HBV 1.0 for maintenance Fat (% total kcal) 30%–35% Patients considered at highest risk for cardiovascular disease; <10% saturated fat emphasis on PUFAc, MUFAd, 250–300 mg cholesterol/day Sodium (mg/d) Unrestricted 2,000 2,000 2,000 Unrestricted; monitor medication effect Potassium (mg/d) Unrestricted Correlated to 2,000–3,000 3,000–4,000 Unrestricted; monitor laboratory values (8–17 mg/kg/d) (8–17 mg/kg/d) medication effect Calcium (mg/d) Unrestricted 1,200 ≤ 2,000 from diet ≤ 2,000 from diet and 1,200 and medications medications Phosphorus (mg/d) Unrestricted Correlated to 800–1,000 800–1,000 Unrestricted unless lab values indicted Fluid (ml/d) Unrestricted Unrestricted with 1,000 + urine Monitored; 1,500–2,000 Unrestricted unless normal urine output indicated output a Meant as guidelines only for initial assessment; individualization to patient’s own metabolic status and co-existing metabolic conditions is essential for optimal care. b HBV=high biological value. c PUFA=polyunsaturated fatty acids. d MUFA=monounsaturated fatty acids. “Reprinted from Journal of the American Dietetic Association, V104: 404-409, Beto JA et al.: “Medical nutrition therapy in chronic kidney failure: integrating clinical practice guidelines” © 2004, with permission from the American Dietetic Association. NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #20 Nutrition in Renal Failure PRACTICAL GASTROENTEROLOGY • SEPTEMBER 2004 47 tant to remember that dietary protein comprises only 25% of the total nitrogen pool that is metabolized by the body each day, and that the difference between 1.0 gm protein/Kg and 1.3 gm protein/kg in a 70 Kg patient is only 21 gm of protein per day. Nitrogen load from GI bleeding, inadequately controlled serum glucose, or no nutritional intake in the setting of acute illness would lead to significantly more urea generation than 10–20 gm of additional protein over 24 hours. Patients with multisystem organ failure frequently require dialysis and specialized nutrition support that meets the calorie and protein requirements for critical illness. The protein requirements for patients receiving dialysis are increased above the requirements for healthy adults. Hemodialysis and peritoneal dialysis increase nitrogen losses. In addition, there is information that hemodialysis itself is an inflammatory and catabolic process (12). The National Kidney Foundation’s guideline is 1.2 g protein/Kg/day for stable maintenance hemodialysis patients, and 1.2–1.3 gm protein/day for stable peritoneal dialysis patients (9). Patients with malnutrition, acute catabolic illness, or with postoperative wounds should receive greater than 1.3 gm protein/Kg/day. There is data that increasing protein to 2.0–2.5 gm protein/Kg will result in improved nitrogen balance in hospitalized patients with acute renal failure (13–15). However, increasing protein intake beyond 1.5–1.6 gm/Kg may increase the rate of urea nitrogen appearance, and increase the need for frequent dialysis (16). There is no prospective study that adequately addresses the question of what protein provision will result in the best outcomes for acutely ill patients requiring dialysis. See Table 2 for protein recommendations in renal failure. NUTRITION INTERVENTION Oral The frequent occurrence of malnutrition in patients with renal failure, and the consistent association between markers of malnutrition and poor outcome in this population emphasize the need for appropriate and timely nutrition intervention. Nutrition assessment and counseling with the patient and family is advisable; but it is the consistent follow-up, with modification of the nutrition plan as clinical status changes, that is essential. Modifying the diet consistency to match dentition, adjusting traditional recipes and foods to fit the current plan, or providing oral liquid supplements can all improve nutrition intake. Non-essential diet restrictions should be avoided. Frequently a multi-disciplinary effort is required to address reversible conditions or to identify medications that may contribute to anorexia or inability to eat. Cohort studies of occult gastroparesis and bacterial overgrowth point to some of the treatable GI manifestations that may contribute to malnutrition (5). Table 3 provides suggestions to enhance oral intake. Renal compensatory mechanisms maintain normal serum potassium levels until GFR drops below 15–20 mL/minute (17). Dietary potassium is generally restricted to 2000–3000 mg/day for patients requiring hemodialysis, and 3000–4000 mg/day for patients requiring peritoneal dialysis. There are a number of non-food factors that can cause or contribute to hyperkalemia (Table 4). Correcting underlying factors causing hyperkalemia, such as inadequate glucose control (18) will frequently allow patients a more liberal diet restriction that will encourage good oral intake. Dietary sodium intake is frequently restricted to 2000–4000 mg per day for patients with chronic kidney disease in an effort to aid in the control of hypertension, and to avoid excessive thirst and fluid consumption in those patients with oliguria or anuria. Salt substitutes frequently contain potassium chloride, and patients should be instructed to avoid salt substitutes that are not approved by their dietitian or physician. Patients with chronic kidney disease frequently experience hyperphosphatemia when their glomerular (continued on page 51) Table 3 Strategies to enhance oral intake • Avoid diet restrictions in patients with poor intake • Offer oral liquid supplements and snacks • Treat gastroparesis and other GI maladies • Achieve glycemic control • Correct electrolyte