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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chronically uremic rat has been used as a model to study amino acid metabolism in uremia. Uremic rats fed low protein diets (6% casein) survived longer than uremic rats receiving either higher levels of dietary protein or a low protein diet supplemented with a mixture of nonessential amino acids. Alterations in plasma amino acid levels were observed in the uremic rats and were similar to those found in patients with renal failure. Plasma concentrations of citrulline, free tryptophan, glycine and the methylhistidines were increased and levels of serine, ornithine, lysine, total tryptophan, tyrosine, and the tyrosine-phenylalanine ratio were reduced. The metabolic basis of the altered tyrosine-phenylalanine ratio in plasma was studied. Tyrosine aminotransferase (TAT) and phenylalanine hydroxylase (PHL) activity were normal in the liver, but renal PHL activity of was decreased as compared to control rats. Tissue concentrations of citrulline were also found to be raised in liver and muscle of uremic rats. The activity of ornithine transcarbamoylase, was reduced in the liver and arginine synthetase activity was decreased in the kidneys of uremic rats. Thus elevated citrulline levels in uremic tissue appear to be caused by a decrease conversion of citrulline to arginine in the kidney. Preliminary studies of tryptophan metabolism in uremic rats have shown elevated brain levels of 5-hydroxyindoleacetic acid and increased hepatic tryptophan oxygenase activity. Increased plasma amine levels were associated with altered activities of monoamine oxidase and diamine oxidase in kidney and other tissues.
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PMID:Amino acid metabolism in the chronically uremic rat. 23 43

Essential amino acids, found in abundance in high-quality dietary protein, are required daily by hospitalized patients and healthy persons to maintain the dynamic process of protein metabolism. One method for assessing dietary protein quality is by determining a diet's chemical score, ie, the ratio of a gram of the limiting amino acid in a test diet to the same amount of the corresponding amino acid in a reference diet (eg, whole-egg protein) multiplied by 100. This investigation used the chemical score to evaluate the protein quality of 9 parenteral and 17 enteral diets commonly used to feed hospitalized patients. Standard parenteral and enteral products (ie, formulas that had not been designed for patients with a specific disease state) had chemical scores that ranged from 46% to 70%. Limiting amino acids were either methionine (plus cysteine) or phenylalanine (plus tyrosine). Products designed for patients with renal failure had the highest scores, which ranged from 85% to 145%. Products that were enriched with branched-chain amino acids for trauma patients had scores that ranged from 38% to 73%. The only product available for patients with pulmonary compromise had a score of 50%. The lowest scores, which ranged from 5% to 13%, were found in products for patients with hepatic failure. All products, except those with chemical scores below 13%, may be fed in relatively small amounts of protein (7 to 33 g) to satisfy the minimum daily requirements of essential amino acids, although such levels would not meet minimal daily nitrogen requirements. We recommend that dietitians use the chemical score to assess the protein quality of parenteral and enteral diets.
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PMID:A chemical score to evaluate the protein quality of commercial parenteral and enteral formulas: emphasis on formulas for patients with liver failure. 190 41

The effect of chronic renal failure (CRF) on the pattern of plasma free amino acid concentrations was studied in 22 healthy controls (group 1); 43 CRF patients of which serum creatinine levels were 2-4.9 mg/dl (group 2, n = 11), 5-10 mg/dl (group 3, n = 10), more than 10 mg/dl (group 4, n = 9), and chronically hemodialysed patients (group 5, n = 13). In all renal failure groups, plasma concentrations of eight free essential amino acids-isoleucine, leucine, lysine, methionine, threonine, tryptophan, tyrosine and valine and those of three non-essential amino acids-alanine, glutamate and serine were significantly lower than those in controls. Plasma concentrations of free arginine, cystine, glutamate and serine were significantly higher in CRF patients. Patterns of change of plasma aminogram were similar among CRF patients regardless of the stages of renal function or dialytic treatment. Stepwise changes of some plasma free amino acids were observed as renal function became worse. The molar ratios of plasma free valine/glycine, serine/glycine and tyrosine/phenylalanine were decreased accordingly. Our study confirms the presence of abnormal plasma aminogram, specifically that of essential amino acids, in CRF. Therapeutic intervention is warranted but still needs further investigations.
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PMID:Plasma amino acid patterns in normal Thais and in patients with chronic renal failure. 194 Jul 7

