Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acid stable trypsin inhibitor (ASTI), with a molecular weight of about 85,000 by gel filtration, specific activity of 1,498 U/mg protein and pI of 1.6, from renal failure patient plasma was first purified. The amino acid composition of the purified ASTI was found to be that of a Gly- and Glu-rich protein which lacked His, closely resembling that of urinary trypsin inhibitor. The NH2-terminal amino acid sequence was Ala-Val-Leu-Pro-Gln-Glu- Glu-Glu-Gly-X-Gly-Gly-Gly-Gln-Leu-Val-Thr-Glu-Val-Thr-Lys-Lys-Glu- Asp-Ser-Ser-Gln-Leu-Gly-Tyr-Ser-Ala-Gly-Pro.
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PMID:Purification and amino acid analysis of plasma acid stable trypsin inhibitor. 378 Jun 58

Patients with varying degrees of renal failure were studied for their blood lactate response to exercise on either a treadmill or a bicycle ergometer. In the group exercised on a treadmill, blood lactate and alanine levels were measured, and in the group exercised on the bicycle ergometer blood lactate levels and oxygen uptake were measured. In both groups regardless of the method of exercise or the degree of azotemia, a rapid rise in blood lactate similar to that previously reported with exercise was observed. Blood alanine levels, which were low in subjects with renal disease, did not change with exercise even with a rise in blood lactate levels. There was no difference in the oxygen uptake between normal controls and subjects with renal disease. We conclude that blood alanine levels are low in renal disease, and that with the degree of exercise studied the rise in blood lactate in patients with renal disease is not accompanied by a change in oxygen uptake and does not evoke a rise in blood alanine levels. The mechanisms for the abnormal rise in blood lactate in these patients does not appear to be due to anoxia.
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PMID:Oxygen uptake in exercising subjects with minimal renal disease. 402 16

Concentrations of N-acetyl-beta-D-glucosaminidase (NAG), alanine-amino-peptidase (AAP) and beta-2-microglobulin (beta 2M) were determined daily in the urine of 28 patients treated with gentamicin (2-3 mg . kg-1 . day-1) for a mean of 15 days. All had normal renal function. Increased activity in NAG and AAP was observed for all patients, either immediately or after 2 or 3 days of treatment. The results were compared with serum creatinine concentrations and urinary beta 2M levels. This study indicates a relationship between the nephrotoxicity of gentamicin and initial urinary enzymic activity(NAGi) prior to any treatment. The degree of NAG response during the first ten days of treatment appeared as a second prognostic factor. Renal failure was observed for one out of the 12 patients with normal NAGi (NAGi less than 200 mumol/day). Seven of them showed a marked enzyme activity response (greater than 1500 mumol/day) with an increase in beta 2M activity. Eleven out of the 16 patients with elevated NAGi (NAGi greater than 200 mumol/day) developed renal failure and showed an elevated maximal response. The concentration of AAP appears to be of little prognostic value. The variation in individual maximal urinary enzyme responses observed among the 28 patients during the first ten days of treatment points to the existence of individual sensitivities to gentamicin, the exact mechanism of which remains unclear.
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PMID:Predictive value of urinary N-acetyl-beta-D-glucosaminidase (NAG), alanine-aminopeptidase (AAP) and beta-2-microglobulin (beta 2M) in evaluating nephrotoxicity of gentamicin. 617 16

Plasma and muscle free amino acid analyses have been performed on four groups of children with different levels of renal failure. Mean plasma creatinine of the groups 1 to 4 was respectively 1.3, 2.3, 3.3, and 4.9 mg/100 ml. Significant but different alterations of plasma and muscle amino acid pattern were found in the four groups of patients. In plasma, aspartic acid, citrulline, OH-proline, 1- and 3-methyl histidine were regularly increased, while threonine, valine, phenylalanine, isoleucine, leucine, tryptophane, tyrosine, and tyrosine/phenylalanine ratio were generally decreased. In muscle, glutamine was usually increased and alanine, valine and valine/glycine ratio decreased; significant increase of total amino acid content was only noted in group 4. Some amino acid alterations became worse with renal failure such as 3-methylhistidine increase or tyrosine/phenylalanine decrease, but group 3 patients had the greatest number of individual amino acid alternations. This group of patients also had the highest protein intake. Relationship between growth velocity and muscle amino acid pattern was found, a poor growth rate was associated with an increase of nonessential and essential amino acids with the exception of valine.
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PMID:Plasma and muscle free amino acids in children at the early stages of renal failure. 739 67

