Medical nutrition therapy when kidney disease meets liver failure.
Hyperammonemia and Protein
Protein restriction and the use of oral or enteral formulas enriched in branched chain amino acids but low in aromatic amino acids are frequently the MNTs chosen in ESLD, however, they are not the most current or effective clinical practice (Krentisky, 2003; Mizock, 1999). Urea cycle activity declines as functional liver mass is lost. Ammonia clearance is reduced when the liver is bypassed by portacaval shunting. Hyperammonemia occurs, but can be readily controlled with anti-encephalopathic medications. Metronidazole and neomycin reduce the ammononiagenic gut flora. Lactulose is metabolized by gut bacteria to products that acidify the gut lumen and convert ammonia to unabsorbable ammonium ion. Dosing lactulose to produce 2 to 4 loose stools per day should prevent hyperammonemia and related hepatic encephalopathy (HE) (Riordan & Williams, 1997). Frequent stooling can interfere with dialysis treatments, leading to noncompliance with lactulose and elevated ammonia levels, however, if dosing of these anti-encephalpathic medications is adequate and compliance is good, protein restriction is seldom needed. Recommended protein intake is in the range of 1.0 to 1.5 gm/kg of dry weight (Krentisky, 2003; Mizock, 1999). Once HE has become refractory to medications or a portacaval shunt must be placed, then protein should be restricted to 0.8 gm/kg of dry weight (Krenfisky, 2003; Riordan & Williams, 1997).
Protein should be consumed in small amounts over the course of the day. Avoiding the consumption of large protein portions at any one time will prevent, overwhelmingly, a urea cycle with limited capacity resulting in hyperammonemia. Other situations that lead to heightened protein catabolism, such as bleeding or sepsis, will also elevate ammonia and should be considered as potential culprits along with diet and medication noncompliance whenever HE unexpectedly occurs (Mizock, 1999).
Oral and enteral formulas that have been enriched in branched chain amino acids (BCAA) and reduced in aromatic amino acids (AAA) are costly and unpalatable. The benefit of these formulas is controversial. High BCAA/low AAA formulas may be most beneficial when HE occurs with a standard oral or enteral formula after sepsis, bleeding, and medication noncompliance has been ruled out. When HE is controlled by medications, the 2 kcal/ml oral supplements designed for patients on dialysis work well. These products provide a concentrated source of protein and calories, especially when ascites-related early satiety is present.
To limit gluconeogenesis and spare protein in ESLD adequate caloric intake is essential. Glycogen synthesis is severely impaired, while hepatic and muscle glycogen stores are exhausted. A sufficient caloric intake is crucial to limit the utilization of BCAA in gluconeogenesis which leads to muscle wasting. Small frequent feedings are important in an attempt to avoid the fasting state. Bedtime snacks are encouraged. An overnight fast in ESLD can be equivalent to a 72-hour fast in an individual with normal hepatic function. An intake of 30 to 35 kcal/kg of dry weight advised for the population on dialysis is also the goal for ESLD (McCann, 2002).
However, aggressive caloric repletion where significant malnutrition is present can lead to refeeding syndrome. In the malnourished patient with ESLD requiring dialysis, feedings should be initiated at 15 to 20 kcal/kg dry weight. Potassium, phosphorus, and magnesium should be closely monitored and any deficits corrected before caloric intake is advanced.
Cholestatic liver disease (CLD) often leads to fat mal-absorption, compromising caloric intake and producing progressive weight loss. With a low bile flow, long chained fatty acids are not absorbed resulting in steatorrhea. Oral or enteral formulas should be chosen that contain medium chained triglycerides (MCT) as 50% or more of the total fat. MCTs are readily absorbed in the absence of adequate bile flow and can provide calories that can help to stabilize weight loss.
Sodium, Potassium, and Phosphorus
To control ascites in ESLD, sodium may be limited to 4 grams per day or less but may be liberalized when oral intake is poor (Krentisky, 2003; Li et al., 2000). If dialysis is initiated, sodium restriction is only required as necessary to control thirst, blood pressure, and intradialytic weight gains.
If the diet is well tolerated, potassium and phosphorus are restricted as per the usual renal diet recommendations. Phosphorus binders are usually needed. Some individuals with ESLD who require dialysis, especially those with ALD-associated ESLD who continue to consume alcohol, are at risk for potassium and phosphorus depletion despite renal failure. Predialysis potassium and phosphorus blood levels should be closely monitored in these individuals. Their diets and/or dialysis regimes should be adjusted accordingly. Supplemental intravenous phosphorus may be necessary, especially when predialysis serum phosphorus is less than 2.0 mg/dl.
