Nutrition in Renal Failure: Myths and Management NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #20 Carol Rees Parrish, R.D., MS, Series Editor Joe Krenitsky, MS, RD, Nutrition Support Specialist, Digestive Health Center of Excellence, University of Virginia Health System, Charlottesville, VA. Malnutrition occurs in up to 40% of patients with renal failure, and is associated with increased morbidity and mortality in this population. The cause of malnutrition in renal failure is multifactorial, but gastrointestinal symptoms frequently contribute to decreased food intake. Treatment of the GI manifestations of renal failure and co-existing conditions can improve nutrition status. Providing calories and protein that are appropriate for a patient’s stage of kidney disease allows adequate nutrition and avoids unnecessary diet restrictions. This article reviews factors that frequently impair nutrition status in patients with renal failure, and provides suggestions for diet, supplements, and specialized nutrition support. Nutrition assessment, monitoring, and guidelines for vitamin and mineral supplements are discussed. (continued on page 42) Joe Krenitsky 42 PRACTICAL GASTROENTEROLOGY • SEPTEMBER 2004 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #20 Nutrition in Renal Failure vation of the acute-phase response related to co-morbid conditions. In addition, it is possible that co-morbid conditions result in increased inflammatory cytokines and are the cause of both malnutrition and the increased m o r t a l i t y. However, there are several studies that demonstrate that the provision of increased nutrition to patients with malnutrition and renal failure may improve patient outcomes (1,6). This article will review some of the factors that affect nutrition status in patients with renal failure, discuss appropriate nutritional needs, and offer strategies for optimizing nutritional intake. DECREASED NUTRIENT INTAKE There are a number of factors that contribute to malnutrition in patients with renal failure (Table 1). Decreased intake of protein and calories is the most evident factor. Studies have demonstrated that even patients with a mild decline in glomerular filtration rate (GFR) (i.e. <50 mL/minute) have a decreased calorie and protein intake (1,2). Studies have also documented that dietary protein intake progressively declines with decreasing GFR (1,2). Co-morbid conditions frequently contribute to decreased intake and malnutrition. Gastroparesis likely contributes to poor intake in those patients with renal failure who have diabetes mellitus. There is increasing evidence that non-diabetic patients with renal failure and poor intake should be evaluated for gastroparesis (4,5). Several studies have documented a high incidence of impaired gastric motility in maintenance dialysis patients (3–5). Those non-diabetic maintenance dialysis patients who had hypoalbuminemia and occult gastroparesis demonstrated improved nutrition status after treatment with erythromycin as a prokinetic agent (5). Overzealous diet restrictions can also contribute to decreased intake. The provision of a “renal diet” that limits protein, salt, potassium, phosphorus and fluid may further limit intake in a patient with existing malnutrition and poor oral intake. Dietary intervention should not be instituted until nutritional status and eating habits have been investigated, and the patient demonstrates a clear need for dietary restriction. Furthermore, underlying causes for electrolyte abnormalities such as poor glucose control, use of potassium containing salt-substitutes, or medications as a cause of hyperkalemia should be addressed before imposing diet restrictions. Patients receiving maintenance dialysis have increased serum leptin and elevated serum acute phase mediators such as IL-6 and TNF (1,2). These mediators would be expected to exacerbate the anorexia and decreased oral intake in patients with renal failure. The presence of uremia is a more obvious factor that adds to the decreased appetite and nutrient intake. INCREASED NUTRIENT LOSSES Patients who receive maintenance dialysis experience a loss of nutrients as a direct result of the dialysis itself. Hemodialysis results in a loss of 6–12 grams of amino acids, 2–3 gms of peptides, and negligible amounts of protein per dialysis session (2). During peritoneal dialysis, patients lose only 2–4 grams of amino acids, but experience a total loss of 8–9 grams of protein per day (including 5–6 grams of albumin) (2). Patients on peritoneal dialysis can lose over 15 grams of protein each day during periods of peritonitis. This increased protein loss can continue for days after the peritonitis is treated (2). Patients receiving maintenance dialysis also have protein losses due to frequent blood sampling for labs. (continued from page 40) (continued on page 44) Table 1 Factors contributing to malnutrition in renal failure • Decreased Intake – Anorexia – Gastroparesis – Intraperitoneal instillation of dialsate in CAPD – Uremia – Increased Leptin • Diet Restrictions • Loss of nutrients in dialysate • Concurrent illness and hospitalizations • Increased inflammatory and catabolic cytokines • Chronic blood loss • Acidosis • Accumulation of toxins such as aluminum • Endocrine disorders – Insulin resistance – Hyperglucogonemia 44 PRACTICAL GASTROENTEROLOGY • SEPTEMBER 2004 A patient with normal hemoglobin will lose approximately 16 grams of protein with each 100 mL of blood removed (1,2). Malabsorption due to bacterial overgrowth is another route for nutrient loss in some patients. In a cohort of 22 patients with chronic renal failure, 36% had small bowel bacterial overgrowth (3). This is