The kinetic of essential amino acids as well as of histidine and alanine in bilateral nephrectomized rabbits was investigated during a 3 hours hemodialysis. Dialysis, elimination and incorporation rates into plasma proteins were determined for all applied amino acids. Total elimination rates of all the investigated amino acids varied. From 5.31% (leucine) to 75.51% (alanine) of the injected labelled amino acids were eliminated in the dialysate. There was an exponential decrease in the dialysis of essential amino acids and histidine during the period of investigation due to the high incorporation rate into plasma proteins. The kinetic of alanine was different due to a slow incorporation rate leading to a higher elimination rate. The fast incorporation of intravenously applied essential amino acids and histidine during dialysis demonstrates that the existing protein deficiency in renal failure can be influenced positively by infusion of amino acids.
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PMID:[Amino acid kinetics during hemodialysis]. 745 1

The impact of hepatic and renal failure on the metabolism of L-alanyl-L-glutamine (Ala-Gln) and glycyl-L-glutamine (Gly-Gln) was investigated in 11 healthy volunteers, five patients with liver cirrhosis, and six patients with chronic renal failure. The clearance (mL.kg-1.min-1) of Ala-Gln was significantly higher than that of Gly-Gln in all three groups. Renal failure significantly reduced clearances of both Ala-Gln and Gly-Gln (13.27 +/- 0.71 and 3.06 +/- 0.28) when compared with control values (21.68 +/- 1.21 and 7.08 +/- 0.38). Liver failure had no significant influence on the clearances of Ala-Gln and Gly-Gln (22.62 +/- 2.89 and 6.20 +/- 0.88). Liver failure delayed and renal failure almost abolished the increases in plasma concentrations of free amino acid residues after peptide injection. It is concluded that other organs can substitute for the peptide-clearing function of the liver, but not of the kidney. Kidney is the most important organ for the clearance of dipeptides and the release of amino acid residues into circulation. Our data show that clearance rates of both Ala-Gln and Gly-Gln are sufficient to avoid accumulation of either peptide if infused in the presently recommended doses. Both Ala-Gln and Gly-Gln could therefore be used as sources for glutamine in parenteral nutrition even in patients with chronic renal failure.
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PMID:Importance of liver and kidney for the utilization of glutamine-containing dipeptides in man. 808 85

We describe the case of a patient in end-stage renal failure due to primary hyperoxaluria type I (PH1) who started hemodialysis in 1977 and is still alive and active. The diagnosis of PH1 was first suspected after a bone biopsy performed in 1981 to investigate hyperparathyroidism. Oxalosis recurred as early as 3 months after transplantation in a cadaver kidney grafted in 1987; nevertheless, graft function remained good enough to make possible the discontinuation of dialysis treatment for 5 months and thereafter to have only 1 dialysis a week for 17 months. The diagnosis of PH1 has been recently confirmed despite the patient being already anuric by means of the determination of plasma oxalate and glycolate levels as well as by determining hepatic alanine:glyoxylate amino-transferase.
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PMID:Long-term survival on renal replacement therapy for primary hyperoxaluria type I. 845 Sep 16

