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Protein restriction

Dietary and phosphorus-containing medication restriction ° Protein restrict to 0.6-0.8 g/kg/d... [Pg.175]

In acute hepatic encephalopathy, temporary protein restriction to decrease the rate of ammonia production can... [Pg.331]

Reduction in dietary protein intake has been shown to slow the progression of kidney disease.8 However, protein restriction must be balanced with the risk of malnutrition in patients with CKD. Patients with a GFR less than 25 mL/minute/ 1.73 m2 received the most benefit from protein restriction 8 therefore, patients with a GFR above this level should not restrict protein intake. The NKF recommends that patients who have a GFR less than 25 mL/minute/1.73 m2 who are not receiving dialysis, however, should restrict protein intake to 0.6 g/kg per day. If patients are not able to maintain adequate dietary energy intake, protein intake maybe increased up to 0.75 g/kg per day.15 Malnutrition is common in patients with ESRD for various reasons, including decreased appetite, hypercatabolism, and nutrient losses through dialysis. For this reason, patients receiving dialysis should maintain protein intake of 1.2 g/kg per day to 1.3 g/kg per day. [Pg.378]

Successful management of urea cycle defects involves a low-protein diet to minimize ammonia production as well as medications that enable the excretion of ammonia nitrogen in forms other than urea. Protein restriction is the mainstay of therapy. In patients with severe disease, tolerance for dietary protein may be so limited that it is not possible to support growth. [Pg.680]

Dietary protein restriction (see Fig. 76-3), lipid-lowering medications, smoking cessation, and anemia management may help slow the rate of CKD progression. [Pg.875]

Dietary protein has long been thought to play a role in the progression of chronic renal disease, but clinical trials have not consistently shown that dietary protein restriction is beneticial. A meta-analysis including the Modification of Diet in Renal Disease (MDRD) Study, of 1413 patients from 1966 to 1994 showed that dietary protein restriction slows the progression of both diabetic and non-diabetic renal disease (see Klahr et al., 1994). It is advisable to restrict protein intake moderately to 1 g/kg daily. [Pg.611]

Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek HW et al. The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. Modification of diet in Renal Disease Study Group. N Engl J Med 1994 330 877-84. [Pg.618]

Heparin-Sepharose Nucleic acid-binding proteins, restriction endonucleases, lipoproteins... [Pg.103]

Sanjuijo P., Ruiz J. I., and Montejo M. (1997). Inborn errors of metabolism with a protein-restricted diet effect on polyunsaturated fatty acids. J. Inherited Metab. Dis. 20 783-789. [Pg.238]

Renal failure has a long history of treatment with protein-restricted diets. Dietary plant protein is a possible therapy mechanism for the treatment of chronic and acute renal failure. [Pg.107]

Ml. Maschio, G., Oldrizi, L, Rugiu, C., and Loschiavo, C., Serum lipids in patients with chronic renal failure on long-term, protein-restricted diets. Am. J. Med. 87, 51N—54N (1989). [Pg.214]

Patients with hyperphenylalaninemia and phenylketonuria consuming a protein-restricted diet have decreased blood plasma TAC (by about 14%) (V3). Blood plasma TAC was significantly lower in subjects with severehyperhomocysteinemia compared with their parents and healthy control subjects (M24). [Pg.262]

The protein restricted mice also expired less CO from labeled DMH than their counterparts fed 40% protein. Using expired 1tC02 as an index of potential genetic toxicity, the burden of... [Pg.299]

The mainstay of therapy in biotinidase deficiency is biotin supplementation. To date, all symptomatic children with biotinidase deficiency have improved after treatment with 5 to 10 mg of biotin per day. Biotin appears to be required in the free form as opposed to the bound form. This is based on the findings of two children who were fed yeast as a form of therapy. Neither improved because essentially all of the biotin in yeast is protein bound, and these children could not recycle the biotin. These children, however, did improve when treated with free biotin. Treatment with biotin is essential and sufficient to prevent or resolve the symptoms. It is not necessary to treat children with biotinidase deficiency with protein-restricted diets as it is in some of the isolated carboxylase deficiencies because with biotin therapy all the carboxylase activities are normal. Symptoms of biotinidase deficiency are preventable if patients are diagnosed and treated at birth or before symptoms occur. [Pg.142]

Question How is the production of a tissue-specific protein restricted to that one tissue since the gene is present in the nucleus of all cells. [Pg.496]

Benzoate, phenylacetate, and arginine would be given to supply a protein-restricted diet. Nitrogen would emerge in hippurate, phenylacetylglutamine, and citrulline. [Pg.1489]

Suppression of bowel flora is thought by some to be useful in hepatic encephalopathy. Here, absorption of products of bacterial breakdown of protein (ammonium, amines) in the intestine lead to cerebral symptoms and even to coma. In acute coma, neomycin 6 g/d should be given by gastric tube as prophylaxis, 1-4 g/d may be given to patients with protein intolerance who fail to respond to dietary protein restriction (see also lactulose, p. 640). [Pg.246]

The cirrhosis patient is in a vicious circle regarding protein metabolism cirrhosis hepatic encephalopathy protein restriction malnutrition catabolism Thus, prolonged protein restriction and catabolism may considerably worsen the prognosis of cirrhosis. In this hazardous situation, the dietary and therapeutic use of branched-chain amino acids (BCAA), i.e. valine, leucine and isoleucine, is a logical therapeutic intervention. [Pg.861]

In treating the uremic patient with the protein-restricted diet, would you use a protein of high or low biological value ... [Pg.478]

Zamenhof, S., Mariheus, E. V, and Grauel, L. 1971), DNA cell number) and protein in neonatal rat brain Alteration by timing of maternal dietary protein restriction. /. Wutr. 101,1265-1270. [Pg.487]


See other pages where Protein restriction is mentioned: [Pg.202]    [Pg.111]    [Pg.113]    [Pg.331]    [Pg.1518]    [Pg.49]    [Pg.312]    [Pg.56]    [Pg.296]    [Pg.21]    [Pg.610]    [Pg.611]    [Pg.210]    [Pg.300]    [Pg.31]    [Pg.88]    [Pg.43]    [Pg.202]    [Pg.203]    [Pg.128]    [Pg.31]    [Pg.213]    [Pg.963]    [Pg.1890]    [Pg.733]    [Pg.489]   


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