kcal/kg/day, adjusted depending upon body weight and severity of the ARF 1. Carbohydrate metabolism : ARF patients may have associated hyperglycaemia. It may be either due to insulin resistance which has been proved

2 in experimental animals 4 or accelerated hepatic gluconeogenesis 5,6. Lipid metabolism : Lipid metabolism is impaired due to lipolysis which can impair reticuloendothelial functions. Few studies have shown that omega-3-fatty acids may enhance immune function and host resistance 7. Water and minerals must be evaluated carefully each day. ARF patients are frequently associated with hyperkalaemia, hyperphosphataemia, and hypocalcaemia due to impaired excretions and increased catabolism 8. In contrast to chronic renal failure (CRF), serum levels of vitamin A and vitamin E (anti-oxidants) are decreased by 50%. To add further, selenium level also exacerbates the degree of ischaemic renal injury hence mortality 9,10. Protein and aminoacid metabolism : The hallmark of metabolic alteration in ARF is activation of protein catabolism with excessive release of amino-acids from skeletal muscles and defective utilisation of amino-acids 11,12. Excessive protein catabolism and inadequate nutrition are responsible for lean body mass 13. Protein requirement in ARF : Protein requirement is exactly calculated by UNA (Urinary nitrogen appearance) as shown in table II. In practice, it is simplified by calculating the rise in BUN during 24 hours 14. Generally three groups of patients have been identified in ARF as shown in table III. The protein requirement as well as calorie requirement is calculated after clinically assessing ARF patient. The routes of nutrition can also be decided from this table. Table II 6 : 1. U.N.A. (gm/day) = urinary urea nitrogen (gm/ 24 hr) + dialysate urea nitrogen (gm/24hr) + change in body urea nitrogen (gm/24hr). 2. For patients on haemodialysis, urea kinetic modeling may also be used to estimate U.N.A 21. Group I. Patients with low U.N.A. (i.e., 4 to 5 gm/ day). Mild type of ARF generally caused by nephrotoxins. These patients are not malnourished and are not undergoing dialysis. Protein recommended is 0.6 gm/kg to minimise accumulation of nitrogen metabolite. Subsequently gradually increased to 0.8 gm/kg as long as BUN remains less than 100 mg/day. They are managed by oral feeding with vitamin supplementation without dialysis support. Group II. Patients with U.N.A. more than 5 gm/ day are hypercatabolic, malnourished, and are undergoing dialysis therapy. Nutritional support is also guided by types of renal replacement therapy. Patients undergoing thrice a week haemodialysis/conventional haemodialysis usually require protein of about gm/kg/day 3,15. It should have combination of both essential and non-essential aminoacids to prevent imbalance. For patients having moderate to severe hypercatabolism (UNA is 5 to 12 gm/day) dietary treatment is complex, requiring enteral and/or parental nutrition 16. In all patients who can tolerate orally, enteral nutrition should be encouraged as it helps to maintain gastrointestinal function especially barrier function of intestinal mucosa 17. In experimental ARF, enteral nutrition can augment renal plasma flow and improve renal function 18,19. Mainly three types of readymade oral and enteral preparations are available depending on the feasibility, various protein contents, and tolerance of the ready-to-use preparations, viz., 1. Elemental powder diet for CRF Low protein (EAA) diet 2. Standard enteral formula (EF) : In ICU patient of ARF amount and type of proteins, viz., glutamine, arginine, nucleotides with high electrolytes. 3. Specific enteral formulae for metabolically altered patients of uraemia Ready-to-use liquid diet is used during haemodialysis. Journal, Indian Academy of Clinical Medicine Vol. 3, No. 3 July-September