Primary hyperoxaluria type 1 (PH1) is a rare recessive autosomal inborn error of glyoxylate metabolism leading to oxalate retention, the first target of which is the kidney. The disease is caused by a defect of the liver-specific peroxisomal enzyme alanine: glyoxylate aminotransferase. Patients with pyridoxine-resistant forms of PH1 usually require organ replacement therapy, i.e. liver transplantation to supply the deficient enzyme and/or kidney transplantation to replace the affected organ. The current experience of the management of PH1 has emphasized two main points: (1) end-stage renal failure must be avoided since it increases dramatically the risk of systemic involvement, (2) the correction of oxalate overproduction and organ overload requires the removal of the host liver. Practical attitudes towards these ideas are difficult to assess and an individualized strategy is therefore required. Isolated kidney transplantation should be limited to adult patients with late-onset and a mild course of the disease. The present experience of combined liver-kidney transplantation was gained mainly in adult patients with severe systemic involvement; the 3-year patient survival rate recently increased to 82%. This figure might be improved if the procedure were performed earlier while the glomerular filtration rate (GFR) is above 25 ml/min per 1.73 m2. Isolated liver transplantation should be considered in carefully selected children with severe forms of pyridoxine-resistance (PH1) before GFR has dropped to less than 30 ml/min per 1.73 m2; it seems to be indicated especially in the presence of a rapid decline of GFR in the preceding year.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Should liver transplantation be performed before advanced renal insufficiency in primary hyperoxaluria type 1? 835 94

Primary hyperoxalurias are inborn errors of metabolism with recessive autosomal transmission. Type 1 is due to the deficiency of the hepatic-specific peroxisomal enzyme alanine: glyoxylate aminotransferase, and type 2 to that of the glyoxylate reductase/D-glycerate dehydrogenase, present in the cytosol of hepatocytes and leucocytes. Type 3 is due to increased intestinal absorption of oxalate of unknown pathophysiology. In the 3 types, increased oxalate load may lead to systemic oxalosis when glomerular filtration rate decreases below 30 ml/min/1.73 m2, calcium oxalate saturation occurring in plasma when oxalate level approximates 50 mumol/l. High fluid intake and long-term co-administration of pyridoxine and orthophosphate could perhaps efficiently prevent renal failure in a majority of patients. However, combined liver-kidney transplantation presently constitutes the most adequate therapy of end-stage renal failure in type 1 and perhaps in type 2 hyperoxaluria.
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PMID:[Primary hyperoxaluria]. 852 46

The objective of this work is to study the relation between the variations of the plasmatic aminogram, and the nutritional state of the patient with chronic kidney failure on hemodialysis. We studied 79 patients with chronic kidney failure undergoing hemodialysis treatment, with and evolution of 46 +/- 37 months. They were subjected to a dietary questionnaire, and anthropometric study after dialysis (body mass index, triceps skin fold, muscular circumference of the arm), and determination of the levels of serum amino acids after a pre-dialysis nocturnal fast half way through the week, and finally a record is made of the number of times each patient was hospitalized in the 6 months prior to the study. In the amino acids with a pyruvate origin, there is a significant reduction of alanine (p: 0.002), serine (p: 0.004), and methionine (p: 0.001), and a significant increase of glycine, cystathionine, and cystine (p: 0.0001), with the Glycine/Serine coefficient being elevated (p: 0.001). All amino acids with a ketoglutarate origin are increased significantly (p < 0.007), except glutamine which is decreased (p: 0.0009), and arginine which does not show any significant differences. The essential amino acids are decreased in relation to the non-essential ones (p: 0.0001), although if they are compared with the normal values, only threonine is decreased (p: 0.001). Of the rest, histidine, isoleucine (p: 0.0001) and phenylalanine (p: 0.001) are significantly increased. The tyrosine/phenylalanine coefficient is decreased (p: 0.001). The daily ingestion of protein is correlated negatively with alanine, proline, hydroxyproline, and aspartic acid. The anthropometric parameters are correlated positively with the branched amino acids, alanine and proline. Finally, the number of hospital admissions in the last 6 months, is correlated positively with valine, leucine, phenylalanine, and glutamic acid. In conclusion, we consider that the increase of the glycine/serine, phenylalanine/serine and non essential/essential coefficients, is related to alterations of the metabolism, intrinsic to the condition of uremia, while the alterations of the levels of branched amino acids is related to the nutritional condition of the patients.
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PMID:[Nutritional status and plasma amino acid levels in hemodialysis]. 859 19


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