abnormalities • Provide foods appropriate for patient’s dentition • Evaluate for, and address depression NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #20 (continued from page 47) Nutrition in Renal Failure PRACTICAL GASTROENTEROLOGY • SEPTEMBER 2004 51 filtration rate (GFR) drops to 20–30 mL/min (19). A dietary phosphorus restriction of 800–1000 mg per day should be implemented when serum phosphorus rises >4.6 mg/dL (19). There is recent evidence that phosphorus excretion is affected when GFR drops below 60 mL/min, contributing to secondary hyperparathyroidism. The increased serum parathyroid hormone normalizes serum phosphorus level until GFR drops below 20–30 (19). A dietary phosphorus restriction of 800–1000 mg/day decreases PTH levels and may reduce bone resorption in those patients with elevated PTH. Patients with hyperphosphatemia frequently receive calcium-containing phosphate binders, which can contribute to hypercalcemia or elevation of the serum calcium-phosphorus product. The National Kidney Foundation recommends that serum calciumphosphorus product be maintained at Effects of chronic protein-calorie malnutrition on the kidney Protein-calorie malnutrition is a widespread public health problem that contributes considerably to mortality and morbidity in areas where it is prevalent [1, 2]. A look at the world distribution of protein-calorie malnutrition indicates that the areas most affected are those countries where large proportions of the population are living under conditions of limited social and economic development [11. The United States has considered itself one of the best-fed nations of the world. While this may be true, its attitude of self-satisfaction was challenged seriously by findings reported recently by the National Nutrition Survey [3]. Many persons, particularly among the lower income groups, were found to be malnourished. The growth of children under six years of age was below desirable standards in a number of areas. A high incidence of iron deficiency anemia was observed in infants and young children and in women during their reproductive years. Protein-calorie malnutrition is more than a medical problem. Social, cultural and economic factors are involved. In underdeveloped countries, it results from two main factors: a diet that is quantitatively and qualitatively inadequate plus superimposed stress, usually of infectious origin [4]. A deficient diet results, in turn, from varying combinations of low food production, inadequate preservation and distribution of foods, restricted purchasing power, poor food habits and deficient knowledge of the relation between diet and health. Excessive incidence of infectious disease is a consequence of poor environmental conditions, inadequate knowledge of epidemiologic factors, poor personal hygiene and insufficient health services. These factors are interrelated and act synergistically to the detriment of nutritional status. The clinical result depends on many determinants: on the severity and duration of the nutritional deficiencies of protein and calories, on the relative importance of the deficiency of protein to that of calories, on the nature and severity of other associated nutritional deficiencies, on the age of the person affected and on the presence of other complications. The mild and moderate forms occurring in children, frequently unrecognized and misinterpreted, are primarily characterized by inadequate growth and development. In adults, malnutrition reduces weight, performance and resistance to infection [4]. © 1973, by the International Society of Nephrology. 129 Before describing the changes in renal structure and function which occur in malnourished humans or animals, it is crucial to appreciate that at this stage of our knowledge it is very difficult to determine which changes reflect a direct deleterious effect of malnutrition on the kidney and which represent an adaptation by the kidney to the nutritional insult. The former state implies a pathological change, the latter a physiologic response. Renal function in malnutrition While a great deal has been written regarding the consequences of renal functional disturbances on the composition of the internal environment and nutrition, much less has been published about the effect of nutritional disturbances on renal function. Investigators in the past have implied that the kidneys are substantially "normal" in malnutrition. The bases for such conclusions are certain observations about which there is no disagreement: 1) malnourished subjects produce urine that is generally free of protein, glucose and formed elements such as casts, red blood cells, etc.; and 2) the blood of these individuals does not exhibit characteristics which tend to appear in renal insufficiency—that is, the levels of blood urea nitrogen, creatinine and other materials which tend to accumulate in renal failure are not elevated [5]. Such negative evidence, however, neither proves the full normality of the kidneys nor provides a picture of the actual renal function in chronic protein malnutrition. In the literature of childhood malnutrition, on the other hand, there is frequent mention of the abnormalities of water and electrolyte metabolismwhich occur, and it seems likely that the kidney plays a major role in initiating and prolonging these abnormalities. Reports of studies on renal function in childhood malnutrition are scarce, though suggestive of significant functional disturbances [6—8]. For the past few years, we have studied the effects of chronic protein malnutrition on renal function in experimental animals, in children from Jamaica and in adult subjects