3 Table III 6 : Patient classification and nutrient requirements in patients with acute renal failure. Extent of catabolism Mild Moderate Severe Excess urea appearance < 5g 5-10 g >10 g (above N intake) Clinical setting (examples) Drug toxicity Elective surgery Sepsis, organ ± infection failure Dialysis/CRRT-frequency Rare As needed Frequent Route of nutritional Oral Enteral and/or Enteral and/or administration parenteral parenteral Energy recommendations (kcal/kgbw/day) Energy substrates Glucose Glucose + fat Glucose +fat Glucose (g/kgbw/day) Fat (g/kgbw/day) Amino acids/protein (g/kg/day) EAA (+NEAA) EAA + NEAA EAA + NEAA Nutrients used Oral/enteral/parenteral Food Enteral formulae Enteral formulae Glucose 50-70% Glucose 50-80% + fat emulsions + fat emulsions 10% or 20% 10% or 20% EAA+specific NEAA solutions (general or nephro ) multi-vitamin and multi trace element preparations. CRRT-continuous renal replacement therapy; EAA-essential amino acids. Though enteral feeding may cause technical problems, infection, or GIT side effects, the volume overload and problems of electrolyte disturbances are never seen in patients with enteral feeding. Only in very few of group II ARF patients dialysis or continuous renal replacement therapy can become necessary. Group III Those who are critically ill patients of ARF with poly-trauma, burns, sepsis, organ failure nutrition can be tried by oral or enteral route. However, mainstay of management is haemodialysis or continuous renal replacement therapy (RRT), i.e., total parenteral nutrition (TPN) or continuous veno-venous haemodialysis (CVVH) 16. Parenteral hyper-alimentation may be associated with significant mechanical, infection related, and metabolic complication. Metabolic complications may be due to volume load or electrolyte disturbances and can be managed by infusion control. The type and frequency of renal replacement therapy can also aggravate protein catabolism. Therefore, it is not initiated until 4th day of ARF or when oral or enteral feeding fails. Solutions containing essential amino acids and non-essential amino acids in standard proportion (nephro solutions) which contain tyrosin diapeptide as it is less soluble in water are recommended. Recently glutamine dipeptide has been introduced 280 Journal, Indian Academy of Clinical Medicine Vol. 3, No. 3 July-September 2002

4 in parenteral nutrition because it has a role in various metabolic functions. It can improve survival in critically ill patients. Infusion of salts complex of a ketoglutarate and ornithine is reported to decrease UNA and improve nitrogen balance. Composition of parenteral nutrition For parenteral nutrition, composition is mainly glucose, amino acids, and fat emulsion with vitamins, electrolytes, trace elements, and insulin. Glucose Glucose is main energy substrate, as it can be used even under hypoxic condition and it reduces nitrogen requirement. However, glucose intake must be restricted to less than 5 gm/kg body weight. Generally, 70% dextrose is used because of its greater caloric density. Insulin is frequently required to maintain normoglycaemia. Amino-acid solutions Specially designed nephromixtures of essential and non-essential amino-acids are available (500 cc of 8.5% to 10% of E.A.A. and N.E.A.A.). These on (a) conventional haemodialysis require 1.0 to 1.2 gm/kg per day, and (b) on C.V.V.H. or C.V.V.H.D. require 1.5 to 2 gm/kg/day 20. Fat emulsion : Lipid solutions should provide 30% of energy intake, 20% lipid emulsion provides the most fat and energy per ml of water. Parenteral solutions (Renal failure fluid) : Standard solution with amino-acid 5-10%, glucose 40-70%, and fat emulsion 10-20% plus addition of vitamin, trace elements, electrolytes, and insulin contained in single bag are available (all in one solution). The infusion should be started at low rate providing 50% of requirement and gradually increased over several days. The daily requirement of parenteral solution is generally to provide the required energy and the intake is 1.5 to 2.0 L/day for patients on haemodialysis thrice a week or conventional haemodialysis; 2.0 to 3.0 L/day for