Vitamins and Zinc
Folate deficiency is common to ALD-associated ESLD and will worsen with dialysis losses if supplemental folate is not provided. Alcohol impairs folate absorption. Hepatic methionine metabolism is inhibited without sufficient folate and can produce additional liver damage (Halsted, Villanueva, Devlin, & Chandler, 2002). The best choices among available renal vitamins for patients with ALD-associated ESLD on dialysis are those containing at least 1 mg of folate.
Vitamin [B.sub.12] levels are often noted to be elevated in ESLD as a consequence of leakage from hepatocellular damage. This does not represent a vitamin [B.sub.12] excess (Baker, Frank, & DeAngelis, 1987). Vitamin [B.sub.12] should be continued to avoid neurological injury as folate is also part of routine water soluble vitamin replacement for those requiring dialysis.
Cholestatic liver disease produces fat soluble vitamin malabsorption. The hypervitaminosis A that occurs in kidney failure may help to counter the vitamin A malabsorption that occurs in CLD. Actual vitamin A status in ESLD with dialysis dependency may be difficult to discern. A serum vitamin A level may not correctly portray vitamin A status given the decline in hepatic protein synthesis, including retinol binding protein with ESLD as well as the additional negative impact of any inflammation. When dietary intake of vitamin A is less than two-thirds of the Dietary Reference Intake (DRI), supplemental vitamin A at the level of the DR[ should be initiated in patients on dialysis (Chazot & Kopple, 1997).
Osteoporosis occurs with CLD and is associated with low levels of 25-hydroxy vitamin D despite the use of water miscible forms of vitamin D. Intravenous calcitriol is used to treat osteoporosis with success in CLD (Shiomi et al., 1999). For the patient who is dialysis dependent and has CLD, intravenous calcitriol or paricalcitol given for the control of renal osteodystrophy may also ameliorate CLD-related osteoporosis. Doxercalciferol is not indicated in ESLD as sufficient hepatic mass may not be present to complete the conversion to calcitriol.
Zinc deficiency occurs with ESLD and is related to poor oral intake as well as diuretic losses that are often no longer incurred once dialysis is necessary (Krenfisky, 2003). When protein intake is adequate and significant gastrointestinal losses are not present, supplemental zinc is not indicated. If protein intake is marginal and/or gastrointestinal losses are consistently noted, then 15 mg/day of supplemental zinc may be beneficial.
When dialysis dependency is complicated by ESLD, there must be a blending of two dietary and medication regimes. A more adequate protein intake is possible with compliance to anti-encephalopathic medications. Depletion of electrolytes, minerals and some vitamins can occur with malnutrition and/or chronic alcoholism. This scenario represents a special challenge to the physician, dietitian, nurse, and social worker in working towards a good quality of life for the patient but can be successfully managed through careful monitoring and teamwork.
Baker, H., Frank, O., & DeAngelis, B. (1987). Plasma vitamin B12 titres as indicators of disease severity and mortality of patients with alcoholic hepatitis. Alcohol and Alcoholism, 22(1), 1-5.
Chazot, C., & Kopple, J. (1997). Vitamin metabolism and requirements in renal disease and renal failure. Baltimore: Williams and Wilkins.
Halsted, C.H., Villanueva, J.A., Devlin, A.M., & Chandler, C.J. (2002). Metabolic interactions of alcohol and folate. Journal of Nutrition, 132(Suppl. 8), 2367S-2372S.
Krentisky, J. (2003). Nutrition for patients with hepatic failure. Practical Gastroenterology, 6, 23.
Li, S.D., Lue, W., Mobarhan, S., Nadir, A., Van Thiel, D.H., & Hagerty, A. (2000). Nutrition support for individuals with liver failure. Nutrition Reviews, 58(8), 242-247.
McCann, L. (2002). Pocket guide to nutrition assessment of the patient with chronic kidney disease (3rd cd.). New York: National Kidney Foundation.
Mizock, B.A. (1999). Nutritional support in hepatic encephalopathy. Nutrition, 15(3), 220-228.
Riordan, S.M., & Williams, R. (1997). Treatment of hepatic encephalopathy. New England Journal of Medicine, 337(7), 473-479.
Shiomi, S., Masaki, K., Habu, D., Takeda, T., Nishiguchi, S., Kuroki, T., et al. (1999). Calcitriol for bone loss in patients with primary biliary cirrhosis. Journal of Gastroenterology, 34(2), 241-245.
Ann Beemer Cotton, MS, RD, CNSD, is Clinical Dietitian Specialist, Methodist Hospital, Indianapolis, IN.
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|Title Annotation:||Issues in Renal Nutrition: Focus on Nutritional Care for Nephrology Patients|
|Author:||Cotton, Ann Beemer|
|Publication:||Nephrology Nursing Journal|
|Article Type:||Clinical report|
|Date:||Nov 1, 2007|
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