We describe a rat model of renal failure that separates catabolic and anabolic states from each other. Muscle protein synthesis was compared during the anabolic period between sham (S) operated and renal failure (RF) rats that were fed different levels of dietary protein. Male rats weighing between 60 and 80 g first had a partial left nephrectomy and then were given a tryptophan deficient diet from four to six days to induce weight loss. On the second day of the diet either a renal decapsulation (S rats) or a simple right nephrectomy (RF rats) was done to enhance the catabolic response in both and to induce renal failure in the RF rats. Following the period of feeding the deficient diet, both groups were fed a nutritionally complete 14, 17, 20 or 30% protein diet for three to five days. This induced a brisk anabolic response as measured by weight gain. Differences in body weight between the S and RF rats after three to five days on the repletion diet generally was less than 10%. The rats then were fasted overnight, fed a standard meal and muscle protein synthesis (Sm%) was measured two hours post-feeding. Sm% was estimated from the incorporation of 3H phenylalanine (PHE) into muscle 10 minutes following the i.v. injection of 3HPHE (25 muCi/100 g body wt) with carrier PHE to flood all the precursor amino acid pools. Weight loss in the catabolic phase was greater and the net weight gain for the two phases was less in the RF group. Overall, renal failure resulted in a significant reduction in Sm% (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of reduced renal function and dietary protein on muscle protein synthesis. 206

The concentration of 18 alpha-amino acids (AAs) in plasma and renal cortical cell water were measured 3 or 24 hr after 1 hr of unilateral renal artery clamping or 24 or 48 hr after 15 mg/kg body weight HgCl2 injection sc as a test of epithelial integrity. Cellular glycine (Gly), hydroxyproline (Hpr), ornithine (Orn), phenylalanine (Phe), serine (Ser), and tryptophan (Trp) concentrations were depressed 24 hr after HgCl2 (p less than 0.05), but the remaining 12 AAs were not distinguishable from control despite the presence of severe renal failure. ARginine (Arg), glutamic acid (Glu), and valine (Val) also were decreased (P less than 0.05) 24 hr later, but concentrations of half of all measured AAs were still normal. Cellular alanine (Ala), Arg, Glu, Gly, Phe, and Ser concentrations were decreased 3 hr after ischemia, p less than 0.05, but 12 AAs were unchanged and only Arg, Phe, Ser, and threonine (Thr) were reduced 24 hr after ischemia was reversed. Concentrations of even the most affected AAs remained notably higher than in plasma in both forms of acute renal failure (ARF). Total loss of AAs from a small proportion of tubular cells would be hidden by essentially normal concentrations in the rest, and such losses may well have occurred. Unless cellular AAs in ARF are almost completely bound, however, the well-maintained cell:plasma AA concentration ratios indicate that cellular energetics were adequate for AA uptake and that epithelial permeability to AAs in the vast majority of cells was not greatly disturbed. Such findings suggest that most of the epithelium, although seriously damaged, had remained viable.
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PMID:Renal epithelial amino acid concentrations in mercury-induced and postischemic acute renal failure. 221 14

A patient with chronic renal failure was investigated after complaining of oral discomfort which was found to be due to macroglossia and generalized involvement of the oral soft tissues by amyloidosis. A search for multiple myeloma proved to be positive. She also had a previous history of Carpal-tunnel syndrome. Despite an initial good response to treatment with phenylalanine nitrogen mustard (melphalan hydrochloride), she finally succumbed to end-stage renal failure.
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PMID:Amyloidosis with oral involvement. Case report. 232 67

Several lines of evidence suggest that tyrosine formation is impaired in renal failure. The concentration of tyrosine is decreased and the phenylalanine/tyrosine ratio is increased in plasma and in skeletal muscle cells. After an oral or intravenous load, the rise of plasma phenylalanine is augmented, the clearance is decreased, oxidation is diminished and the corresponding rise of plasma tyrosine level is blunted. Tyrosine elimination and oxidation are not altered in uremia. The defect in tyrosine formation may be especially important in uremic patients on a low protein diet supplemented with tyrosine-free essential amino acid preparations and in subjects on artificial nutritional support. Thus, tyrosine should be regarded as a conditionally essential amino acid in renal failure and should be supplied exogenously, at least in these patient groups. Oral tyrosine supplementation was shown to replete plasma and intracellular pools and improve nitrogen balance in chronic renal failure patients on a low protein diet. However, because of poor solubility in aqueous solutions, tyrosine cannot be included in the free form in amino acid solutions for parenteral nutrition. To circumvent stability or solubility problems, tyrosine containing dipeptides and/or N-acetyl-tyrosine may serve as tyrosine sources for parenteral supply. Renal failure does not affect alanyl-tyrosine hydrolysis, and there is an immediate increase of plasma tyrosine concentration after peptide infusion. Elimination and hydrolysis of glycine-tyrosine is retarded in renal failure, but the clearance exceeds clinically relevant infusion rates. After infusion of N-acetyl-tyrosine, no increase in plasma tyrosine is seen, and the half-life N-acetyl-tyrosine is grossly prolonged in uremia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phenylalanine and tyrosine metabolism in renal failure: dipeptides as tyrosine source. 251 76