patients undergoing continuous veno-venous haemodialysis. Conclusions All patients of acute renal failure require adequate nutritional support to maintain protein stores, body mass, maintaining milieu interior, to correct preexisting disease by which to enhance renal recovery. Prognosis of patient depends upon the severity of underlying illness and amount of hypercatabolism. First of all, these patients are started on oral or enteral feeding. Oral feeding is safe in all respects. If oral or enteral nutrition is impossible, then only parenteral feeding is recommended, though this is not without complications. Nutritional therapy, just like dialysis, should be viewed as means of supporting the patient until underlying illness is controlled and hypercatabolism is reversed. Inadequate nutrition may contribute to lean body mass and can potentiate the catabolic response of ARF not only by substrate losses but also by activation of protein breakdown, hence mortality. Future advances will require metabolic intervention to control accelerated catabolism. References 1. Drumil W, Mitch WE. Metabolic abnormalities in acute renal failure. Seminars Dialysis 1996; 9: Schneeweiss B, Graninger W, Stockenhuber F et al. Energy metabolism in acute and chronic renal failure. Am J Clin Nutr 1990; 52: Drumil W. Nutritional support in acute renal failure, in Mitch W.E. Klahr S (eds): Nutrition and the Kidney, Boston, MA, Little Brown,1998; pp May RC, Clark AS, Goheer MA, Mitch WE. Specific defects in insulin-mediated muscle metabolism in acute uremia. Kidney Int 1985; 28: Cianciaruso B, Bellizzi V, Napoli R et al. Hepatic uptake and release of glucose, lactate and amino-acids in acutely uremic dogs. Metabolism 1991; 40: Drumil W. Nutritional management of ARF. Am J Kid Dis 2001; 37 (1): S89-S Drumil W, Zechner R, Magometschnigg D et al. Postheparin lipolytic activity in acute renal failure. Clin Nephrol 1985; 23: Drumil W, Schwarzenhofer M, Apsner R, Horl WH. Fat soluble vitamins in patients with acute renal failure. Miner Electrolyte Metab 1998; 24: Journal, Indian Academy of Clinical Medicine Vol. 3, No. 3 July-September

5 9. Metnitz GH, Fischer M, Bartens S et al. Impact of acute renal failure on antioxidant status in patients with multiple organ failure. Acta Anaesthesiol Scand 2000; 44: Angstwurm MW, Schottdorf J, Schopohl J, Gaertner R. Selenium replacement in patients with severe systemic inflammatory response syndrome imporves clinical outcome. Crit Care Med 1999; 27: Drumil W. Protein metabolism in acute renal failure. Miner Electrolyte Metab 1998; 24: Price SR, Reaich D, Marinovic AC et al. Mechanisms congibuting to muscle wasting in acute uremia: activation of amino acid catabolism. J Am Soc Nephrol 1998; 9: Drumil W, Fischer M, Liebisch B et al. Elimination of amino acids in renal failure. Am J Clin Nutr 1994; 60: Maroni JM, Steinman TI, Mitch W. A method of estimating nitrogen intake of patients of chronic renal failure. Kidney Int 1985; 27: Macias WL, Alaka KJ, Murphy MH et al. Impact of nutritional regimen on protein catabolism and nitrogen balance in patients with acute renal failure. J Parenter Enteral Nutr 1996; 20: Drumil W. Metabolic aspects of continuous renal replacement therapies. Kidney in Suppl 1999; 72: S56- S Drumil W, Mitch WE. Enteral nutrition in renal disease, in Rombeau JL, Holandelli RH (eds): Enteral and Tube Feeding. Philadelphia, PA, Sauders, 1997; pp Roberts PR, Black KW, Zaloga GP. Enteral feeding improves outcome and protects against glycerol-induced acute renal failure in the rat. Am J Respir Crit Care Med 1997; 156: Fiaccadori E, Leonardi S, Lombardi M et al. Enteral nutrition in patients with acute renal failure: Nutritional effects and adequacy of nutrient intakes. JASN 1996; 7: 1372A. 20. Griffiths RD, Jones CJ, Palmer TEA. Six-month outcome of critically ill patients given glutamine-supplemented parenteral nutrition. Nutrition 1997; 13: Journal, Indian Academy of Clinical Medicine Vol. 3, No. 3 July-September 2002