very likely an underappreciated route of fecal nutrient losses considering that over 25% of these patients did not have overt gastrointestinal symptoms. INCREASED CATABOLISM Patients with renal failure are frequently “anabolism challenged.” The increased acute-phase reactants observed with renal failure and dialysis inhibit hepatic production of albumin and increase catabolism of skeletal muscle tissue (1,2). Acidosis is an additional factor that precipitates catabolism in this population (7). Recent research documents the ability of acidosis to activate the ubiquitin-proteasome proteolytic system in muscle, one of the primary pathways of cell protein catabolism (8). Provision of bicarbonate to maintenance dialysis patients decreases the protein catabolic rate, and improves nutrition status (7,8). Acidosis also inhibits osteoblast and increases osteoclast activity, contributing to the osteodystrophy associated with renal failure (7). NUTRITION NEEDS Before any discussion of calorie and protein needs in patients with renal failure can proceed, one important point must be made. There are no large, prospective controlled trials that have randomized patients to receive graded levels of protein and calories to determine the intake that will lead to the best outcomes in nutritional status, morbidity, and mortality. Current recommendations have been based on surrogate markers of nutrition status, indirect calorimetry measurements, and studies of protein catabolic rate. Considering the revelations that medical outcomes research has yielded in the last 10 years, realize that the finest recommendations cannot reliably tell us how to feed this nutritionally vulnerable population in a way that will yield the best outcomes. Several studies have investigated the calorie needs of maintenance hemodialysis patients under metabolic balance conditions. A review of these studies concluded that caloric expenditure of stable hemodialysis and CAPD patients were not significantly increased above normal (1). However, a review of surveys of food intake in the dialysis population suggests that calorie intake is frequently inadequate, and is compromised to a greater degree than protein intake (1,2). The National Kidney Foundation’s guidelines for stable dialysis patients are 30–35 calories/Kg (9) and can be found on Table 2. Patients who receive peritoneal dialysis with a dextrose containing dialysate solution can absorb up to 70% of the dextrose from the solution that is instilled (10). Many patients absorb 200–300 dextrose calories per day from chronic ambulatory peritoneal dialysis (CAPD), and this must be taken into account when estimating calorie intake and needs or when attempting to control hyperglycemia. CALCULATING CALORIE NEEDS Generally, caloric calculations should be done with actual edema-free body weight, determined post-dialysis for hemodialysis, and “post-drain” for peritoneal dialysis. The National Kidney Foundation recommends that when patients are ><95% or >115% of the median standard weight (as determined from the NHANES II data), that an adjusted body weight be used (9). If actual body weight is used to calculate calorie requirements in patients that are obese, energy requirements may be overestimated. Adjusted body weight is calculated as follows: Adjusted weight = ideal weight + [(actual edema-free weight – ideal weight) × 0.25] Estimation of calorie needs remains an issue of some controversy among nutrition experts. From a practical standpoint, any estimation of calorie requirements is only a starting point to avoid gross overfeeding or underfeeding. Monitoring a patients clinical status and trends in their edema-free weigh, with timely adjustment in the nutritional plan as needed, is far more important than absolute precision of the initial assessment of calorie needs. NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #20 Nutrition in Renal Failure (continued from page 42) (continued on page 46) Nutrition in Renal Failure PROTEIN REQUIREMENTS Chronic Renal Failure Protein requirements for patients with renal failure are dependent on the acute or chronic nature of the renal failure and the presence and type of dialysis. The nutritional status and adequacy of current intake of the patient should also be considered. Adults with chronic renal failure who are not receiving dialysis can usually maintain a neutral nitrogen balance consuming 0.6 g of protein per kilogram if adequate calories are ingested and most of the protein is of high biological value (11). A reduced protein intake may decrease uremic symptoms and delay the need for dialysis in a stable patient with chronic renal insufficiency. However, a reduced protein intake is not advisable in the setting of significant malnutrition, or inadequate calorie intake. Acute Renal Failure There is no data to suggest that a protein restriction is of any benefit in the setting of acute renal failure associated with severe illness or multi-organ dysfunction. In patients who are acutely ill with increasing uremia, there is a temptation to focus on the protein content of nutrition support as a major contributor to uremia. It is impor46 PRACTICAL GASTROENTEROLOGY • SEPTEMBER 2004 (continued from page 44) Table 2 Selected nutritional parameters for varying levels of kidney failurea Stages 1–4 Normal kidney Chronic Stage 5 Stage 5 Nutritional parameter function kidney disease Hemodialysis Peritoneal dialysis Transplant Calories (kcal/kg/d) 30–37 35 < 60 yrs 35 < 60 yrs 35 < 60 yrs 30-35 initial 30–35 ≥ 60 yrs 30–35 ≥ 60 yrs 30–35 ≥ 60 yrs include 25–30 for maintenance calories from dialysate Protein (gm/kg/d) 0.8 0.6–0.75 1.2 1.2–1.3 1.3–1.5 initial 50% HBVb 50% HBV 50%