To examine granulocyte oxidative metabolism (GOM) quantitatively, we evaluated two methods, one for assaying luminol-dependent chemiluminescence (CL) and the other for changes in fluorescence by dichlorofluorescin (DCF). The CL assay was carried out using a lumiphotometer (TD-4000, Laboscience) after stimulating granulocytes in whole blood by n-formyl-methonyl-leucyl-phenylalanine (FMLP, 100 nmol/l) or by opsonized zymosan (OZ, 2 mg/ml). To reduce hemoglobin (Hb) interference, each sample was diluted with autologous plasma to a Hb concentration of 3 g/dl. The DCF assay was performed on whole blood samples (100 microliters) labeled with DCF (5 mumol/l) following stimulation by phorbol myristate acetate (PMA, 100 ng/ml). Changes in fluorescence were determined using a flow cytometer that gave the delta mean channel fluorescence intensity (DMCF) as an indicator of GOM. The coefficients of variance (CV) in within-run assays for the CL and the DCF were 10% and 5%, respectively. These CV-values were almost the same even when separated granulocytes as a test sample were used instead of whole blood. CL determined by FMLP stimulation in 27 renal failure patients on hemodialysis (HD), was significantly lower than that in 10 normal controls, but no difference was found in that determined by OZ stimulation. In HD patients, the DMCF values tended to increase in those at 15 min and the end of HD sessions compared to the value prior to HD. This suggested that the HD membrane and/or extracorporeal circulation stimulates GOM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Evaluation of leukocyte oxidative metabolism using whole blood samples by chemiluminescence and flow cytometric assays]. 260 54

The uremic syndrome is multifactorial, and affects most tissues and organs. Disturbances in protein and amino acid metabolism may play important roles, especially in chronic uremia, either directly or by production of toxic metabolites, with resultant negative nitrogen (N) balance, muscle wasting, reduced protein synthesis, and characteristically abnormal intracellular free amino acid concentrations. There are also grossly abnormal amino acid levels in the plasma of uremic patients, e.g., increases in conjugated amino acids, high levels of several nonessential and low levels of essential amino acids. The ratios of tyrosine/phenylalanine and of valine/glycine are decreased. The low tryptophan levels may contribute to encephalopathy as a result of an imbalance in neurotransmitter synthesis. Citrulline is found in excess; the explanation is unresolved. There are elevated concentrations of the sulfur-containing amino acids: cystine, taurine, cystathionine, and homocysteine. Excess of the latter is implicated in the atherogenesis of renal failure. Disturbed metabolism and interorgan exchange of amino acids in the uremic state explains some of the abnormalities in tissue and plasma concentrations of individual amino acids. Enzymatic defects are involved in the disturbed metabolism of branched chain amino acids (BCAA), with possible antagonism among them, which impairs growth and amino acid utilization. Carbohydrate intolerance, associated with insensitivity of peripheral tissues to insulin and hyperinsulinemia, elicits decreased plasma BCAA. Protein synthesis rates in normal and pathological conditions are more closely related to the intracellular amino acid pool than to plasma amino acid levels. Concentrations of individual amino acids in the plasma pool are poor indicators of their intracellular concentrations. Muscle contains the largest pool of protein and free amino acids in the body. In chronic renal failure patients, the intracellular concentrations of valine, threonine, lysine, and carnosine are low. With low protein diets and in hemodialysis, serine, tyrosine, and taurine often are also low. The low taurine may be related to fatigue and to uremic cardiomyopathies. The commonly used amino acid supplements generally fail to correct the intracellular amino acid deficits. A "New Formula" has been developed to correct these intracellular amino acid abnormalities, and to supplement a low protein diet. It provides more valine than leucine, increased tyrosine and threonine, and less histidine, leucine, isoleucine, lysine, methionine, and phenylalanine than in formulas customarily used for patients with chronic renal failure. It is uncertain whether other ap
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PMID:Amino acid metabolism in uremia. 267 58

A randomized, double-blind study was conducted to determine the possible effects of aspartame on the plasma amino acid profiles of 23 diabetic patients with renal failure who were undergoing maintenance hemodialysis. Subjects were given a single dose of 10 mg aspartame/kg (approximately equivalent to 25 packets of Equal [NutraSweet Consumer Products, Inc, Chicago, IL] or the amount of phenylalanine in a 300-mL glass of milk) or a placebo in a crossover study design. Three postdialysis blood samples were drawn just before and 1 and 2 h after aspartame or placebo consumption. After aspartame consumption statistically significant increases in only two amino acids, phenylalanine and tyrosine, were noted at 1 and 2 h when compared with placebo values. The increases in phenylalanine were within the normal postprandial range for healthy subjects; no other increases in essential or nonessential amino acids, except for tyrosine, were detected. This study supports the view that aspartame is safe for diabetic subjects with chronic renal failure.
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PMID:Effect of aspartame on plasma amino acid profiles of diabetic patients with chronic renal failure. 272 70


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